The SET-2400W is a newly designed whole-body PET scanner with a large axial field of view (20 cm). Its physical performance was investigated and evaluated. The scanner consists of four rings of 112 BGO detector units (22.8 mm in-plane x 50 mm axial x 30 mm depth). Each detector unit has a 6 (in-plane) x 8 (axial) matrix of BGO crystals coupled to two dual photomultiplier tubes. They are arranged in 32 rings giving 63 two-dimensional image planes. Sensitivity for a 20-cm cylindrical phantom was 6.1 kcps/kBq/ml (224 kcps/microCi/ml) in the 2D clinical mode, and to 48.6 kcps/kBq/ml (1.8 Mcps/microCi/ml) in the 3D mode after scatter correction. In-plane spatial resolution was 3.9 mm FWHM at the center of the field-of-view, and 4.4 mm FWHM tangentially, and 5.4 mm FWHM radially at 100 mm from the center. Average axial resolution was 4.5 mm FWHM at the center and 5.8 mm FWHM at a radial position 100 mm from the center. Average scatter fraction was 8% for the 2D mode and 40% for the 3D mode. The maximum count rate was 230 kcps in the 2D mode and 350 kcps in the 3D mode. Clinical images demonstrate the utility of an enlarged axial field-of-view scanner in brain study and whole-body PET imaging.

Abstract. Cisplatin causes chronic interstitial disease with fibrosis, but the development mechanism of interstitial fibrosis is not yet understood. We examined the effect of an antioxidant, N,N'-diphenyl-1,4-phenylenediamine (DPPD), on development of interstitial fibrosis induced by cisplatin. Cisplatin increased blood urea nitrogen (BUN), plasma creatinine, and elicited glucosuria and enzymuria at 3 days after administration, but these changes were restored to the normal level after 14 days. Type III collagen increased from 7 days after administration of cisplatin and the expansion of the interstitial fibrosis area became evident at 14 days. Sustained renal fibrosis worsened renal function again at 56 days. Administration of DPPD, which was started at 3 days after cisplatin treatment, significantly inhibited the increase in renal type III collagen contents and the expansion of the interstitial fibrosis area without affecting enzymuria and increased BUN. These results indicate that anti-fibrotic action of DPPD is not secondary due to the inhibition of acute renal injury but is rather a direct effect on renal fibrogenesis. DPPD did not prevent the infiltration of macrophages by cisplatin, suggesting that anti-fibrotic action of DPPD was not mediated by the inhibition of inflammatory cellular influx. It is suggested that reactive oxygen species are involved in cisplatin-induced renal interstitial fibrosis.

The results of our study suggest that not all atherosclerotic plaques show high FDG accumulation. FDG-PET studies of plaques with the use of fused images can potentially provide detailed information about atherosclerosis.

We report a case of MPA with cerebral infarction and hemorrhage. A 72-year-old man was admitted to our hospital because of high fever, speech failure, and weakness of the left limbs in April 2008. Magnetic resonance imaging of the head showed cerebral infarction at the right corona radiata. Mononeuropathy multiplex and renal dysfunction (Cr 1.46 mg/dl) were noted. Urinalysis revealed occult blood, proteinuria and granular casts. White blood cell count was 11960/ul, CRP concentration was 12.9 mg/dl, and the MPO-ANCA titer was 330 EU. Computed tomography of the abdomen revealed arterial aneurysms in the kidney. The patient was diagnosed with microscopic polyangiitis (MPA). On the 8th day after hospital admission, a new cerebral hemorrhage occurred at the right thalamus. Prednisolone (1 mg/kg/day) and intravenous pulse cyclophosphamide (200 mg) were initiated. Because the patient's MPA was refractory, methylprednisolone pulse therapy (1000 mg/dayx3 days) was added to his treatment regimen, and he received plasma exchange (20 U/day) and double filtration plasmapheresis twice each ; after this, his MPA recovered. Cerebral infarction and hemorrhage are rare complications in MPA and are associated with poor prognosis. Published literature on these complications is reviewed.

-Zinc is an essential nutrient that can also be toxic. We have previously reported that zincrelated renal toxicity is due, in part, to free radical generation in the renal epithelial cell line, LLC-PK 1 cells. We have also shown that an MEK1/2 inhibitor, U0126, markedly inhibits zinc-induced renal cell injury. In this study, we investigated the role of an upstream MEK/ERK pathway, Raf-1 kinase pathway, and the transcription factor and ERK substrate Elk-1, in rat renal cortical slices exposed to zinc. Immediately after preparing slices from rat renal cortex, the slices were incubated in medium containing Raf-1 and MEK inhibitors. ERK1/2 and Elk-1 activation were determined by Western blot analysis for phosphorylated ERK (pERK) 1/2 and phosphorylated Elk-1 (pElk-1) in nuclear fractions prepared from slices exposed to zinc. Zinc caused not only increases in 4-hydroxynonenal (4-HNE) modified protein and lipid peroxidation, as an index of oxidant stress, and decreases in PAH accumulation, as that of renal cell injury in the slices. Zinc also induced a rapid increase in ERK/Elk-1 activity accompanied by increased expressions of pERK and pElk-1 in the nuclear fraction. A Raf-1 kinase inhibitor and an MEK1/2 inhibitor U0126 significantly attenuated zinc-induced decreases PAH accumulation in the slices. The Raf-1 kinase inhibitor and U0126 also suppressed ERK1/2 activation in nuclear fractions prepared from slices treated with zinc. The present results suggest that a Raf-1/MEK/ERK1/2 pathway and the ERK substrate Elk-1 are involved in free radical-induced injury in rat renal cortical slices exposed to zinc.