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Objective. To examine whether nuclear factor κB (NF‐κB) is activated in cultured synovial cells in response to tumor necrosis factor α (TNFα) and to investigate the correlation between NF‐κB activation and synovial cell proliferation. Methods. Activation of NF‐κB was detected by electrophoretic mobility shift assay. The transcription of several NF‐κB–dependent genes was evaluated by reverse transcriptase polymerase chain reaction and transient expression assay using human immunodeficiency virus–long terminal repeat chloramphenicol acetyltransferase. Proliferative activity was determined by measurement of 3H‐thymidine incorporation. Results. Stimulation of synovial cells with TNFα activated NF‐κB and subsequent transcription of several genes. Treatment of synovial cells with N‐acetyl‐L‐cysteine (NAC), an antioxidant agent, inhibited TNFα‐induced NF‐κB activation and transcription. Moreover, NAC also inhibited synovial cell proliferation induced by TNFα. Conclusion. Our results suggest that NF‐κB plays a pivotal role in synovial cell activation by TNFα. Thus, suppression of NF‐κB could be a potential therapeutic modality for synovitis such as that of rheumatoid arthritis.

This paper describes a variable supply-voltage (VS) scheme. From an external supply, the VS scheme automatically generates minimum internal supply voltages by feedback control of a buck converter, a speed detector, and a timing controller so that they meet the demand on its operation frequency. A 32-b RISC core processor is developed in a 0.4-m CMOS technology which optimally controls the internal supply voltages with the VS scheme and the threshold voltages through substrate bias control. Performance in MIPS/W is improved by a factor of more than two compared with its conventional CMOS design. Index Terms-Buck converter, low power CMOS circuits, low threshold voltage, low voltage.