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Littérature scientifique sur le sujet « Scas15 »

Auteur : Grafiati
Publié le 25 juillet 2024

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Articles de revues sur le sujet "Scas15"

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Silva, Iago Castro da, Eveson Oscar Almeida Conceição, Daniel Santiago Pereira, Hervé Rogez et Nilton Akio Muto. « Evaluation of the Antimicrobial Capacity of Bacteria Isolated from Stingless Bee (Scaptotrigona aff. postica) Honey Cultivated in Açai (Euterpe oleracea) Monoculture ». Antibiotics 12, no 2 (20 janvier 2023) : 223. http://dx.doi.org/10.3390/antibiotics12020223.

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Many antimicrobial compounds have been seeking to protect the human body against pathogenic microbial infections. In recent times, there has been considerable growth of pathogens resistant to existing drugs due to the inappropriate use of antibiotics. In the present study, bacteria isolated from the honey of stingless bees native to the Amazon called Scaptotrigona aff. postica and Apis mellifera were used to determine their potential antimicrobial properties and characterize the medium cultivated with isolated bacteria. The results showed inhibition of nine isolates. Among these isolates, SCA12, SCA13, and SCA15 showed inhibitory activity similar to that of vancomycin, which was used as a positive control. The SCA13 strain obtained the best results with antimicrobial extract against the tested pathogens; the species was identified as Enterococcus faecalis, and its lyophilized extract was characterized by temperature, pH, and trypsin, in which they showed antimicrobial activity. This work shows that bacteria isolated from the stingless bee honey, Scaptotrigona aff. postica, have the potential to produce antimicrobial substances.
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Gardner, R. J. M. « "SCA16" is really SCA15 ». Journal of Medical Genetics 45, no 3 (22 octobre 2007) : 192. http://dx.doi.org/10.1136/jmg.2007.056341.

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Kaur, Jaslovleen, Shaista Parveen, Uzma Shamim, Pooja Sharma, Varun Suroliya, Akhilesh Kumar Sonkar, Istaq Ahmad et al. « Investigations of Huntington’s Disease and Huntington’s Disease-Like Syndromes in Indian Choreatic Patients ». Journal of Huntington's Disease 9, no 3 (8 octobre 2020) : 283–89. http://dx.doi.org/10.3233/jhd-200398.

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Background: The diagnostic workup for choreiform movement disorders including Huntington’s disease (HD) and those mimicking HD like phenotype is complex. Objective: The aim of the present study was to genetically define HD and HD-like presentations in an Indian cohort. We also describe HTT-CAG expansion manifesting as neuroferritinopathy-like disorder in four families from Punjab in India. Materials and methods: 159 patients clinically diagnosed as HD and HD-like presentations from various tertiary neurology clinics were referred to our centre (CSIR-IGIB) for genetic investigations. As a first tier test, CAG-TNR for HTT was performed and subsequently HD-negative samples were screened for JPH3 (HDL2), TBP (SCA17), ATN1 (DRPLA), PPP2R2B (SCA12) and GGGGCC expansion in C9orf72 gene. Four families presenting as neuroferritinopathy-like disorder were also investigated for HTT-CAG expansion. Results: 94 of 159 (59%) patients were found to have expanded HTT-CAG repeats. Pathogenic repeat expansion in JPH3, TBP, ATN1 and C9orf72 were not found in HD negative cases. Two patients were positive for SCA12-CAG expansion in pathogenic length, whereas 5 cases harboured TBP-CAG repeats falling in reduced penetrance range of 41– 48 repeats for SCA17. Four unrelated families, presented with atypical chorea and brain MRI findings suggestive of basal ganglia abnormalities mimicking neuroferritinopathy were found to harbour HTT-CAG expansion. Conclusion: We present SCA12 as a new reported phenocopy of HD which should be considered for diagnostic workout along with SCA17 for HD-like syndromes. This study also illustrates the necessity, to consider evolving HD like phenotype, as a clinical diagnosis for cases with initial manifestations depicting neuroferritinopathy.
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Seixas, Ana I., Martin H. Maurer, Mark Lin, Colleen Callahan, Alka Ahuja, Tohru Matsuura, Christopher A. Ross, Fuki M. Hisama, Isabel Silveira et Russell L. Margolis. « FXTAS, SCA10, and SCA17 in American patients with movement disorders ». American Journal of Medical Genetics Part A 136A, no 1 (2005) : 87–89. http://dx.doi.org/10.1002/ajmg.a.30761.

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Ghanem, Mustafa H., Andrew J. Shih, Himanshu Vashistha, Latanya N. Coke, Wentian Li, Sun Jung Kim, Kim R. Simpfendorfer et Peter K. Gregersen. « Investigations into SCAMP5, a candidate lupus risk gene expressed in plasmacytoid dendritic cells ». Lupus Science & ; Medicine 8, no 1 (novembre 2021) : e000567. http://dx.doi.org/10.1136/lupus-2021-000567.

