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  • The results of the present study

    2018-10-30

    The results of the present study contribute to an increased understanding of the mechanisms involved in cWAD. However, the results are drawn from a relatively small sample size composed only of women. While the sample size of the study is an important factor for the interpretation of the results related to neurological scores, it has relatively limited relevance for the group comparison of rCBF performed in the voxel-based analysis, since 12 repetitions of the H215O PET scan were performed per subject. These repeated measurements reinforce the statistical analysis controlling for within-subject variance. In addition, similar results were obtained in the changes of rCBF in cWAD when the group comparison was performed using only the first acquisition of each condition (Table 1s and Fig. 1s in Appendix B of the Supplementary Material section). Finally, the regional results might be influenced by sub-optimal registration of c-Myc tag structures in the absence of individual MRI images, the limited spatial resolution of the PET camera (4 to 5mm FWHM), or the absence of correction for partial volume effects. Finally, while no differences in the rCBF were observed between conditions, the complete absence of a habituation effect to the electrical stimulation of the neck cannot be completely excluded and must be considered when comparing the results with other studies at rest. The current research data, so far, clearly show that the brain reacts to whiplash injury by changes in the perfusion of certain regions. However, these data do not reveal the underlying mechanism that produces these alterations. Are the mechanisms described by Moskowitz and Buzzi (1991) or the hypothesis proposed by Vállez García et al. (2014) the key to the disease or are both mechanisms, in combination or even triggered by each other, responsible for disease development? Is the brain reshaping its function over time after whiplash injury, a phenomenon observed after spinal cord injury, crossed cerebellar diaschisis, and other brain plasticity processes (Otte, 2001; Otte et al., 1998b)? In this context, the study by Obermann et al. (2009) on neuroplasticity in a longitudinal study following whiplash injury found adaptive gray matter changes of pain processing structures occurring in response to pain, but brain changes resolved in those where symptoms reduced, and only remained in those with persistent symptoms. Hence, possibly these symptoms relate to the persistence of the percept of pain, and given that it is possible that tissue lesions are likely in cWAD, it may be that peripheral mechanisms drive this process. Therefore, further functional neuroimaging studies in cWAD patients are mandatory for a better understanding of the pathophysiology. As long as the pathophysiology is not understood, an evidence-based approach to any treatment option cannot be developed (Otte et al., 2014).
    Conclusion
    Author Contributions
    Role of the Funding Source
    Conflict of Interest Statement
    Leber\'s hereditary optic neuropathy (LHON) is one of the most common causes of blindness in young adults. Unfortunately, there is currently no effective treatment. The most common point mutation that leads to the development of LHON is the mitochondrial DNA 11778 G-to-A point mutation (). In China, the G11778A point mutation is present in 90% of LHON patients (). Therefore, we selected this mutation as the target for gene therapy. After a series of successful animal experiments (), a total of 9 patients were administered an intravitreal injection of rAAV2-ND4 (recombinant adeno-associated virus carrying the NADH–ubiquinone oxidoreductase subunit 4 gene) in 2011 and 2012. Early therapy outcomes for these patients have been previously reported (), but the patients were only monitored for 9months in that study.
    Introduction The prevalence of myopia has rapidly increased in recent decades, resulting in a significant global public health concern (Morgan et al., 2012; Pan et al., 2012). Globally, there are approximately 153 million people over the age of 5years who suffer from visual defects (8million of whom suffer from blindness) caused by uncorrected myopia and other refractive errors (Resnikoff et al., 2008). Myopia is an important and often undertreated eye disease. Although most cases of myopia can be corrected with glasses, contact lenses, or refractive surgery, uncorrected refractive errors still account for ~33% of visual impairments (Dandona and Dandona, 2001; McCarty, 2006). High-degree myopia is an especially important visual affliction because of the higher risks of macular and retinal complications. Myopia results primarily from abnormal elongation of the vitreous chamber of the eye (Curtin, 1985). This condition is recapitulated in the monocular form deprivation (MFD) animal model, which has been used to study myopia pathogenesis (McKanna and Casagrande, 1981). Eye elongation is associated with remodeling of the sclera (Marzani and Wallman, 1997; McKanna and Casagrande, 1981), loss of scleral tissue via reduced connective tissue synthesis, and increased collagen I (COL1) degradation, resulting in changes in the composition and ductility of the sclera (McBrien et al., 2000; Rada et al., 2002). Recent studies in monkeys showed that the retina—specifically, photoreceptors and retinal pigment epithelium—plays an important role in modulating eye growth and axial length (Smith et al., 2009; Smith et al., 2005; Smith et al., 2007) by producing activating signals that promote scleral tissue remodeling (Chen et al., 2012).