Curved planar reformatted CT angiography: usefulness for the evaluation of aneurysms at the carotid siphon.

BACKGROUND AND PURPOSE: Three-dimensional CT angiography uses the data obtained on a contrast-enhanced CT brain scan to generate 3D images of the intracranial vasculature. We describe the methodology of curved planar reformatting (CPR) for CT angiography and characterize its usefulness in the evaluation of aneurysms at the carotid siphon, comparing it with the shaded surface display technique (SSD). METHODS: Eighty-seven patients with suspected intracranial aneurysms at CT angiography were examined by conventional cerebral angiography, and the patients with aneurysm(s) at the carotid siphon were selected for study. For these patients, the visibility of the neck and fundus of the aneurysms on CT angiograms was compared for those obtained with SSD and those with CPR, and observer reproducibility was evaluated with the kappa statistic. RESULTS: Eighteen patients were confirmed to have an aneurysm at the carotid siphon on conventional angiograms. Seventeen aneurysms were depicted at CT angiography with SSD; 18 aneurysms with CPR. The number of visible aneurysmal necks and fundi was nine and 12, respectively, with SSD; 18 and 18, respectively, with CPR. CONCLUSION: CPR allows better demonstration of the body and neck of an aneurysm at the carotid siphon, which has a tortuous course and is surrounded by complex bony structures. CPR may be a useful adjunct for the evaluation of aneurysms in this region.     

The roles of TNFR1 in lipopolysaccharide‐induced bone loss: Dual effects of TNFR1 on bone metabolism via osteoclastogenesis and osteoblast survival

LPS (lipopolysaccharide), a major constituent of Gram‐negative bacteria, regulates proliferation and differentiation of osteoclasts directly or indirectly. This study sought to investigate the functions of the RANK/RANKL pathway in LPS‐induced bone loss in vivo. Wild‐type mice or TNFR1?/? mice were injected LPS with or without osteoprotegerin (OPG) and analyzed histologically. Bone volume was reduced by LPS injection in all groups, and OPG administration prevented the LPS‐induced bone loss regardless of genotypes. LPS‐induced enhancement of osteoclastogenesis in wild‐type mice was blocked by OPG administration. LPS or OPG did not affect osteoclastogenesis in TNFR1?/? mice. Interestingly, osteoblast surface was remarkably reduced in LPS‐treated TNFR1?/? mice as a result of enhanced osteoblast apoptosis. TRAIL, induced by TNF‐α in BMC, triggered apoptosis of primary osteoblast only when TNFR1 signal was ablated in vitro. In conclusion, RANK signaling plays a prominent role in osteoclastogenesis downstream of LPS. Furthermore, TNFR1 regulates bone metabolism through not only the regulation of osteoclast differentiation but also osteoblast survival. © 2009 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 28:657–663, 2010     

Radiological predictive factors on preoperative multimodality imaging are related to Oncotype DX recurrence score in estrogen-positive/human epidermal growth factor receptor 2-negative invasive breast cancer: a cross-sectional study

Annals of Nuclear Medicine - The Oncotype DX (ODX) estimates the 10-year risk of metastasis or recurrence of breast cancer and indicates whether chemotherapy is likely to be effective; however, the...     

Autologous chondrocytes transplantation

Hunter's observation in 1743 that cartilage "once destroyed, is not repaired" has not essentially changed for two and a half centuries. At present, there is no well-established procedure for the repair of cartilage defect with articular cartilage. Transplantation of human autologous chondrocytes in suspension, as reported by Brittberg et al., provided a potential procedure for articular cartilage repair. We have improved their procedure and developed a new technique, which creates new cartilage-like tissue by cultivating autologous chondrocytes embedded in atelocollagen gel for 3 weeks before transplantation. Good clinical results suggest that this technique should be a promising procedure for repairing articular cartilage defect.     

Detection of c-Ki- ras point mutation from pancreatic juice

Summary Cytological diagnosis of pancreatic carcinoma sometimes poses difficulties in distinguishing malignant from benign cells. Recent molecular study of pancreatic carcinoma has revealed a very high incidence of a point mutation of the c-Ki-ras oncogene at codon 12 in this neoplasm. To take advantage of this technique for the diagnosis of pancreatic carcinoma, we attempted to amplify the c-Ki-ras gene from endoscopically obtained pancreatic juice by isolation of DNA and polymerase chain reaction (PCR) coupled with restriction fragment length polymorphism (RFLP). PCR was possible in approx 70% of the cases. A point mutation was nonradioisotopically detected in 4 of 6 pancreatic carcinomas and in one intraductal papillary neoplasm, whereas no mutation was detected in other cases. Thus, this method was thought to be useful for the diagnosis of pancreatic carcinoma.     

Inhibition of endotoxin- and antigen-induced airway inflammation by fudosteine, a mucoactive agent

We evaluated the effect of a mucoactive agent (-)-(R)-2-amino-3-(3-hydroxypropylthio) propionic acid (fudosteine), on airway inflammation using endotoxin- and antigen-induced models. Time courses of growth related oncogene/cytokine-induced neutrophil chemoattractant-1 (GRO/CINC-1) production, neutrophil migration and goblet cell hyperplasia were examined in endotoxin-induced rat airway inflammation. GRO/CINC-1 in bronchoalveolar lavage fluid (BALF) increased in response to intratracheal instillation of endotoxin and peaked within 4 h. Neutrophils in BALF and goblet cells on trachea peaked 24 and 96 h after endotoxin instillation, respectively. Fudosteine significantly inhibited increases in GRO/CINC-1 at 10-100 mg/kg, and neutrophils and goblet cells at 30 and 100 mg/kg. These results suggest that inflammatory events including neutrophil chemoattractant production and neutrophil migration play important roles for goblet cell hyperplasia in endotoxin-induced airway inflammation, and fudosteine inhibits goblet cell hyperplasia by inhibiting GRO/CINC-1 production and/or neutrophil migration. Furthermore, fudosteine (100 mg/kg) inhibited ovalbumin-induced eosinophil infiltration into BALF, suggesting it attenuates asthmatic inflammation.