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Register transfer level (RTL) development is a time cost step that requires high diligence and fidelity to get the valid interpretation of abstraction function of digital circuit. In this research, we introduce and prove that Model-Based Design Process (MBDP) is an effective and efficient way to develop a RTL complex system such as wireless communication. Using MBDP flow, we interpret, develop, and verify the physical layer RTL of a new standard that ratified on the end 2009, i.e. IEEE 802.11n wireless local area network (WLAN). The result of this research is a prototyping FPGA StratixII EP2S180 that has properly worked as a 2x2 MIMO WLAN with maximum throughput 144 Mbps.

It has been shown that hepatitis C virus (HCV) populations in vivo are composed of different but highly homologous HCV genomes (quasispecies) as shown in the hypervariable region (HVR) that exists in the N-terminal of the envelope 2 gene of HCV, and that the predominant sequence of the HVR of HCV genomes changes rapidly over time. To further investigate genetic backgrounds of the change in the HVR of HCV genomes, 45 plasma samples serially obtained from nine patients with chronic hepatitis C were studied using population-based analyses. Total RNA was recovered and the envelope gene containing the HVR was amplified by the reverse transcription and nested polymerase chain reaction. The amplified cDNA was examined by the single strand conformation polymorphism (SSCP) analysis. Furthermore, 43 HCV sequences, separated by the SSCP analysis from three patients were determined by the dideoxy chain termination method, and the phylogenetic analysis was performed using the neighbor joining method. The SSCP analysis demonstrated that HCV population within each individual were composed of 1 to 6 quasispecies. These quasispecies populations in vivo changed sequentially in eight of nine patients, Gradual selections of coexisting quasispecies were observed over 6- to 18-month periods in three patients, whereas complete replacements of previous quasispecies by new quasispecies were repeatedly observed over few-month intervals in five patients. The phylogenetic analysis on these quasispecies revealed the continuous accumulation of mutations in two patients and discontinuous appearance of evolutionarily distant quasispecies in one patient. These results indicate that HCV genomes in vivo form quasispecies populations, and that these quasispecies populations change during the natural course of chronic infection. Genetic mechanisms underlining the change of the HVR of HCV genome appear to be either continuous accumulation of mutations or selective overgrowth of preexisting minor variants from the large spectrum of quasispecies populations.

To investigate the correlation between the replication of hepatitis C virus in liver and the clinical and histopathological features, we detected and quantified plus and minus strands of HCV-RNA in plasma and in livers of patients with chronic hepatitis C by a quantitative polymerase chain reaction. RNA was extracted from the plasma and liver tissue of ten patients with biopsy-proven chronic hepatitis C. The plus and minus strands of HCV-RNA were detected by a strand-specific reverse transcription with either sense or anti-sense oligonucleotide primers deduced from the hepatitis C virus genome, and a standard HCV-RNA with an enzyme restriction site was used to quantify the amount of HCV-RNA. Both plus and minus strands of HCV-RNA were detected from the liver tissue of all patients included. The amount of plus-stranded HCV-RNA in the liver was 10 times higher than that of minus-stranded HCV-RNA. Plus-stranded HCV-RNA was detected in the plasma in all patients, while the minus strand was not detected in any patient. There was a weak correlation between the amount of both strands of HCV-RNA in the liver and that of the plus strand in plasma. There was no significant correlation between the amount of liver HCV-RNA and serum alanine transaminase and aspartate transaminase levels, or histopathological findings in the liver. The present method of detecting and quantifying liver HCV-RNA is simple and sensitive; it may be used to detect residual hepatitis C virus replication after the disappearance of plasma HCV-RNA in acute hepatitis or in chronic hepatitis after interferon treatment.

There is a hypervariable region in the envelope 2 gene of the hepatitis C virus genome, whose heterogeneity in different hepatitis C virus isolates has been suggested to be a result of the immune selection of escape variants. To determine the role of hypervariable region variants in the mechanism of resistance to interferon observed in 75-80% of interferon-treated patients with chronic hepatitis C, hypervariable region sequences were compared before and after interferon treatment. Eight patients with chronic hepatitis C were treated with recombinant interferon-alpha-2b. DNA containing the hypervariable region was obtained by reverse transcription-polymerase chain reaction from serial plasma samples of each patient and directly sequenced without cloning to determine changes in the predominant sequence. In two patients, hepatitis C virus-RNA was eliminated by interferon treatment. In the remaining six patients, hepatitis C virus-RNA was not eradicated. The predominant hepatitis C virus which survived interferon treatment was the mutant hepatitis C virus with 3-19 out of 81 nucleotide substitutions in the hypervariable region, resulting in 2-14 out of 27 amino acid changes. Most of the nucleotide substitutions were nonsynonymous, indicating that there were positive selections for amino acid changes in the hypervariable region. The change rate was significantly higher in patients whose plasma hepatitis C virus-RNA was consistently detectable during and after interferon treatment than in patients whose plasma hepatitis C virus-RNA became undetectable during treatment and reappeared after the cessation of the treatment (4.23 +/- 0.43 vs 0.77 +/- 0.20 x 10(-1)/site/year, p0.01). This suggests that the evolution of the hypervariable region was associated with the effect of interferon treatment. These results suggest that hypervariable region variants play an important role in maintaining persistent infection during interferon treatment by evading host immune surveillance.

