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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.

In 1911, Alois Alzheimer published a detailed report (Zbl. ges. Neurol. Psych. 4: 356-385) on a peculiar case of the disease that had been named after him by Emil Kraepelin in 1910. Alzheimer describes a 56-year-old male patient (Johann F.) who suffered from presenile dementia and who was hospitalized in Kraepelin's clinic for more than 3 years. Post-mortem examination of the patient's brain revealed numerous amyloid plaques but no neurofibrillary tangles in the cerebral cortex, corresponding to a less common form of Alzheimer disease which may be referred to as 'plaque only'. We have identified well-preserved histological sections of this case and performed mutational screening of exon 17 of the amyloid precursor protein gene and genotyping for apolipoprotein E alleles. The patient was shown to be homozygous for apolipoprotein allele epsilon3 and lacked APP mutations at codons 692, 693, 713 and 717. This case is of historical importance as it may have convinced Kraepelin to name the disease after his co-worker, Alois Alzheimer.

We have succeeded in obtaining magnetized star models that have extremely strong magnetic fields in the interior of the star. In our formulation, arbitrary functions of the magnetic flux function appear in the expression for the current density. By appropriately choosing the functional form for one of the arbitrary functions that corresponds to the distribution of the toroidal current density, we have obtained configurations with magnetic field distributions that are highly localized within the central part and near the magnetic axis region. The absolute values of the central magnetic fields are stronger than those of the surface region by two orders of magnitude. By applying our results to magnetars, the internal magnetic poloidal fields could be 10