Life-style activities in systemic lupus erythematosus.

OBJECTIVE: We evaluated the life-style activities of outpatients with SLE and factors that reduce their social activities. SUBJECTS: SLE group = 60 patients, Control 1 = 30 healthy subjects and Control 2 = 30 patients with other autoimmune diseases. The Frenchay Activity Index (FAI), Zung's self-rating depression scale (SDS), and the Japanese version of the Philadelphia Geriatric Center morale scale-revised (MS) were compared between groups. Relation between FAI and age, disease duration, steroid dose, SDS, and MS were examined in the SLE group, Control 1, and Control 2. RESULTS: Total scores by FAI was 28.1 +/-8.0 points in Control 1, whereas it was 26.5 +/- 5.8 points in Control 2 and 24.5 +/- 7.7 points in the SLE group. While there was no statistical difference between the SLE group and Control 2, the scores were significantly lower in the SLE group than in Control 1 (P < 0.05). In SLE patients, age, the duration of the disease, and the steroid dose had no correlation, but MS had a positive correlation (P < 0.05) and SDS had a negative correlation (P < 0.05). In Control 2, age, the duration of the disease, the steroid dose, MS and SDS had no correlation whereas there was significant negative relation between FAI and SDS in Control 1 (r= -0.516, P<0.005). CONCLUSION: The significant relation between life-style activities and subjective well-being, and depression in SLE suggests that detection and treatment of mental status is important in improving the life-style activities of SLE patients.

Novel human TEF-1 isoforms exhibit altered DNA binding and functional properties.

The transcriptional enhancer factor-1 (TEF-1) is a member of the TEA/ATTS domain family. TEF-1 binds to GT-IIC (GGAATG), SphI (AGTATG), SphII (AGCATG), and M-CAT (GGTATG) response elements and is involved in the transactivation of a variety of genes, including the SV40 large T antigen, mammalian muscle-specific genes, and human chorionic somatomammotropin genes. Also, TEF-1 acts as a transcriptional repressor in placental cells, possibly through interaction with the TATA binding protein (TBP), preventing TBP binding to the TATA box. Here we describe the cloning, tissue-specific expression pattern, and functional characterization of two novel TEF-1 isoforms, TEF-1beta and TEF-1gamma. These isoforms most likely arise from alternative splicing of mRNA transcribed from a single gene and involve substitutions and/or insertions in a region immediately following the DNA binding domain. TEF-1beta appears to be widely distributed like the prototypic TEF-1, designated TEF-1alpha, whereas TEF-1gamma exhibits a narrower tissue-specific expression pattern that includes pancreas, kidney, and skeletal and heart muscle. The relatively limited sequence alterations among these isoforms cause significant changes in their DNA binding and transcriptional activities. TEF-1beta and TEF-1gamma bind to GT-IIC sequences with higher affinity and repress hCS promoter more efficiently than TEF-1alpha. These results suggest that each TEF-1 isoform may play unique regulatory roles in various tissues.

Lysophosphatidylcholine up-regulates IL-1 beta-induced iNOS expression in rat mesangial cells.

BACKGROUND: Nitric oxide (NO), a simple molecule synthesized from L-arginine by NO synthases (NOS), has been identified to play an important role in cell communication, cell defense and cell injury. Several studies have shown that glomeruli from rats with immune-mediated glomerular inflammation have increased production of NO. Recently, it was also reported that inducible NOS (iNOS) is localized in mesangial cells, glomerular epithelial cells and infiltrating cells in the diseased human glomeruli. On the other hand, while oxidized low density lipoprotein (ox-LDL) has been suggested to be related to progression of glomerular disease, the mechanism remains unknown. We investigated the effect of lysophosphatidylcholine (LPC), a modified phospholipid produced during LDL oxidation, on iNOS expression in rat mesangial cells. METHODS AND RESULTS: Treatment of mesangial cells with interleukin-1 beta (IL-1 beta) induced iNOS activity measured as nitrite levels in cell culture supernatants. Treatment with LPC had no effect. In contrast, coincubation with LPC and IL-1 beta resulted in a markedly higher nitrite content compared to that after incubation with IL-1 beta alone. Western blot analysis revealed that LPC caused a significant increase in the formation of iNOS protein in the presence of IL-1 beta. CONCLUSION: These findings suggest that LPC may contribute to progression of glomerular inflammation by augmenting IL-1 beta-induced iNOS expression.

[A case of malignant rheumatoid arthritis with lupus anticoagulant and cerebral infarction].

We reported a case of malignant rheumatoid arthritis (MRA) with cerebral infarction associated with a possible cause of lupus anticoagulant. The patient was a 68-year-old woman who had received treatment for rheumatoid arthritis (RA) from 15 to 16 years ago. She consulted to our hospital with a major complaint of right hemiplegia. Brain CT revealed a low density area in the left hemisphere. She was diagnosed as cerebral infarction and hospitalized. Since she was noted to have hypocomplementemia, interstitial pneumonia and pericarditis, she was diagnosed as MRA. Coagulation test disclosed positive lupus anticoagulant (LA). Generally, CNS disorders in MRA are uncommon. Cerebral infarction was complicated in the present case, suggesting the involvement of antiphospholipid antibodies as its pathogenesis.