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ObjectiveWe have investigated the molecular function of SCAMP5, a candidate risk gene for SLE exclusively expressed in plasmacytoid dendritic cells (pDCs) among peripheral leucocytes.MethodsWe tested the independence of the association in SCAMP5 with SLE by performing conditional analyses. We profiled the expression pattern of SCAMP5 among circulating leucocytes at the transcript and protein levels. Using lentiviral vectors, we localised the subcellular distribution of SCAMP5 alongside the interferon secretory pathway. We analysed pDCs for the expression of SCAMP5 and interferon production capacity by SCAMP5 genotype. Finally, we examined pDC-specific SCAMP5 isoforms by total RNAseq analysis and examined for genotype-associated quantitative differences therein.ResultsA conditional analysis revealed evidence of an independent genetic association of SCAMP5 with SLE. Among circulating leucocytes, SCAMP5 is uniquely expressed in pDCs at the transcript and protein levels, with main presence in the Golgi apparatus and minor presence at the cell periphery. In live cells, SCAMP5 displayed dynamic Golgi-cell surface trafficking and localised with the interferon secretory pathway. SCAMP5 did not differ in expression levels in pDCs between genotyped donors; however, a transient interferon secretory defect was noted in pDCs from donors carrying the risk genotype.ConclusionsSCAMP5 constitutes a novel SLE risk gene on the basis of genomic data and expression in a cell type widely implicated in SLE pathogenesis. While we could not find evidence of quantitative expression differences in SCAMP5 between genotyped donors, SCAMP5 remains an attractive gene to explore given its highly restricted expression pattern and colocalisation with interferon secretion.
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Pouw, Juliëtte N., Michel A. M. Olde Nordkamp, Tom G. O'Toole, Timothy R. D. J. Radstake, Emmerik F. A. Leijten et Marianne Boes. « Activation-induced colocalisation of SCAMP5 with IFNα in human plasmacytoid dendritic cells ». Lupus Science & ; Medicine 9, no 1 (mars 2022) : e000680. http://dx.doi.org/10.1136/lupus-2022-000680.

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IntroductionPlasmacytoid dendritic cells (pDCs) are the main producers of type I interferon (IFN) in SLE. pDCs express high secretory carrier membrane protein 5 (SCAMP5). Recent work in transfected HEK cells connects SCAMP5 to the type I IFN secretory pathway. To further study the role of SCAMP5 in IFNα secretion by pDCs, we focused on the subcellular distribution of SCAMP5 in human pDCs freshly isolated from peripheral blood.MethodsWe measured SCAMP5 expression by flow cytometry in peripheral blood mononuclear cells of healthy subjects (n=8). Next, we assessed the colocalisation of SCAMP5 with IFNα in pDCs of healthy subjects (n=4) by evaluating bright detail similarity (BDS) scores using ImageStream technology.ResultsWe confirm that SCAMP5 is highly expressed by pDCs derived from peripheral blood. In activated pDCs, we show that SCAMP5 colocalises with IFNα (mean BDS 2.0±0.1; BDS >2.0 in 44% of pDCs).ConclusionSCAMP5 colocalises with IFNα in activated human pDCs, in support of a role of this trafficking protein in the secretion of type I IFN by pDCs.
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Flockerzi, Fidelis Andrea, Johannes Hohneck, Matthias Saar, Rainer Maria Bohle et Phillip Rolf Stahl. « SCARA5 Is Overexpressed in Prostate Cancer and Linked to Poor Prognosis ». Diagnostics 13, no 13 (29 juin 2023) : 2211. http://dx.doi.org/10.3390/diagnostics13132211.

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Prostate cancer is one of the most common malignancies worldwide, showing a wide range of clinical behaviors. Therefore, several treatment options arise out of the diagnosis “prostate cancer”. For this reason, it is desirable to find novel prognostic and predictive markers. In former studies, we showed that THSD7A expression is associated with unfavorable prognostic parameters in prostate cancer and is linked to a high expression of focal adhesion kinase (FAK). Recently, scavenger receptor class A member 5 (SCARA5) was reported to be the downstream gene of THSD7A in esophageal squamous cell carcinoma. SCARA5 is believed to play an important role in the development and progression of several different tumor types. Most studies describe SCARA5 as a tumor suppressor. There is also evidence that SCARA 5 interacts with FAK. To examine the role of SCARA5 as a potential biomarker in prostate cancer, a total of 461 prostate cancers were analyzed via immunohistochemistry using tissue microarrays. Furthermore, we compared the expression level of SCARA5 with our previously collected data on THSD7A and FAK. High SCARA5 expression was associated with advanced tumor stage (p < 0.001), positive nodal status (p < 0.001) and high Gleason-score (p < 0.001). At least, strongly SCARA5-positive cancers were associated with THSD7A-positivity. There was no significant association between SCARA5 expression level and FAK expression level. To our knowledge, we are the first to investigate the role of SCARA5 in prostate cancer and we demonstrated that SCARA5 might be a potential biomarker in prostate cancer.
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Flockerzi, Fidelis Andrea, Johannes Hohneck, Frank Langer, Wolfgang Tränkenschuh et Phillip Rolf Stahl. « The Role of SCARA5 as a Potential Biomarker in Squamous Cell Carcinoma of the Lung ». International Journal of Molecular Sciences 25, no 13 (4 juillet 2024) : 7355. http://dx.doi.org/10.3390/ijms25137355.

