[Case of Fusobacterium necrophorum sepsis (Lemierre's syndrome) with pulmonary septic emboli and liver abscess].

The present article documents a case of Fusobacterium sepsis with a transient anticardiolipin antibody increase in an otherwise healthy 24-year-old patient. He was presented to the emergency room with headache and fever. His temperature was 39.5°C, laboratory results revealed a white blood count of 15.2×10(3)/µl and C reactive protein 22.6 mg/dl. The patient was admitted. Chest X-ray showed the infiltrate in bilateral lower lung area. He received 400 mg of clarithromycin per day. His all symptoms did not change. On the 8(th) day in the hospital, the patient's antibiotics were switched to pazufloxacin. Chest and abdominal CT scan showed some irregular patchy nodules of around 1 cm in diameter in the bilateral lower lung fields and a round low density lesion 3 cm in diameter in the right upper segment (S8) in the liver. Blood culture revealed Fusobacterium necrophorum. On the 10(th) day, the antibacterial agent was changed from pazufloxacin to ampicillin sulbactam. On the 17(th) day, we added clindamycin. As a result his temperature gradually returned to normal. It is reported that the titer of anticardiolipin antibody increases in the sepsis patients caused by Fusobacterium necrophorum. As his symptoms disappeared, his titer of anticardiolipin antibody also decreased. So we considered he had a transient anticardiolipin titer increase.

DNA topoisomerase II inhibitor, etoposide, induces p21WAF1/CIP1 through down-regulation of c-Myc in K562 cells.

BACKGROUND: Anticancer agents modulate gene expression and these changes are essential for tumor cell killing. To investigate the mechanism by which etoposide acts as an anticancer agent, the relationship between p21WAF1/CIP1 (p21) and c-Myc was studied. MATERIALS AND METHODS: K562 cells with and without ectopic c-Myc expression were studied. Apoptosis was detected using propidium iodide and Hoechst 33342 double staining. The c-Myc and p21 levels were studied by RT-PCR and immunoblot. The p21 promoter (from -205 to +67) was investigated by the luciferase reporter gene assay. RESULTS: Ectopic c-Myc-expressing K562 (K562/c-Myc) cells showed more extensive apoptosis than K562 cells after continuous exposure to 200 microM etoposide for 24 hours. During this treatment, p21 expression was not observed in K562/c-Myc cells, and the expression of c-Myc and p21 was mutually exclusive. Etoposide activated the p21 promoter in a concentration-dependent manner, and etoposide-induced luciferase activity was suppressed by co-transfection of c-Myc. CONCLUSION: p21 promoter activity was repressed by c-Myc in proliferating K562 cells, and detoposide-induced down-regulation of c-Myc released this suppression, resulting in the induction of p21.