Rasmussenfoley9213

BACKGROUND Use of a microsensor has been suggested to monitor patching adherence. Application has been limited because the microsensor's small size makes it easy to lose and a swallowing risk. We designed the Eye Patch Assistant (EPA) to hold the small microsensor in place and reduce the risk of loss or swallowing. This study reports the accuracy, precision, ease of use, and comfort for patching with EPA (patch+EPA) to monitor adherence. METHODS Adults (N = 13) wore an adhesive patch alone or a patch+EPA for 2 hours each, recorded wear time, and completed an ease of use/comfort questionnaire; 30 children wore a patch or patch+EPA and completed the questionnaire. Sensor sampling interval was every 5 minutes or every 1 minute. Sensor accuracy and precision were evaluated by Bland-Altman analysis and 95% limits of agreement, and questionnaire scores compared by Wilcoxon tests. RESULTS With 5-minute sampling, we found excellent accuracy for adults (mean actual vs recorded time difference, 1.4 minutes) and children (mean difference, -0.9 min). We found high precision for both adults and children (95% limits of agreement half widths of 6.4 minutes and 1.9 minutes, respectively). In adults, the ease of use score for the patch+EPA was lower than the patch (P less then 0.01), but the comfort score for the patch+EPA was higher (P less then 0.01). For children, scores did not differ significantly. The patch+EPA functioned well between 45° and 82°F. CONCLUSIONS The patch+EPA was well accepted and monitored adherence accurately and precisely. PURPOSE To assess the extent to which strabismus in children was associated with motor difficulties and to examine which parameters of strabismus were most closely associated with motor development. METHODS The motor skills of children who were suffering from strabismus, were tested binocularly using the Movement Assessment Battery for Children, Second Edition (MABC-2) and compared with the motor performance of monocularly tested healthy controls without any ophthalmologic disease. RESULTS A total of 40 children with strabismus (mean, 7.25 ± 3.83 years; 19 females) and 18 controls (mean age, 8.33 ± 5.42 years; 6 females) were tested. According to the MABC-2 test, of the 40, 19 had no motor disability, and 21 were at risk of or already presented significant motor disabilities. Results of the MABC-2 were significantly lower for strabismic children without binocularity compared to those with binocularity (P = 0.002). Lack of binocularity was associated with significantly lower performance for static balance (P = 0.003) as well as for catching tasks (P = 0.042). CONCLUSIONS Lack of binocularity and stereopsis in children is associated with significant motor skills impairment, in particular for static balance and catching tasks. (E/Z)BCI These results should be confirmed with a larger sample, including older patients, to assess the compensation mechanisms that develop with age and the actual effects of strabismus on overall motor performance. Geminiviruses are single-stranded DNA viruses that cause devastating diseases in many crops worldwide. The replication enhancer proteins (REn), encoded by the C3 (AC3, and AL3) ORFs of geminiviruses, have critical roles in viral DNA accumulation and symptom development in infected plants. In the current study, we have constructed an infectious clone of the Tobacco curly shoot virus (TbCSV) C3 mutant, TbCSVΔC3, that contains two start codon mutations that abrogated C3 ORF expression, but did not alter the amino acid sequence of the C2 ORF. As predicted, the absence of the C3 protein reduced TbCSV DNA accumulation, and over-expression of the C3 protein enhanced TbCSV DNA accumulation in infected leaves of Nicotiana benthamiana. The C3 mutation reduced the expression levels of both virion- and complementary-sense TbCSV genes whereas over-expression of the C3 protein increased TbCSV gene expression. Furthermore, the expression of the wild-type and site-directed mutants of C3 proteins using the potato virus X (PVX) system showed that Y93A mutation reduced the replication enhancement activity of the C3 protein in N. benthamiana. All the available evidence demonstrates that the C3 protein is tightly coupled with TbCSV DNA accumulation. However, the TbCSVΔC3 mutant was nearly as infectious in N. benthamiana as TbCSVWT and only had slightly delayed and attenuated symptom expression. Our findings demonstrate that TbCSV C3 protein enhances viral replication and gene expression, but has only moderate effects on symptom development in N. benthamiana. V.Human cytomegalovirus (HCMV) is a ubiquitous member of the Betaherpesvirinae subfamily, causing life-threatening diseases in individuals with impaired, immature, or senescent immunity. Accordingly, HIV-infected AIDS patients, transplant recipients, and congenitally infected neonates frequently suffer from symptomatic episodes of HCMV replication. Like all viruses, HCMV has a split relationship with the host proteome. Efficient virus replication can only be achieved if proteins involved in intrinsic, innate, and adaptive immune responses are sufficiently antagonized. Simultaneously, the abundance and function of proteins involved in the synthesis of chemical building blocks required for virus production, such as nucleotides, amino acids, and fatty acids, must be preserved or even enriched. The ubiquitin (Ub) proteasome system (UPS) constitutes one of the most relevant protein decay systems of eukaryotic cells. In addition to the regulation of the turn-over and abundance of thousands of proteins, the UPS also generates the majority of peptides presented by major histocompatibility complex (MHC) molecules to allow surveillance by T lymphocytes. Cytomegaloviruses exploit the UPS to regulate the abundance of viral proteins and to manipulate the host proteome in favour of viral replication and immune evasion. After summarizing the current knowledge of CMV-mediated misuse of the UPS, we discuss the evolution of viral proteins utilizing the UPS for the degradation of defined target proteins. We propose two alternative routes of adapter protein development and their mechanistic consequences.