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Lung cancer is the leading cause of cancer-related deaths in the western world. Squamous cell carcinoma is one of the most common histological subtypes of this malignancy. For squamous cell carcinoma of the lung (LSCC), prognostic and predictive markers still are largely missing. In a previous study, we were able to show that the expression of THSD7A shows an association with unfavorable prognostic parameters in prostate cancer. There is also a link to a high expression of FAK. There is incidence that SCARA5 might be the downstream gene of THSD7A. Furthermore, there is evidence that SCARA5 interacts with FAK. We were interested in the role of SCARA5 as a potential biomarker in LSCC. Furthermore, we wanted to know whether SCARA5 expression is linked to THSD7A positivity and to the expression level of FAK. For this reason, we analyzed 101 LSCC tumors by immunohistochemistry. Tissue microarrays were utilized. No significant association was found between SCARA5 expression and overall survival or clinicopathological parameters. There was also no significant association between THSD7A positivity and SCARA5 expression level. Moreover, no significant association was found between FAK expression level and SCARA5 expression level. SCARA5 seems not to play a major role as a biomarker in squamous cell carcinoma of the lung.
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Yousaf, Hammad, Ambrin Fatima, Zafar Ali, Shahid M. Baig, Mathias Toft et Zafar Iqbal. « A Novel Nonsense Variant in GRM1 Causes Autosomal Recessive Spinocerebellar Ataxia 13 in a Consanguineous Pakistani Family ». Genes 13, no 9 (17 septembre 2022) : 1667. http://dx.doi.org/10.3390/genes13091667.

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Background and objectives: Autosomal recessive spinocerebellar ataxia-13 (SCAR13) is an ultra-rare disorder characterized by slowly progressive cerebellar ataxia, cognitive deficiencies, and skeletal and oculomotor abnormalities. The objective of this case report is to expand the clinical and molecular spectrum of SCAR13. Methods: We investigated a consanguineous Pakistani family with four patients partially presenting with clinical features of SCAR13 using whole exome sequencing. Segregation analysis was performed by Sanger sequencing in all the available individuals of the family. Results: Patients presented with quadrupedal gait, delayed developmental milestones, non-progressive peripheral neuropathy, and cognitive impairment. Whole exome sequencing identified a novel pathogenic nonsense homozygous variant, Gly240*, in the gene GRM1 as a cause of SCAR13 that segregates with the recessive disease. Discussion: We report a novel homozygous nonsense variant in the GRM1 gene in four Pakistani patients presenting with clinical features that partially overlap with the already reported phenotype of SCAR13. In addition, the family presented quadrupedal gait and non-progressive symptoms, manifestations which have not been recognized previously. So far, only four variants in GRM1 have been reported, in families of Roma, Iranian, and Tunisian origins. The current study adds to the mutation spectrum of GRM1 and provides a rare presentation of SCAR13, the first from the Pakistani population.
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Lee, Unghwi, Chunghon Choi, Seung Hyun Ryu, Daehun Park, Sang-Eun Lee, Kitae Kim, Yujin Kim et Sunghoe Chang. « SCAMP5 plays a critical role in axonal trafficking and synaptic localization of NHE6 to adjust quantal size at glutamatergic synapses ». Proceedings of the National Academy of Sciences 118, no 2 (28 décembre 2020) : e2011371118. http://dx.doi.org/10.1073/pnas.2011371118.

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Glutamate uptake into synaptic vesicles (SVs) depends on cation/H+ exchange activity, which converts the chemical gradient (ΔpH) into membrane potential (Δψ) across the SV membrane at the presynaptic terminals. Thus, the proper recruitment of cation/H+ exchanger to SVs is important in determining glutamate quantal size, yet little is known about its localization mechanism. Here, we found that secretory carrier membrane protein 5 (SCAMP5) interacted with the cation/H+ exchanger NHE6, and this interaction regulated NHE6 recruitment to glutamatergic presynaptic terminals. Protein–protein interaction analysis with truncated constructs revealed that the 2/3 loop domain of SCAMP5 is directly associated with the C-terminal region of NHE6. The use of optical imaging and electrophysiological recording showed that small hairpin RNA–mediated knockdown (KD) of SCAMP5 or perturbation of SCAMP5/NHE6 interaction markedly inhibited axonal trafficking and the presynaptic localization of NHE6, leading to hyperacidification of SVs and a reduction in the quantal size of glutamate release. Knockout of NHE6 occluded the effect of SCAMP5 KD without causing additional defects. Together, our results reveal that as a key regulator of axonal trafficking and synaptic localization of NHE6, SCAMP5 could adjust presynaptic strength by regulating quantal size at glutamatergic synapses. Since both proteins are autism candidate genes, the reduced quantal size by interrupting their interaction may underscore synaptic dysfunction observed in autism.
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Thèses sur le sujet "Scas15"

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Salimbeni, Simona. « Déficience en TDP1 et instabilité génomique dans les cellules non-réplicatives ». Thesis, Toulouse 3, 2020. http://www.theses.fr/2020TOU30065.