To evaluate the clinical significance of sequence variations in the hypervariable region of hepatitis C virus during the course of chronic infection, we performed pairwise comparison of the predominant nucleotide sequences. Hepatitis C virus RNA was extracted from two plasma samples obtained from 12 chronically infected Japanese patients over approximately 1 yr. Complementary DNA containing the hypervariable region was amplified by means of reverse transcription-polymerase chain reaction and was directly sequenced for determination of predominant sequences. In all 12 individuals, the predominant sequence of the hypervariable region at the second time point differed from that at the first time point, and significant sequence variation was observed during this short period. A high proportion of these nucleotide substitutions (90%) resulted in changes of predicted amino acid sequences, indirect evidence of in vivo positive selection for these variants. There appeared to be an important difference in the rate of nucleotide sequence variation of the hypervariable region between four patients with flare-ups of their ALT levels (1.54 to 2.24 x 10(-1)/genome site/yr) and eight patients with quiescent courses (0.13 to 1.21 x 10(-1)/genome site/yr). These results demonstrate that rapid sequence variations of the hypervariable region of predominant virus population take place during the natural course of chronic hepatitis C virus infection. These sequence variations seem to occur as an adaptive response of hepatitis C virus to evade host immunity and may play a major role in the establishment of persistent infection and in the occasional flare-up of hepatitis.

We reported a case of asymptomatic pancreatic AVM, incidentally found on routine ultrasonography and diagnosed noninvasively by means of Doppler ultrasonography and MRI. The diagnosis was confirmed by angiography. This is the first report to demonstrate the characteristics of pancreatic AVM by these two imaging techniques. They proved to be useful in identifying the vascular nature of AVM without the use of a contrast material, which is a definite advantage over DSA and CT. The quality of the image obtained was equivalent or superior to that obtained by DSA and contrast-enhanced CT. Doppler ultrasonography and MRI may serve as the primary imaging techniques of choice in suspected cases of AVM.

Backgrounds: In viral hepatitis including chronic hepatitis C (CH-C), interferon (IFN) mediates antiviral response, which involves the action of multiple IFN-inducible proteins, such as a dsRNA-dependent protein kinase (PKR) system, a 2'-5' oligoadenylate synthetase (2,5-AS) and latent cellular endoribonuclease (RNase L) system, and MxA protein. While involvement of PKR in the anti-hepatitisC virus (HCV) effect of IFN was suggested, relativecontributionof other JFN-inducible protein is unknown. The aim was to clarify the intrahepatic mRNA expression profile of these IFN-inducible genes in CH-C. Methods: Sixty patients without IFN treatment who had undergone liver biopsy were included: CH-C (n= 28), chronic hepatitis B (CH-B)(n=6), autoimmune hepatitis (AIH)(n=9), primary biliary cirrhosis (PBC)(n=5), alcoholic liver disease (ALD)(n=7), and normal liver (NL)(n=5). Total RNA was extracted, and doublestranded eDNA was synthesized. The amount of mRNA for PKR, 2,5-AS, RNase L, RNase L inhibitor (RNase L-I), and MxA was quantified by competitive PCR. The values were corrected by the GAPDH mRNA expression. The expressionof each gene was compared~mo~g .diseases by Mann-Whitney's U test. Results: In our system, detection limits of PKR, 2,5-AS, RNase L, RNase L-I, and MxA mRNA were 0.2, 0.005, 0.1, 0.03, and 0.5 kcopy/10ng eDNA. PKRlGAPDH ratios (xlO-) were as follows (median [range]): CH-C; 2.9 [0.026-110], CH-B; 0.79 [0.02-8.3], AIH; 0.56 [0.14-9.1], PBC; 0.55 [0.25-0.74], ALD; 0.23 [0.042-8.3], and NL; 0.74 [0.12-0.89]. PKR mRNA was significantly overexpressed in CH-C (p=0.OO68). In addition, the amount of the PKR mRNA positively correlated with serum ALT levels in CH-C (r=0.51, p=0.0054). RNase L-U GAPDH ratios (xI0-) were as follows: CH-C; 0.011 [0-143], CH-B; 41 [0-723], AIH; 109 [0-209}, PBC; 0 [0-301], ALD; 51 [O-I13}, and NL; 4.2 [0.024-7.9], showing significant reduction of RNase L-I mRNA in CH-C (p=O.OI). Expression levels of 2,5-AS, Rl'llase L, and MxA were not different in above diseases. Conclusions: Among several IFN-inducible proteins, only PKR and RNase L-I showed altered expression patterns in the CH-C liver. While the functionalsignificance of the down-regulation of RNase L-I remains to be elucidated, the overexpression ofPKR mRNAand its correlation with serum ALT values suggests that the PKR system may playa role in the antiviral mechanism against HCV in vivo.