Purpose: To characterize longitudinal changes in molecular water diffusion, blood microcirculation, and their contributions to the apparent diffusion changes using intravoxel incoherent motion (IVIM) analysis in an experimental mouse model of liver fibrosis. Materials and Methods:Liver fibrosis was induced in male adult C57BL/6N mice (22-25 g; n ¼ 12) by repetitive dosing of carbon tetrachloride (CCl 4 ). The respiratorygated diffusion-weighted (DW) images were acquired using single-shot spin-echo EPI (SE-EPI) with 8 b-values and single diffusion gradient direction. True diffusion coefficient (D true ), blood pseudodiffusion coefficient (D pseudo ), and perfusion fraction (P fraction ) were measured. Diffusion tensor imaging (DTI) was also performed for comparison. Histology was performed with hematoxylineosin and Masson's trichrome staining.Results: A significant decrease in D true was found at 2 weeks and 4 weeks following CCl 4 insult, as compared with that before insult. Similarly, D pseudo values before injury was significantly higher than those at 2 weeks and 4 weeks after CCl 4 insult. Meanwhile, P fraction values showed no significant differences over different timepoints. For DTI, significant decrease in ADC was observed following CCl 4 administration. Fractional anisotropy at 2 weeks after CCl 4 insult was significantly lower than that before insult, and subsequently normalized at 4 weeks after the insult. Liver histology showed collagen deposition, the presence of intracellular fat vacuoles, and cell necrosis/apoptosis in livers with CCl 4 insult.Conclusion: Both molecular water diffusion and blood microcirculation contribute to the alteration in apparent diffusion changes in liver fibrosis. Reduction in D true and D pseudo values resulted from diffusion and perfusion changes, respectively, during the progression of liver fibrosis. IVIM analysis may serve as valuable and robust tool in detecting and characterizing liver fibrosis at early stages, monitoring its progression in a noninvasive manner.
Purpose: To characterize changes in relaxation times of liver using quantitative magnetic resonance imaging (MRI) in an experimental mouse model of liver fibrosis. Quantitative MRI is a potentially robust method to characterize liver fibrosis. However, correlation between relaxation times and fibrosis stage has been controversial. Materials and Methods:Liver fibrosis was induced in male adult C57BL/6N mice (22-25 g; n ¼ 12) by repetitive dosing of carbon tetrachloride (CCl 4 ). The animals were examined with a series of spin-echo (SE) images with varying TRs and multiecho SE imaging sequence at 7 T before and 2, 4, 6, and 8 weeks after CCl 4 insult. Hepatic T 1 and T 2 values were measured. Histology was performed with hematoxylin-eosin staining and Masson's trichrome staining.Results: Significant increase (P < 0.001) in hepatic T 1 was found at 2, 4, 6, and 8 weeks following CCl 4 insult as compared with that before insult. Meanwhile, hepatic T 2 at 2, 4, 6, and 8 weeks after CCl 4 insult was significantly higher (P < 0.001) than that before the insult. Liver histology showed collagen deposition, edema, and infiltration of inflammatory cells in livers with CCl 4 insult. Conclusion:Both longitudinal and transverse relaxation times may serve as robust markers for liver fibrosis. With the advent of single breath-hold sequences for MR relaxometry, quantitative mapping of relaxation times can be routinely and reliably performed in abdominal organs and hence may be valuable and robust in detecting liver fibrosis at early phase and monitoring its progression.
Vitiligo is a common chronic acquired pigmentation disorder characterized by loss of functional melanocytes from the epidermis and follicular reservoir. Among multiple hypotheses which have been proposed in the pathogenesis of vitiligo, autoimmunity and oxidative stress-mediated toxicity in melanocytes remain most widely accepted. Macroautophagy is a lysosome-dependent degradation pathway which widely exists in eukaryotic cells. Autophagy participates in the oxidative stress response in many cells, which plays a protective role in preventing damage caused by oxidative stress. Recent studies have enrolled autophagy as an important regulator in limiting damage caused by UV light and lipid oxidation, keeping oxidative stress in a steady state in epidermal keratinocytes and maintaining normal proliferation and aging of melanocytes. Impairment of autophagy might disrupt the antioxidant defense system which renders melanocytes to oxidative insults. These findings provide supportive evidence to explore new ideas of the pathogenesis of vitiligo and other pigmentation disorders.
MR diffusion characterization of IMCL droplet size provides a unique means to examine the intracellular lipid dynamics and metabolic abnormalities in vivo.
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