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L'ataxie spinocérébelleuse avec neuropathie axonale (SCAN1) est un rare syndrome neurodégénératif récessif associé à une atrophie cérébelleuse et à une neuropathie périphérique. Il est causé par une mutation homozygote dans le gène tyrosyl-ADN phosphodiestérase-1 (TDP1) (A1478G). Cette mutation entraîne une substitution de l'histidine 493 par une arginine (H493R) dans le site catalytique de TDP1, ce qui conduit à une diminution de l’activité de TDP1. TDP1 hydrolyse la liaison entre une extrémité 3' de l'ADN et une tyrosine au sein d'un complexe de clivage de la topoisomérase I (TOP1cc) piégé sur la chromatine. TDP1 n'excise pas seulement les TOP1cc piégés, mais répare également d'autres lésions bloquant l'extrémité 3', notamment les 3'-phosphoglycolates qui résultent d’une oxydation. Toutefois, le mécanisme par lequel la mutation TDP1 H493R entraine le phénotype SCAN1, qui est associé avec la mort des neurones post-mitotiques, est peu connu. Les cassures double-brin (DSBs) de l'ADN sont peu fréquentes mais parmi les lésions génomiques les plus sévères. Un défaut de réparation peut induire la mort cellulaire, et elles ont été impliquées dans la pathogénèse de nombreuses maladies humaines, incluant des syndromes neurodégénératifs. Mon objectif de doctorat a été de déterminer si le phénotype SCAN1 pouvait être lié à une accumulation de DSBs dans des cellules non réplicatives portant la mutation TDP1 H493R. Les seuls modèles disponibles pour étudier l'impact de cette mutation étaient des lignées de cellules lymphoblastoïdes provenant de patients SCAN1 comparées à celles d'individus sains. Nous avons donc généré des modèles de cellules d'ostéosarcome U2OS homozygotes pour TDP1 H493R ou TDP1 KO en utilisant la technique CRISPR-Cas9. Nous avons également généré des cellules primaires de poumon WI38 hTERT TDP1 KO. Nous avons observé que les cellules TDP1 H493R et TDP1 KO accumulent des DSBs endogènes, principalement dans la phase G1 du cycle cellulaire par rapport à la phase S. Une augmentation de DSBs a également été observée après déplétion de TDP1 par siRNA dans les cellules WI38 hTERT quiescentes, suggérant la nature réplication-indépendante de ces DSBs. Le traitement des cellules TDP1 H493R et TDP1 KO par la camptothécine, qui induit spécifiquement des TOP1ccs, suggère en outre que l'accumulation de DSBs pourrait être liée au défaut d'élimination des TOP1ccs. Ensuite, nous nous sommes demandé si l'accumulation de DSBs dans ces cellules pouvait être liée à une augmentation de la production de ces DSBs et/ou à un défaut dans leur réparation. Notamment, les structures R-loops qui se forment lors de la transcription peuvent induire des DSBs dans les cellules non réplicatives. Nous avons montré que la déficience en TDP1 modulait les R-loops sur certains gènes, ce qui soulève la possibilité de leur implication dans la formation de DSBs. L'analyse de la réparation des DSBs après traitement par la camptothécine a révélé que les cellules TDP1 H493R et TDP1 KO étaient toutes deux défectueuses dans la réparation des DSBs en G1 mais pas en S, la mutation TDP1 H493R ayant l'effet le plus prononcé. Ces résultats suggèrent que les DSBs pourraient s'accumuler spécifiquement dans les cellules déficientes en TDP1 qui ne répliquent pas en raison d'une réparation défectueuse de ces cassures. L’ensemble des notre résultats apporte de nouvelles informations sur l'étiologie du syndrome neurodégénératif SCAN1. Ce travail a été soutenu par une bourse de doctorat dans le cadre du programme universitaire franco-italien VINCI 2016
Spinocerebellar ataxia with axonal neuropathy (SCAN1) is a rare recessive neurodegenerative syndrome associated with cerebellar atrophy and peripheral neuropathy. It is caused by a homozygous missense mutation in the tyrosyl-DNA phosphodiesterase-1 (TDP1) gene (A1478G). This results in a substitution of histidine for arginine-493 (H493R) in the TDP1 catalytic site, leading to a reduced TDP1 activity. TDP1 hydrolyses the bond between a DNA 3’-end and a tyrosyl moiety within a trapped topoisomerase I cleavage complex (TOP1cc). TDP1 not only excises trapped TOP1ccs but also processes other 3’-end-blocking lesions, including 3’-phosphoglycolates that result from oxidation. Even so, how TDP1 H493R mutation promotes the SCAN1 phenotype, which is associated with the death of post-mitotic neurons, is unclear. DNA double-strand breaks (DSBs) are infrequent but among the most harmful genomic lesions. Their defective repair can induce cell death, and they have been implicated in the pathogenesis of several human diseases, including neurodegenerative syndromes. Hence, my Ph.D. objective was to investigate whether the SCAN1 phenotype could be related to an accumulation of DSBs in non-replicating cells harboring the H493R mutation of TDP1. The only available models to study the impact of TDP1 H493R mutation were lymphoblastoid cell lines derived from SCAN1 patients compared to those of healthy individuals. Hence, we have generated models of osteosarcoma U2OS cells homozygous for TDP1 H493R or TDP1 KO employing the CRISPR-Cas9 technique. We have also generated primary lung WI38 hTERT fibroblasts TDP1 KO. We found that both TDP1 H493R and TDP1 KO cells accumulate endogenous DSBs, primarily in the G1 phase of the cell cycle compared to S phase. A similar increase of DSBs was observed in quiescent WI38 hTERT cells following depletion of TDP1 with siRNA, suggesting the replication-independent nature of DSBs. Treatment of TDP1 H493R and TDP1 KO cells with camptothecin to induced trapped TOP1ccs, further suggests that accumulation of DSBs could be related to the defective removal of TOP1ccs. Next, we asked whether DSB accumulation in those cells could be related to an increase in DSB production and/or a defect in their repair. Notably, R-loop structures that form co-transcriptionally can induce DSBs in non-replicating cells. We found that TDP1 deficiency modulated R-loop levels at some gene loci, raising the possibility of their implication in DSB formation. Analysis of DSB repair following camptothecin treatment revealed that both TDP1 H493R and TDP1 KO cells were defective in the repair of DSBs in G1 but not in S, with TDP1 H493R having the most pronounced effect. These results suggest that DSBs would accumulate specifically in TDP1-deficient cells that do not undergo replication, due to a defective repair of those breaks. Together, our results provide insights on the etiology of the SCAN1 neurodegenerative syndrome. This work was supported by a PhD fellowship under the French-Italian University VINCI Program 2016
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Vuillaume, Isabelle. « Identification d'un nouveau locus responsable d'une ataxie spinocérébelleuse héréditaire (SCA21) : approche gène-candidat ». Lille 2, 2003. http://www.theses.fr/2003LIL2MT27.

