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AJ  Fay  T  McMahon  C  Im  C  Bair-Marshall  KJ  Niesner  H  Li  A  Nelson  SM  Voglmaier  Y-H  Fu  LJ  Ptáček 《Neurogenetics》2021,22(3):171-185

Paroxysmal kinesigenic dyskinesia is an episodic movement disorder caused by dominant mutations in the proline-rich transmembrane protein PRRT2, with onset in childhood and typically with improvement or resolution by middle age. Mutations in the same gene may also cause benign infantile seizures, which begin in the first year of life and typically remit by the age of 2 years. Many details of PRRT2 function at the synapse, and the effects of mutations on neuronal excitability in the pathophysiology of epilepsy and dyskinesia, have emerged through the work of several groups over the last decade. However, the age dependence of the phenotypes has not been explored in detail in transgenic models. Here, we report our findings in heterozygous and homozygous Prrt2 knockout mice that recapitulate the age dependence of dyskinesia seen in the human disease. We show that Prrt2 deletion reduces the levels of synaptic proteins in a dose-dependent manner that is most pronounced at postnatal day 5 (P5), attenuates at P60, and disappears by P180. In a test for foot slippage while crossing a balance beam, transient loss of coordination was most pronounced at P60 and less prominent at age extremes. Slower traverse time was noted in homozygous knockout mice only, consistent with the ataxia seen in rare individuals with biallelic loss of function mutations in Prrt2. We thus identify three age-dependent phenotypic windows in the mouse model, which recapitulate the pattern seen in humans with PRRT2-related diseases.

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ObjectivesThe aim of this study was to retrospectively examine trends in percutaneous exposure incidences (PEIs) at the School of Dentistry (SoD) from 2009 to 2019 and to report on the underreporting rate of PEIs, current attitudes, and awareness of PEI safety protocols from clinical staff and students at the SoD in 2019.MethodsRetrospective data were collected from deidentified archival incident reports from 2009 to 2019 from the SoD's incident reporting system (UQSafe and Legacy Database). Additionally, cross-sectional data were collected via the validated Percutaneous Exposure Incident Questionnaires (PEIQ) completed by clinical staff and students of the SoD in 2019.ResultsFrom the archival data, the majority (79.9%) of the 618 reported PEIs involved students. Local anaesthetic-related procedures were the most common cause in the archival (31.5%) and survey data (23.7%), whereas the needle-prick was the most common causative instrument in both data sets. Additionally, the finger was the most common site of injury found in the archival (53.0%) and survey data (52.8%). From 345 responses to the survey, 42.1% of PEIs sustained were not reported.ConclusionsStudents were at a higher risk of sustaining a PEI than staff members between 2009 and 2019. The reported knowledge on PEI classification and preventative measures is inadequate, suggesting that further PEI education is necessary. The study provides evidence of the trends in PEIs as well as data on the attitudes and awareness of student and staff at a dental teaching faculty to support the development of PEI safety management protocols.  相似文献   
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We aimed to investigate the impact of genetic alterations on the efficacy of poziotinib in a phase II clinical trial of patients with heavily treated HER2-positive metastatic breast cancer (BC). We performed targeted ultra-deep sequencing with a customized cancer gene panel and RNA expression assay using BC specimens. Of 106 patients, biomarker data were available for 85. Copy number (CN) amplifications of HER2 were observed in 72 patients (85%), and CN >8 in 50 (59%). Single nucleotide variants (SNVs) of HER2 were found in 16 patients (19%). Genetic alterations of PIK3CA pathway were found in 40 patients (47%). Median progression free survival (PFS) of the biomarker analysis group was 3.61 months. In terms of PFS, HER2 with CN >8 prolonged (hazard ratio (HR) 0.61, 95% CI: 0.38, 0.97, p = 0.037) and alteration of PIK3CA pathway shortened the duration of survival (HR 2.25, 95% CI: 1.39, 3.63, p = 0.001). SNVs of HER2 increased survival duration, but the effect was not significant (HR: 0.58, 95% CI: 0.31, 1.08, p = 0.085). In addition, SNVs in the ERBB3 cytoplasmic domain decreased poziotinib response (HR: 4.58, 95% CI: 2.02, 10.37, p < 0.001). In multigene analysis, BC with HER2 CN >8 and intact PIK3CA pathway had significantly longer PFS compared to others (HR: 0.37, 95% CI: 0.21, 0.66, p = 0.001), while SNVs in the ERBB3 cytoplasmic domain predicted poor prognosis (HR: 4.28, 95% CI: 1.71, 10.71, p < 0.001). In conclusion, HER2 CN amplification, PIK3CA pathway alteration, and ERBB3 cytoplasmic mutation showed predictive roles on clinical outcomes of HER2-positive MBC treated with poziotinib.  相似文献   
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Although poly(3,4‐ethylenedioxythiophene):poly(styrenesulfonate) (PEDOT:PSS) has good electrical conductivity and high transparency in most applications, its usage in stretchable applications is limited because of its rigidity, reduced conductivity after elongation, and poor environmental stability. This study addresses these issues by incorporating the soft and relatively hydrophobic moiety poly(ethylene glycol) methacrylate (PEGMA). By incorporating PEGMA randomly in the rigid PSS chain, a soft and hydrophobic copolymer P(SS‐co‐PEGMA) is obtained. The conducting P(SS‐co‐PEGMA)‐based polymer‐coated PET film exhibits good resistance even after 400% elongation. In addition, PEDOT:P(SS‐co‐PEGMA) has better environmental stability than PEDOT:PSS because of the presence of the relatively hydrophobic PEGMA moiety in the chain. Moreover, the potential applicability of the synthesized flexible and stretchable electronic material as a stretchable matrix is established, which includes inorganic conductors (AgNW). When this material is stretched, it can be applied as a conductive interconnector to maintain the electrical pathway, instead of the other insulating matrices.  相似文献   
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