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Purpose To clarify the components primarily responsible for diffusion abnormalities in pancreatic cancerous tissue. Materials and Methods Subjects comprised 10 patients with surgically confirmed pancreatic cancer. Diffusion‐weighted (DW) echo‐planar imaging (b value = 0, 500 s/mm2) was employed to calculate the apparent diffusion coefficient (ADC). ADC values of cancer and noncancerous tissue were calculated. Furthermore, ADC values of the cancer were compared with histopathological results. Results The mean (±standard deviation) ADC value was significantly lower for tumor (1.27 ± 0.52 × 10−3 mm2/s) than for noncancerous tissue (1.90 ± 0.41 × 10−3 mm2/s, P < 0.05). Histopathological examination showed similar proportions of fibrotic area, cellular component, necrosis, and mucin in each case. Regarding the density of fibrosis in cancer, three cases were classified in the loose fibrosis group and the remaining seven cases were classified in the dense fibrosis group. The mean ADC value was significantly higher in the loose fibrosis group (1.88 ± 0.39 × 10−3 mm2/s) than in the dense fibrosis group (1.01 ± 0.29 × 10−3 mm2/s, P < 0.05). In quantitative analysis, ADC correlated well with the proportion of collagenous fibers (r = −0.87, P < 0.05). Conclusion Collagenous fibers may be responsible for diffusion abnormalities in pancreatic cancer. J. Magn. Reson. Imaging 2008;27:1302–1308. © 2008 Wiley‐Liss, Inc.

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Three novel diterpenoids, excoecarins D, E, and K (1-3), were isolated from Excoecaria agallocha. The structures of 1-3 were established as 3alpha,18-dihydroxy-3beta,20-epoxybeyer-15-ene, (15R, 16S)-ent-15,16-epoxybeyeran-3-one, and ent-3beta-hydroxykaur-16-en-2-one, respectively, on the basis of extensive NMR experiments and, in the case of 1, by X-ray analysis.

Arterial transit time (ATT) is most crucial for measuring absolute cerebral blood flow (CBF) by arterial spin labeling (ASL), a noninvasive magnetic resonance (MR) perfusion assessment technique, in patients with chronic occlusive cerebrovascular disease. We validated ASL-CBF and ASL-ATT maps calculated by pulsed continuous ASL (pCASL) with multiple post-label delay acquisitions in patients with occlusive cerebrovascular disease. Fifteen patients underwent MR scans, including pCASL, and positron emission tomography (PET) scans with 15O-water to obtain PET-CBF. MR acquisitions with different post-label delays (1.0, 1.5, 2.0, 2.5 and 3.0 sec) were also obtained for ATT correction. The theoretical framework of 2-compartmental model (2CM) was also used for the delay compensation. ASL-CBF and ASL-ATT were calculated based on the proposed 2CM, and the effect on the CBF values and the ATT correction characteristics were discussed. Linear regression analyses were performed both on pixel-by-pixel and region-of-interest bases in the middle cerebral artery (MCA) territory. There were significant correlations between ASL-CBF and PET-CBF both for voxel values (r = 0.74 ± 0.08, slope: 0.87 ± 0.22, intercept: 6.1 ± 4.9) and for the MCA territorial comparison in both affected (R2 = 0.67, y = 0.83x + 6.3) and contralateral sides (R2 = 0.66, y = 0.74x + 6.3). ASL-ATTs in the affected side were significantly longer than those in the contralateral side (1.51 ± 0.41 sec and 1.12 ± 0.30 sec, respectively, p <0.0005). CBF measurement using pCASL with delay compensation was feasible and fairly accurate even in altered hemodynamic states.

Arterial transit time (ATT) prolongation causes an error of cerebral blood flow (CBF) measurement during arterial spin labeling (ASL). To improve the accuracy of ATT and CBF in patients with prolonged ATT, we propose a robust ATT and CBF estimation method for clinical practice. The proposed method consists of a three‐delay Hadamard‐encoded pseudo‐continuous ASL (H‐pCASL) with an additional‐encoding and single‐delay with long‐labeled long‐delay (1dLLLD) acquisition. The additional‐encoding allows for the reconstruction of a single‐delay image with long‐labeled short‐delay (1dLLSD) in addition to the normal Hadamard sub‐bolus images. Five different images (normal Hadamard 3 delay, 1dLLSD, 1dLLLD) were reconstructed to calculate ATT and CBF. A Monte Carlo simulation and an in vivo study were performed to access the accuracy of the proposed method in comparison to normal 7‐delay (7d) H‐pCASL with equally divided sub‐bolus labeling duration (LD). The simulation showed that the accuracy of CBF is strongly affected by ATT. It was also demonstrated that underestimation of ATT and CBF by 7d H‐pCASL was higher with longer ATT than with the proposed method. Consistent with the simulation, the 7d H‐pCASL significantly underestimated the ATT compared to that of the proposed method. This underestimation was evident in the distal anterior cerebral artery (ACA; P = 0.0394) and the distal posterior cerebral artery (PCA; 2 P = 0.0255). Similar to the ATT, the CBF was underestimated with 7d H‐pCASL in the distal ACA (P = 0.0099), distal middle cerebral artery (P = 0.0109), and distal PCA (P = 0.0319) compared to the proposed method. Improving the SNR of each delay image (even though the number of delays is small) is crucial for ATT estimation. This is opposed to acquiring many delays with short LD. The proposed method confers accurate ATT and CBF estimation within a practical acquisition time in a clinical setting.