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Kelp, Alexandra [Verfasser]. « Generierung und Charakterisierung eines transgenen Rattenmodells der Spinozerebellären Ataxie Typ 17 (SCA17) / Alexandra Kelp ». München : Verlag Dr. Hut, 2015. http://d-nb.info/1075409616/34.

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Schuster, Stefanie [Verfasser]. « Deciphering the effect of mutant STUB1 on the heat shock response in SCAR16 patient-derived cells / Stefanie Schuster ». Tübingen : Universitätsbibliothek Tübingen, 2020. http://d-nb.info/1216501882/34.

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Öhlund, Rebecca. « Könsskillnader i välbefinnande utifrån val av fysisk aktivitet ». Thesis, Örebro universitet, Institutionen för juridik, psykologi och socialt arbete, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-43343.

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Samhället uppmuntrar individer att se över sina hälsovanor för att öka välbefinnandet. Syftet var att undersöka om val av fysisk aktivitet hade effekt på den generella hälsan i ökat subjektivt välbefinnande samt om det fanns könsskillnader i dessa. Sextio män och kvinnor mellan 25-50 år valdes slumpmässigt ut från träningsanläggningar för att besvara the 12-item General Health Questionnaire (GHQ-12) samt Swedish Core Affect Scale (SCAS). Resultatet visade på signifikant ökning av välbefinnande efter fysisk aktivitet samt inga könsskillnader. Dock fanns en signifikant interaktionseffekt mellan kön och fysisk aktivitet, de män som promenerade och kvinnor som konditionstränade hade högst välbefinnande och generell hälsa. Slutsatsen blev att välbefinnandet ökade oavsett kön efter fysisk aktivitet dock gav olika aktiviteter varierande ökningar mellan könen.
The society encourages individuals to promote their health habits in order to improve their well-being. The aim was to investigate the effect of different types of physical activity on experience of general health in well-being in men and woman. Sixty men and women in ages 25-50 years old were randomly chosen from training facilities to answer the 12-item General Health Questionnaire (GHQ-12) and Swedish Core Affect Scale (SCAS). The results showed a significant increase in positive well-being due to the practice of physical activity, but there were no gender difference. However, it was found a significant interaction effect of age and physical activity on health, the men who walked and women who conditioning trained showed highest well-being and general health. The conclusion was that the well-being increase regardless of sex after physical activity, however, different activities gave varying increases between the sexes.
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Bampi, Giovana Bavia. « Estudo de haplótipos em famílias com ataxia espinocerebelar tipo 10(SCA10) : evidências de um efeito fundador da mutação ». reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2015. http://hdl.handle.net/10183/119618.

