13C MR imaging of methionine-rich gliomas at 4.7T: a pilot study.

We explored the feasibility of using carbon-13 ((13)C) magnetic resonance imaging ((13)C-MRI) to depict (13)C-labeled methionine-enriched gliomas at 4.7 tesla. We transplanted 2 types of glioma cells separately to 2 subcutaneous tissue sites on the backs of mice weighing 15 to 20 g. After confirming tumor growth, we used (13)C-MRI and (1)H-MRI to scan 4 mice that had been administered (13)C-labeled methionine and 2 control mice. (13)C-MRI of all 4 transplanted mice administered with (13)C-labeled methionine revealed 2 areas of hyperintensity that corresponded to the tumor sites on (1)H-MR images, but no such areas were visualized in transplanted controls. Our data suggest that (13)C-MRI can show the accumulation of (13)C-labeled tracer by gliomas.

Low-frequency conductivity tensor of rat brain tissues inferred from diffusion MRI.

Conductivity tensor maps of the rat brain were obtained using diffusion magnetic resonance imaging (MRI). Signal attenuations in the cortex and the corpus callosum were measured using the stimulated echo acquisition mode (STEAM) sequence with b factors up to 6000 s/mm(2). Our previously published method was improved to infer 3 x 3 conductivity tensor at the low-frequency limit. The conductivity tensor of the tissue was inferred from the fast component of the diffusion tensor and a fraction of the fast component. The mean conductivity (MC) of the cortex and the corpus callosum was 0.52 and 0.62 S/m, respectively. Diffusion-weighted images were obtained with b factors up to 4500 s/mm(2). Conductivity tensor images were calculated from the fast diffusion tensor images. Tissues with highly anisotropic cellular structures, such as the corpus callosum, the internal capsule, and the trigeminal nerve, exhibited high anisotropy in conductivity. The resulting values corresponded to conductivities at the low-frequency limit because our method assumed electric currents flowing only through extracellular fluid.

Dependence of the spin-spin relaxation time of water in collagen gels on collagen fiber directions.

In this study, we investigated the effect of structural differences in collagen fibers in relation to the spin-spin (T2) relaxation time of surrounding water molecules. We propose a simple experimental model of the magic angle effect based on magnetically oriented collagen gels. Experiments were performed with a 4.7T magnetic resonance imaging (MRI) system with a quadrature radio frequency coil operated at 200 MHz for 1H resonance. Collagen gels were polymerized from collagen solutions exposed to a 4.7T magnetic field for 120 min. The T2 relaxation time was measured with the Carr-Purcell-Meiboom-Gill (CPMG) sequence. The apparent diffusion coefficient (ADC) was measured with the stimulated echo acquisition mode (STEAM) sequence with a motion-probing gradient (MPG). Orienting the collagen fibers at an angle of about 55 degrees to the main magnetic field caused an increase in the T2 relaxation times of water molecules in the collagen gels. The ADC in the direction parallel to the fibers was larger than that in the direction perpendicular to the fibers. The increase in the T2 relaxation time and ADC are attributed to a change in the magnetic interaction between the water molecules and collagen fibers.

Continuous blockade of L-type Ca2+ channels suppresses activation of calcineurin and development of cardiac hypertrophy in spontaneously hypertensive rats.

We examined whether Ca2+ channel blockers inhibit the activation of the Ca2+-dependent phosphatase calcineurin and the development of cardiac hypertrophy in spontaneously hypertensive rats (SHR). We randomly divided 12-week-old SHR into three groups, one each receiving vehicle, bolus injection or continuous infusion of nifedipine (10 mg/kg/day) from 12 to 24 weeks of age. Systolic blood pressure (BP) and heart rate were measured every week after the treatment using the tail-cuff plethysmography method. After 4, 8 and 12 weeks of treatment, 6 rats of each group were subjected to examinations that included an assay for calcineurin activity in the heart, magnetic resonance imaging (MRI), histology and Northern blot analysis. Continuous infusion of nifedipine consistently reduced BP, whereas bolus injection resulted in a fluctuation of BP. Continuous infusion of nifedipine not only reduced left ventricular mass but also decreased the transverse diameter of cardiomyocytes, interstitial fibrosis and the expression of the atrial natriuretic peptide and brain natriuretic peptide genes in the heart, while bolus injection of nifedipine did not significantly attenuate any of these hypertrophic responses in SHR. The activity of calcineurin in the heart was strongly suppressed by continuous but not bolus infusion of nifedipine in SHR. The results indicate that continuous blockade of Ca2+ channels with nifedipine effectively suppresses the development of cardiac hypertrophy in SHR, possibly through inhibition of the calcineurin activity.