When channel state information is known at a transmitter in multiple-input multiple-output systems, the optimum capacity is given by eigenmode channel division with water-pouring power control. In this eigenbeam-space division multiplexing (E-SDM), bit assignments to substreams based on the capacity is not optimum due to the fact that the number of assigned bits is expressed by discrete quantity. In the paper, a method to assign both bit and transmit power to each substream based on the criterion minimizing total bit error rate (BER) is developed, and the BER performance is numerically analyzed in comparison to spatial division multiplexing (SDM). The simulation results assuming 5-transmit and 2-receive antennas show that the E-SDM provides about 10 dB gain compared to the conventional SDM at average BER of 10 −3 . 0-7803-7467-3/02/$17.00 ©2002 IEEE.

Objective. To identify the cells that synthesize EDA-containing fibronectin (FN) and examine the role of EDA+ FN in the pathogenesis of rheumatoid joint lesions.Methods. Localization of EDA+ FN and c-Fos protein in rheumatoid joints was studied immunohistochemically by utilizing antibodies for EDA+ FN and c-Fos. Expression of EDA+ FN was studied by immunoelectron microscopy and in situ hybridization. The amount of EDA+ FN was measured by enzymelinked immunosorbent assay.Results. EDA+ FN was specifically localized in the synovial lining layer of synovium with active rheumatoid arthritis (RA) (n = 17), but not in that with osteoarthritis (n = 4) or with inactive fibrous RA (n = 2).EDA+ FN messenger RNA was localized in the synovial lining layer. EDA+ FN was immunoelectron microscopically localized in the synovial lining fibroblast-like (type B) cells. EDA+ FN was also detected at the cartilagepannus junction and on the surface of RA cartilage. Double staining showed that EDA+ FN colocalized with c-Fos protein in the rheumatoid synovial lining layer. Quantification of EDA+ FN showed that it was highly concentrated in rheumatoid synovial fluids.Conclusion. EDA+ FN is synthesized by the synovial lining fibroblast-like (type B) cells in situ in rheumatoid synovium, and appears to be expressed in association with activated or transformed states of synovium.Fibronectin (FN), synthesized in rheumatoid synovium (1) and specifically located in rheumatoid pannus and on cartilage surface (2,3), may be important in rheumatoid joint destruction (4). FN is composed of more than 2 subunits of protein with molecular weights of 220-250 kd (5). Multiple isoforms of FN are produced from a single gene by alternative splicing at 3 distinct sites: EDA, EDB, and IIICS (5). Recent studies indicate that isoforms containing the EDA or EDB regions are expressed in early stages of fetal development, malignant transformation, and wound healing ( 5 ) , which suggests that EDAcontaining or EDB-containing FN may be expressed in association with cellular proliferation and transformation. The EDA-or EDB-containing FN is found in the synovial lining cells and small blood vessels of rheumatoid joints (6,7), and plasma levels of EDA+ FN in rheumatoid arthritis (RA) patients are higher than those in healthy individuals (8).We used immunohistochemistry techniques to show that EDA+ FN, which is specifically localized in the rheumatoid synovial lining layer, is synthesized by the synovial lining fibroblast-like (type B) cells. EDA+ FN is also detected in invasive fronts of active cellular pannus and on rheumatoid cartilage surfaces that are free of pannus. EDA+ FN is also colocalized with c-Fos protein in the rheumatoid synovial lining layer.Kazuo Hino, BS, Shunichi Shiozawa, MD, Yasuo Kuroki, MD, Hitoshi Ishikawa, MD, Kazuo Chihara, MD: Kobe University, Kobe, Japan; Kazuko Shiozawa, MD: Kakogawa National Hospital, Kakogawa, Japan; Kiyotoshi Sekiguchi, PhD: Osaka Medical Center for Maternal and Child Health, Osaka, Japan; Hisanobu Hirano, MS, Eiji Sakash...