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A ataxia espinocerebelar tipo 10 (SCA10) é uma doença neurodegenerativa rara de herança autossômica dominante caracterizada por atrofia cerebelar com alterações da marcha e, em alguns casos, convulsões. A SCA10 é causada por expansões de repetições pentanucleotídicas ATTCT no íntron 9 do gene ATXN10, o qual se localiza no locus 22q13. Alelos normais apresentam entre 10 a 29 repetições e o alelo patogênico apresenta entre 800 a 4.500 repetições. Até o momento, casos de SCA10 foram descritos apenas em pacientes miscigenados de países do continente americano como México, Brasil, Argentina, Venezuela, Colômbia, Estados Unidos e, mais recentemente, Peru. A origem ameríndia auto declarada pelos pacientes com SCA10 e a ausência de casos em países europeus e asiáticos indicam a hipótese de ocorrência de um efeito fundador da mutação nas populações nativas americanas. O objetivo deste trabalho foi investigar a hipótese de origem ancestral comum da mutação no gene ATXN10. As amostras analisadas foram proveniente de 16 famílias brasileiras e de 21 famílias peruanas com SCA10. Além do grupo de pacientes, um grupo controle composto por 48 indivíduos saudáveis da população indígena Quechua do Peru foi também incluída na análise assim como 51 controles brasileiros de um estudo anterior. Os resultados obtidos mostraram que o haplótipo 19CGGC14 associado ao alelo da expansão está presente em 46,8% das famílias de brasileiros e 62,8% das famílias de peruanos. As frequências de ambos os grupos não é estatisticamente diferente dos controles Quechua (57,3%), sendo diferente dos controles brasileiros (11,8%) (p<0,001). Entretanto, origem etnogeográfica da mutação ainda é desconhecida. O haplótipo comum mínimo foi expandido incluindo outros dois marcadores polimórficos, os quais integram dois haplótipos com alta prevalência em populações nativo americanas com o intuito de obter uma aproximação da origem da região cromossômica onde a mutação está inserida. Dois haplótipos mais frequentes 19-13-CGGC-14-10 e 19- 15-CGGC-14-10 foram identificados nos controles indígenas Quechua, com frequências relativas de 14,3% e 13,3% respectivamente. O segundo haplótipo mais frequente em Quechuas, 19-15-CGGC-14-10, é encontrado em 50,0% das famílias brasileiras e em 64,7% das famílias Peruanas com SCA10. Esses achados corroboram a hipótese de origem ameríndia da mutação.
Spinocerebellar ataxia type 10 is a rare autosomal dominant neurodegenerative disorder characterized by progressive cerebellar ataxia and epilepsy in some cases. The disease is caused by a pentanucleotide ATTCT expansion in intron 9 of the ATXN10 gene, which is located at locus 22q13.3. Normal alleles range from 10 to 29 repeats while mutant allele range from 800 to 4,500 repeats. SCA10 has only been described so far in admixed patients from American countries such as Mexico, Brazil, Argentina, Venezuela, Colombia, United States and more recently Peru. The self-declared Amerindian ancestry by patients and the absence of SCA10 in European and Asian countries leads to the hypothesis of a mutation founder effect in the Native American populations. The aim of this study was to investigate the hypothesis of a common ancestral origin of ATXN10 mutation. Samples analyzed were from 16 Brazilian families, 21 Peruvian families with SCA10. In addition to patient samples, 48 healthy individuals of Indigenous Quechua from Peru were also included in the laboratorial analyses along with 51 Brazilian controls from a previous study. Our data has shown that 19CGGC14-shared haplotype was found in 46.8% of Brazilian and in 62.8% of Peruvian families. Frequencies from both groups are not statistically different from Quechua controls (57.3%), but they are statistically different from Brazilian controls (11.8%) (p<0.001). However, the mutation ethno-geographical origin remains unclear. The minimal common haplotype was expanded by including two additional polymorphic markers that are found at high prevalence in two haplotypes in Native American populations aiming to shed light on the chromosome region ancestry where the mutation arose. Two frequent haplotypes, 19-13-CGGC-14-10 and 19-15- CGGC-14-10 were identified in Indigenous Quechua controls, with relative frequencies of 14.3% and 13.3% respectively. The second most frequent haplotype in Quechuas, 19-15- CGGC-14-10, is found in 50.0% of Brazilian and in 64.7% of Peruvian families with SCA10. These findings corroborate the hypothesis of a Native American ancestry of the mutation.
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Tang, Matthew Y. « Gene reprogramming by K48R mutant ubiquitin in a mouse model of SCA1 ». Thesis, University of Ottawa (Canada), 2005. http://hdl.handle.net/10393/27054.

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Spinocerebellar ataxia type 1 (SCA1) is an incurable neurodegenerative disease resulting from the loss of Purkinje neurons within the cerebellum. The causative agent of the disease is the expansion of a trinucleotide repeat in its gene product ataxin-1. The ubiquitin proteasome pathway (UPP) has been implicated in SCA1 but the role of proteolysis in the disease is still poorly understood. To further investigate this issue in vivo , genetic crosses were performed between a well established mouse model of SCA1 and novel strains expressing elevated levels of wild type or mutant isoforms of ubiquitin. The K48R mutant isoform of ubiquitin (a dominant negative inhibitor of proteolysis) was found to significantly delay the deterioration of Purkinje neurons as evidenced by behavioral, morphological, and molecular indicators. This delay was accompanied by the restoration of genes involved in calcium and glutamate signalling and by the stabilization of postsynaptic density proteins whose abundance/activity would otherwise decline in the course of the SCA1 disease. These results are consistent with transcriptional dysregulation as a key mechanism in neurodegeneration and suggest that the UPP is a useful target for the development of novel therapies.
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Keiser, Megan Kathryn. « Gene therapies for spinocerebellar ataxia type 1 ». Diss., University of Iowa, 2013. https://ir.uiowa.edu/etd/2540.

