Evaluation of muscular changes by ultrasound Nakagami imaging in Duchenne muscular dystrophy.

Duchenne muscular dystrophy (DMD) is the most common debilitating muscular disorder. Developing a noninvasive measure for monitoring the progression of this disease is critical. The present study tested the effectiveness of using ultrasound Nakagami imaging to evaluate the severity of the dystrophic process. A total of 47 participants (40 with DMD and 7 healthy controls) were recruited. Patients were classified into stage 1 (presymptomatic and ambulatory), stage 2 (early nonambulatory), and stage 3 (late nonambulatory). All participants underwent ultrasound examinations on the rectus femoris, tibialis anterior, and gastrocnemius. The results revealed that the ultrasound Nakagami parameter correlated positively with functional severity in the patients with DMD. The median Nakagami parameter of the gastrocnemius muscle increased from 0.50 to 0.85, corresponding to the largest dynamic range between normal and stage 3. The accuracy, sensitivity, and specificity of diagnosing walking function were 85.52%, 76.31%, and 94.73%, respectively. The Nakagami parameter of the rectus femoris and gastrocnemius muscles correlated negatively with the 6-minute walking distance in the ambulatory patients. Therefore, changes in the Nakagami parameter for the gastrocnemius muscle are suitable for monitoring disease progression in ambulatory patients and for predicting ambulation loss. Ultrasound Nakagami imaging shows potential for evaluating patients with DMD.

Quantitative analysis of the therapeutic effect of magnolol on MPTP-induced mouse model of Parkinson's disease using in vivo 18F-9-fluoropropyl-(+)-dihydrotetrabenazine PET imaging.

18F-9-Fluoropropyl-(+)-dihydrotetrabenazine [18F-FP-(+)-DTBZ] positron emission tomography (PET) has been shown to detect dopaminergic neuron loss associated with Parkinson's disease (PD) in human and neurotoxin-induced animal models. A polyphenol compound, magnolol, was recently proposed as having a potentially restorative effect in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)- or 6-hydroxydopamine-treated animal models. In this study, 18F-FP-(+)-DTBZ PET was used to determine the therapeutic efficacy of magnolol in an MPTP-PD mouse model that was prepared by giving an intraperitoneally (i.p.) daily dose of 25 mg/kg MPTP to male C57BL/6 mice for 5 consecutive days. Twenty-minute static 18F-FP-(+)-DTBZ PET scans were performed before MPTP treatment and 5 days after the termination of MPTP treatment to set up the baseline control. Half of the MPTP-treated mice then received a daily dose of magnolol (10 mg/kg dissolved in corn oil, i.p.) for 6 days. 18F-FP-(+)-DTBZ PET imaging was performed the day after the final treatment. All 18F-FP-(+)-DTBZ PET images were analysed and the specific uptake ratio (SUr) was calculated. Ex vivo autoradiography (ARG) and corresponding immunohistochemistry (IHC) studies were conducted to confirm the distribution of dopaminergic terminals in the striatum. The striatal SUr ratios of 18F-FP-(+)-DTBZ PET images for the Sham, the MPTP, and the MPTP + Magnolol-treated groups were 1.25 ± 0.05, 0.75 ± 0.06, and 1.00 ± 0.11, respectively (n = 4 for each group). The ex vivo 18F-FP-(+)-DTBZ ARG and IHC results correlated favourably with the PET imaging results. 18F-FP-(+)-DTBZ PET imaging suggested that magnolol post-treatment may reverse the neuronal damage in the MPTP-lesioned PD mice. In vivo imaging of the striatal vesicular monoamine transporter type 2 (VMAT2) distribution using 18F-FP-(+)-DTBZ animal PET is a useful method to evaluate the efficacy of therapeutic drugs i.e., magnolol, for the management of PD.