Time course of axial and radial diffusion kurtosis of white matter infarctions: period of pseudonormalization.

BACKGROUND AND PURPOSE: Diffusion kurtosis is a statistical measure for quantifying the deviation of the water diffusion profile from a Gaussian distribution. The current study evaluated the time course of diffusion kurtosis in patients with cerebral infarctions, including perforator, white matter, cortical, and watershed infarctions. MATERIALS AND METHODS: Subjects were 31 patients, representing 52 observations of lesions. The duration between the onset and imaging ranged from 3 hours to 122 days. Lesions were categorized into 4 groups listed above. Diffusion kurtosis images were acquired with b-values of 0, 1000, and 2000 s/mm(2) applied in 30 directions; variables including DWI signal, ADC, fractional anisotropy, radial diffusivity, axial diffusivity, radial kurtosis, and axial kurtosis, were obtained. The time courses of the relative values (lesion versus contralateral) for these variables were evaluated, and the pseudonormalization period was calculated. RESULTS: Diffusion kurtosis was highest immediately after the onset of infarction. Trend curves showed that kurtosis decreased with time after onset. Pseudonormalization for radial/axial kurtosis occurred at 13.2/59.9 days for perforator infarctions, 33.1/40.6 days for white matter infarctions, 34.8/35.9 days for cortical infarctions, and 34.1/28.2 days after watershed infarctions. For perforator infarctions, pseudonormalization occurred in the following order: radial kurtosis, ADC, axial kurtosis, and DWI. CONCLUSIONS: Diffusion kurtosis variables in lesions increased early after infarction and decreased with time. Information provided by diffusion kurtosis imaging, including axial and radial kurtosis, seems helpful in conducting a detailed evaluation of the age of infarction, in combination with T2WI, DWI, and ADC.

Lymphotropic hepatitis C virus has an interferon-resistant phenotype.

Hepatitis C virus (HCV) infects and associates with B cells, leading to abnormal B-cell activation and development of lymphoproliferative and autoimmune disorders. This immune perturbation may in turn be associated with the resistance of HCV against the host immune system. The objective of this study was to analyse the effects of HCV infection of B cells on the efficacy of interferon (IFN)-based therapy. The study enrolled 102 patients with chronic hepatitis C who were treated with pegylated IFN plus ribavirin. HCV RNA titres in B cells were compared in patients with rapid viral responder (RVR) vs non-RVR, sustained viral responder (SVR) vs non-SVR and null viral responder (NVR) vs VR. The levels of HCV RNA in B cells were significantly higher in non-RVR, non-SVR and NVR groups. Association between the therapy outcome and the positive B-cell HCV RNA was also investigated in relation to other known viral and host factors. Multivariable analyses showed that the positive B-cell HCV RNA and the minor single-nucleotide polymorphism near the IL28B gene (rs8099917) were independent factors associated with NVR in patients infected with HCV genotype 1. When these two factors were combined, the sensitivity, specificity, positive and negative predictive values for NVR were 92.3%, 98.2%, 92.3% and 98.2%, respectively. Genotype 1 and the presence of one or no mutations in the IFN-sensitivity determining region were associated with higher levels of B-cell HCV RNA. B-cell-tropic HCV appears to have an IFN-resistant phenotype. B-cell HCV RNA positivity is a predictive factor for resistance to IFN-based therapy.

Observation of the one-dimensional diffusion of nanometer-sized dislocation loops.

Dislocations are ubiquitous linear defects and are responsible for many of the properties of crystalline materials. Studies on the glide process of dislocations in bulk materials have mostly focused on the response of dislocations with macroscopic lengths to external loading or unloading. Using in situ transmission electron microscopy, we show that nanometer-sized loops with a Burgers vector of (1/2)111 in alpha-Fe can undergo one-dimensional diffusion even in the absence of stresses that are effective in driving the loops. The loop size dependence of the loop diffusivity obtained is explained by the stochastic thermal fluctuation in the numbers of double kinks.