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Spinocerebellar ataxia type 1 (SCA1) is an adult onset, autosomal dominant neurodegenerative disease caused by a CAG repeat expansion in ataxin-1, which encodes the ataxin-1 protein. SCA1 is one of nine polyQ-expansion gain-of-function diseases which includes Huntington's disease, spinal-bulbar muscular atrophy, dentatorubral-pallidoluysian atrophy and other ataxias. Clinical symptoms of SCA1 include ataxia, dysarthria, ophthalmoparesis, muscle wasting, and extrapyramidal and bulbar dysfunction. Cerebellar Purkinje cells (PCs), neurons in the inferior olive and nuclei of the brainstem are affected. No disease-modifying therapy exists for SCA1. The goals of my thesis were to assess the safety and efficacy of AAV-delivered artificial miRNAs targeting ataxin-1 to alleviate neuropathological and behavioral phenotypes in the knock-in and transgenic SCA1 mouse models. In the knock-in SCA1 mouse model AAVs expressing an artificial miRNA (miSCA1) targeting sequences conserved in mouse and human ataxin-1 were injected directly to the deep cerebellar nuclei. This achieved long term silencing of ataxin-1 mRNA and significantly improved rotarod performance, gait deficiencies, and neuropathology of the cerebellum. In the transgenic SCA1 mouse model the same method of delivery was executed with an artificial microRNA (miR) (miS1) designed to optimize potency, efficacy and safety to suppress Atxn1 expression. Additionally the therapeutic potential of continuous overexpression of ataxin-1-like was examined. Delivery of either ataxin-1-like or miS1 viral vectors to SCA1 mouse cerebellum resulted in widespread cerebellar Purkinje cell transduction. There was significant improvement to rotarod performance, gait deficiencies, coordination and balance, as well as the neuropathology of cerebellar Purkinje cells. In summary, these data indicate the utility of these approaches as possible therapies for SCA1 patients.
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Zhou, Tong. « ROLE OF TYROSYL-DNA PHOSPHODIESTERASE (TDP 1) ON REPAIR OF 3′-PHOSPHOGLYCOLATE (3′- PG) TERMINATED DNA DOUBLE-STRAND BREAKS (DSBS) AND IN RESPONSE TO OXIDATIVE STRESS ». VCU Scholars Compass, 2012. http://scholarscompass.vcu.edu/etd/2933.

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DNA DSBs are most toxic to cells because they can lead to genomic rearrangements and even cell death. Most DSBs induced by ionizing radiation or radiomimetic drugs such as calicheamicin and bleomycin, bear 3′-phosphate or 3′- PG moieties that must be removed to allow subsequent gap filling and ligation. DSBs can be repaired by two main pathways: the homologous recombination (HR) pathway and the non-homologous end-joining (NHEJ) pathway, NHEJ is the primary repair pathway in mammalian cells. While HR repairs single strand breaks (SSBs) or DSBs accurately by using an undamaged copy of the sequence mostly at late S phase and G2 phase, the NHEJ pathway repairs DSBs without the requirement for sequence homology in a processing that may be error-free or error- prone and is most active at G1 phase. TDP1 is a DNA repair enzyme in both pathways, It associates with DNA SSB repair proteins XRCC1 and DNA ligase III and plays a role in processing of topoisomerase I- mediated SSBs. Our early results suggested that TDP1 also can remove protruding 3’- PG and other 3’ blocks from DSBs ends in vitro. A homozygous H493R mutation in the active site of TDP1 causes spinocerebellar ataxia with axonal neuropathy (SCAN1), a rare autosomal recessive genetic disease with neurological symptoms including peripheral neuropathy. DNA damage and misrepair can be determined by measuring the incidence of chromosomal aberrations such as rings, breaks, dicentrics, acentric fragments, and translocations in metaphase cells, and micronuclei in interphase cells. To assess the possible role of TDP1 in DSB repair in intact cells, the radiosensitivity of SCAN1 cells was determined by using a dose-fractionation method of irradiation. The data indicated that, when exposed to fractionated radiation doses, the SCAN1 cells were more sensitive than normal cells. Moreover, following treatment of cells with calicheamicin, SCAN1 cells showed a significantly higher incidence of dicentric chromosomes, acentric fragments, and micronuclei compared to normal cells, indicating that calicheamicin-induced DSBs were repaired less accurately and less efficiently, or more slowly in SCAN1 cells than in normal cells. All these results are consistent with a role for TDP1 in repair of 3’-PG DSBs in vivo. Oxidative stress is thought to induce replicative senescence and DNA damage in mouse embryo fibroblasts (MEFs). To determine the possible roles of oxidative stress on Tdp1-deficient MEFs, Tdp1-knockout MEFs and normal MEFs were cultured in 20% oxygen (atmospheric) and 3% (physiological) oxygen. The data from growth assays indicated that normal MEFs showed replicative senescence in 20% oxygen but not in 3% oxygen. Tdp1-knockout MEFs showed very poor growth compared to Tdp1 normal MEFs in both oxygen conditions, clearly suggesting an influence of repair of Tdp1 on oxidative stress induced DNA-DSBs in MEFs. Taken together, our results indicated that TDP1 is capable of removing protruding 3’-PG from DSB ends in intact cells. Moreover, DSBs induced by oxidative stress were repaired more slowly or inefficiently in MEFs when Tdp1 is absent, resulting in cell cycle arrest and poor cell growth.
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Patterson, Erika K. « The social class attitudes scale (SCAS) : instrument development and estimates for reliability and validity / ». free to MU campus, to others for purchase, 2003. http://wwwlib.umi.com/cr/mo/fullcit?p3099621.

