[Seizure characteristics in Kawasaki disease].

It is well known that convulsions may occur in clinical course of Kawasaki disease. However, the features of such seizures remain unclear. Recent reports have hypothesized that proinflammatory cytokines may contribute to the genesis of febrile convulsions (FC). In the acute phase of Kawasaki disease, proinflammatory cytokines are elevated in serum and CSF. If cytokines play a role in seizure phenomena in patients with Kawasaki disease, FC and seizures in Kawasaki disease might share some clinical features. To clarify the clinical features of convulsion in Kawasaki disease, we investigated 7 patients with Kawasaki disease with convulsions who were diagnosed and treated from November 2003 to November 2005. We found several features of the seizures, as well as the onset age, were diffrent among these clinical entities. The onset of Kawasaki disease was characteristically before six months of age in all patients. Seizure clustering was seen in 5 patients and partial seizures in 4. Prolonged unconsciousness after seizures was seen in one patient, syndrome of inappropriate secretion of ADH (SIADH) in one other. One patient had markedly elevated IL-6 in CSF. These observations led us to speculate that the convulsion of Kawasaki disease may be attributable to an encephalitis. The results of this study suggest that seizure pathophysiology differs between FC and Kawasaki disease.

Evaluation of edge effect due to phase contrast imaging for mammography.

It is well-known that the edge effect produced by phase contrast imaging results in the edge enhancement of x-ray images and thereby sharpens those images. It has recently been reported that phase contrast imaging using practical x-ray tubes with small focal spots has improved image sharpness as observed in the phase contrast imaging with x-ray from synchrotron radiation or micro-focus x-ray tubes. In this study, we conducted the phase contrast imaging of a plastic fiber and plant seeds using a customized mammography equipment with a 0.1 mm focal spot, and the improvement of image sharpness was evaluated in terms of spatial frequency response of the images. We observed that the image contrast of the plastic fiber was increased by edge enhancement, and, as predicted elsewhere, spectral analysis revealed that as the spatial frequencies of the x-ray images increased, so did the sharpness gained through phase contrast imaging. Thus, phase contrast imaging using a practical molybdenum anode tube with a 0.1 mm-focal spot would benefit mammography, in which the morphological detectability of small species such as microcalcifications is of great concern. And detectability of tumor-surrounded glandular tissues in dense breast would be also improved by the phase contrast imaging.

[Application of phase contrast imaging to mammography].

Phase contrast images were obtained experimentally by using a customized mammography unit with a nominal focal spot size of 100 microm and variable source-to-image distances of up to 1.5 m. The purpose of this study was to examine the applicability and potential usefulness of phase contrast imaging for mammography. A mammography phantom (ACR156 RMI phantom) was imaged, and its visibility was examined. The optical density of the phantom images was adjusted to approximately 1.3 for both the contact and phase contrast images. Forty-one observers (18 medical doctors and 23 radiological technologists) participated in visual evaluation of the images. Results showed that, in comparison with the images of contact mammography, the phantom images of phase contrast imaging demonstrated statistically significantly superior visibility for fibers, clustered micro-calcifications, and masses. Therefore, phase contrast imaging obtained by using the customized mammography unit would be useful for improving diagnostic accuracy in mammography.

Cholesteryl-hemisuccinate-induced apoptosis of promyelocytic leukemia HL-60 cells through a cyclosporin A-insensitive mechanism.

We reported previously that alpha-tocopheryl-succinate (VES) induced apoptosis of cultured human promyelocytic leukemia cells (HL-60) (Free Radic Res 2000;33:407-18). We have now studied the effect of cholesteryl-hemisuccinate (CS) on the fate of HL-60 cells to clarify whether CS has an effect similar to that of VES. CS inhibited the growth of HL-60 cells without differentiation to granulocytes and induced DNA fragmentation and ladder formation. CS inhibited the phosphorylation of pleckstrin homology domain-containing protein kinase B (Akt) and initiated the activation of a caspase cascade. CS triggered the reaction leading to the cleavage of Bid and also released cytochrome c (Cyt. c) from mitochondria. In addition, CS induced mitochondrial membrane depolarization and translocation of Bax to mitochondria in HL-60 cells. However, CS did not induce an increase in the concentration of intracellular calcium ions in HL-60 cells. The membrane depolarization, Cyt. c release, and DNA fragmentation were inhibited by z-VAD-fluoromethylketone (z-VAD-fmk), a pan-caspase inhibitor, but not by cyclosporin A, an inhibitor of membrane permeability transition. These results suggested that CS-induced apoptosis of HL-60 cells might be caused by inhibiting Akt phosphorylation following cleavage of Bid through caspase-8 activation and subsequently via an Apaf complex-caspase cascade pathway.

Molecular mechanisms of decreased steroid responsiveness induced by latent adenoviral infection in allergic lung inflammation.

BACKGROUND: We recently reported that allergic lung inflammation in guinea pigs became steroid resistant in the presence of latent adenoviral infection. OBJECTIVE: We sought to investigate the molecular mechanisms that underlie steroid resistance in adenoviral infection. METHODS: Guinea pigs with a latent adenoviral infection were sensitized and challenged with ovalbumin (OVA) and given daily injections of budesonide (20 mg/kg administered intraperitoneally). Sham-infected animals received either saline challenge without budesonide injection or OVA challenge with or without budesonide. The inflammatory response in the lung was measured by means of quantitative histology. Eotaxin, monocyte chemoattractant protein 1 (MCP-1), and RANTES expression in the lung were analyzed by means of Northern blotting, and the binding activity of activator protein 1 (AP-1) and nuclear factor kappaB in nuclear extracts from the lung was analyzed with electrophoretic mobility shift assays. RESULTS: OVA challenge increased eosinophil infiltration and eotaxin and MCP-1 mRNA expression in the lungs, and glucocorticoids reduced these increases in the sham-infected, but not the adenovirus-infected, animals. Changes in binding activity of AP-1, but not nuclear factor kappaB, paralleled changes in eotaxin and MCP-1 mRNA. CONCLUSION: We conclude that latent adenoviral infection inhibits the anti-inflammatory effects of glucocorticoids on allergen-induced eotaxin and MCP-1 expression through AP-1, leading to steroid-resistant allergic lung inflammation.