Results: Inflow temporal resolution of 200 msec was demonstrated, revealing arterial transit times of 750, 950, and 1100 msec to consecutive segments of the middle cerebral artery from distal to the circle of Willis to deep regions of the midbrain. Selective labeling resulted in an average of eightfold suppression of contralateral vessels relative to the labeled vessel. Signal-to-noise ratios and contrast-to-noise ratios on maximum intensity projection selleckchem images obtained with 88-second volumetric acquisitions (60 +/- 15 [standard deviation] and 57 +/- 15, respectively) and 11-second single-projection
acquisitions (19 +/- 5 and 17 +/- 5, respectively) were comparable with standard TOF acquisitions, in which a 2.7-fold longer imaging duration for a 2.6-fold lower pixel area was used. Normal variations of the vasculature were identified with ASL angiography.
Conclusion: ASL angiography can be used to acquire hemodynamic vessel-specific information LB-100 clinical trial similar to that obtained with x-ray DSA. (C) RSNA, 2010″
“Objectives: It was the aim of this study to explore the effects of 3-(5′-hydroxymethyl-2′-furyl)-l-benzyl
indazole (YC-1) on transcription activity, cell proliferation and apoptosis of hypoxic human bladder transitional carcinoma cells (BTCC), mediated by hypoxia-inducible factor l alpha (HIF-1 alpha). Methods: BTCC cell line T24 cells were incubated under normoxic or hypoxic conditions, adding different doses of YC-1.
The protein expression of HIF-l alpha and HIF-1 alpha-mediated genes was detected by Western blotting. RT-PCR was used to detect HIF-1 alpha mRNA expression. Cell proliferation, apoptosis and migration activity were determined by 3-(4,5-dimethylthiazol-2-y1)-2,5-diphenyltetrazolium bromide assay, flow Selleck Tozasertib cytometry and transwell migration assay. The cells were pretreated by two ERK/p38 MAPK pathway-specific inhibitors, PD98059 or SB203580, and then incubated with YC-1 treatment under hypoxic condition. HIF-1 alpha protein expression was detected by Western blotting. Results: Hypoxic T24 cells expressed a higher level of HIF-1 alpha, vascular endothelial growth factor, matrix metalloproteinases-2, B-cell lymphoma/leukemia-2 protein and HIF-1 alpha mRNA compared with normoxic controls, in which the above-mentioned expression was downregulated by YC-1 in a dose-dependent manner. Cell proliferation and migration activity were inhibited while apoptosis was induced by YC-1 under hypoxic condition. Moreover, YC-1-downregulated HIF-1 alpha expression was reversed by PD98059 and SB203580, respectively. Conclusions: YC-1 inhibits HIF-1 alpha and HIF-1 alpha-mediated gene expression, cell proliferation and migration activity and induces apoptosis in hypoxic BTCC. The ERK/p38 MAPK pathway may be involved in YC-1-mediated inhibition of HIF-1 alpha. Copyright (C) 2011 S.