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AIM:To analyze the risk factors of hepatocellular carcinoma (HCC) recurrence after radiofrequency ablation (RFA) treatment with HCV-associated hepatitis. METHODS:Twenty-six patients with HCV-associated HCC who were followed-up for more than 12 mo were selected for this study. Risk factors for distant intrahepatic recurrences of HCC were evaluated for patients in whom complete coagulation was achieved without recurrence in the same subsegment as the primary nodule. Twelve clinical and tumoral factors were examined: Age, gender, nodule diameter, number of primary HCC nodule, Child-Pugh classification, serum platelet, serum albumin, serum AST, post RFA AST, serum ALT, post RFA ALT, post RFA treatment. RESULTS:Distant recurrences of HCC in remnant liver after RFA were observed in 14 cases and in the number of primary HCC nodules (P = 0.047), and the serum platelets (P = 0.030), the clear difference came out by the recurrence group and the non-recurrence group. The cumulative recurrence rates after 1 and 2 years were 30.8% and 86.8%, respectively for primary multinodular HCC, and 15.4% and 29.5% respectively, for primary uninodular HCC. In addition the 1-year recurrence rates for patients with serum albumin more than 3.4 g/dL and less than 3.4 g/dL were 23.1% for both, but the 2-years recurrence rates were 89.0% and 23.1%, respectively. The number of primary HCC nodules (relative risk, 6.970; P = 0.016) were found to be a statistically significant predictor for poor distant intrahepatic recurrence by univariate analysis. CONCLUSION:Patients who have multiple HCC nodules, low serum platelets and low serum albumin accompanied by HCV infection, should be carefully followed because of the high incidence of new HCC lesions in the remnant liver, even if coagulation RFA is complete.

Cyclooxygenase (COX)-2 is upregulated in a variety of human cancers, including in hepatocellular carcinoma (HCC), whereas it is undetectable in most normal tissue. Evidence suggests that COX-2 is likely to be involved in hepatocarcinogenesis and, thus, COX-2 may be involved in an early process in carcinogenesis, dedifferentiation. To address this possibility, we investigated the effect of COX-2 inhibitors on TNF-related apoptosis, inducing ligand (TRAIL) sensitivity and its molecular mechanisms, with special attention to anti-apoptotic proteins. We used the highly selective COX-2 inhibitors, NS398 and CAY10404. We also used the MTT assay and cytological analysis of DAPI-stained DNA to assess viability and apoptosis in two HCC cells (SK-Hep1 and HLE). In order to ask what led to increased sensitivity to TRAIL in HCC cells, cell surface expression of TRAIL and TRAIL-receptors was investigated using flow cytometry analysis. Expression of survivin, X-chromosomelinked IAP (XIAP), Bcl-xL, AKT and phospho-AKT was also investigated using immunoblotting. COX-2 inhibitors resulted in a concentration-dependent decrease in cell viability in the two HCC cell lines tested. Subtoxic levels of COX-2 inhibitors did not significantly augment TNF•-induced apoptosis but did dramatically enhance TRAIL-induced apoptosis in both cell lines. TRAIL receptor 2/death receptor 5 (TRAIL-R2/DR5) expression was significantly up-regulated in SH-Hep1 and HLE cells. TRAIL receptor 1/death receptor 4 (TRAIL-R1/DR4) expression was up-regulated only in SK-Hep1. Expression of survivin and Bcl-xL was down-regulated in SK-Hep1 and HLE cells in the presence of CAY10404 but XIAP was not affected. Expression of survivin, Bcl-xL and XIAP was down-regulated in SK-Hep1 cells in the presence of NS398. Survivin expression was also down-regulated in the presence of NS398 in HLE cells. Finally, NS398 also decreased phospho-AKT in SK-Hep1 cells. These results demonstrate that COX-2 inhibitors can induce apoptosis and augment TRAIL sensitivity by up-regulation of TRAIL receptors and down-regulation of both survivin and AKT signaling.