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Livres sur le sujet "Scas15"

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Gatti, Paula. Juan Antonio Scasso. Montevideo] : IHA, 2009.

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Museo degli arazzi Scassa (Asti, Italy), dir. Museo degli arazzi Scassa. Milano : Skira, 2010.

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Calabrese, Angelo, et Ugo Scassa. Scassa arazziere : L'arazzeria di Asti. Città di Castello : Petruzzi, 2010.

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Avanzo, Donatella, et Silvana Cincotti. Da Kandinsky a Botero : Tutti in un filo : l'Arazzeria Scassa e l'arte del '900. Milano : Skira, 2018.

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State Collaborative of Assessment and Student Standards. Health Education Assessment Project., Council of Chief State School Officers. et ToucanEd Publications (Firm), dir. Assessing health literacy : CCSSO-SCASS Health Education Project. Soquel, CA : ToucanEd Publications, 1999.

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(Firm), SWAT, et Institute of Chartered Accountants in England and Wales., dir. SCAS & VSCAS companies' accounts disclosure checklist. (s.l.) : Accountancy Books, 1992.

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Assumpção, Paschoalino. O teatro amador em Santo André : A Sociedade de Cultura Artística (SCASA) e o Teatro de Alumínio. Santo André, SP : Alpharrabio Edições, 2000.

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A palazzo e in villa : Busti antichi e all'antica di Gio. Vincenzo Imperiale patrizio genovese. Genova : Sagep editori, 2017.

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Ferraris, Massimo. Banda Di Scassi. Lulu Press, Inc., 2014.

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Whitehill and SWAT Ltd Clark. The Scas & Vscas Model Audit File. Accountancy Books, 1993.

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Chapitres de livres sur le sujet "Scas15"

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Toyoshima, Yasuko, et Hitoshi Takahashi. « Spinocerebellar Ataxia Type 17 (SCA17) ». Dans Polyglutamine Disorders, 219–31. Cham : Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-71779-1_10.

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de Vos, C. M., J. D. Bregman et U. J. Schwarz. « Pupil Plane Interferometry : Some Conclusions from SCASIS ». Dans Very High Angular Resolution Imaging, 419–21. Dordrecht : Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-011-0880-5_85.

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Manto, Mario, et Christophe Habas. « Ataxies autosomales dominantes (SCAs) ». Dans Le cervelet, 205–13. Paris : Springer Paris, 2013. http://dx.doi.org/10.1007/978-2-8178-0447-7_23.

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Ishikawa, Kinya. « Molecular Pathogenesis in Spinocerebellar Ataxia Type 31 (SCA31) ». Dans Contemporary Clinical Neuroscience, 507–16. Cham : Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-75817-2_26.

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Klir, George J. « Soft Computer-Aided System Theory and Technology (SCAST) ». Dans Computer Aided Systems Theory — CAST '94, 13–27. Berlin, Heidelberg : Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/3-540-61478-8_64.

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Vos, C. M., J. D. Bregman et U. J. Schwarz. « SCASIS, Diffraction Limited Imaging using a Redundant Pupil Plane Interferometer ». Dans Diffraction-Limited Imaging with Very Large Telescopes, 379–88. Dordrecht : Springer Netherlands, 1989. http://dx.doi.org/10.1007/978-94-009-2340-9_24.

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Hernández-Ferrándiz, Daniel, Juan J. Pantrigo et Raul Cabido. « SCASA : From Synthetic to Real Computer-Aided Sperm Analysis ». Dans Bio-inspired Systems and Applications : from Robotics to Ambient Intelligence, 233–42. Cham : Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-06527-9_23.

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Mariotti, Caterina, Mario Fichera et Lorenzo Nanetti. « How to Design a Therapeutic Trial in SCAs ». Dans Contemporary Clinical Neuroscience, 265–89. Cham : Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-24345-5_8.

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Zijlstra, Timo, Karim Bigou et Arnaud Tisserand. « FPGA Implementation and Comparison of Protections Against SCAs for RLWE ». Dans Lecture Notes in Computer Science, 535–55. Cham : Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-35423-7_27.

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Okazawa, Hitoshi, et Hikari Tanaka. « Molecular Dissection and Therapeutic Application of SCA1 Pathologies Revealed by Comprehensive Approaches ». Dans Contemporary Clinical Neuroscience, 479–86. Cham : Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-75817-2_24.

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Actes de conférences sur le sujet "Scas15"

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Wu, Jiejian, Linghe Kong, Haifeng Tang et Tom Z. J. Fu. « SCASys ». Dans SIGCOMM '21 : ACM SIGCOMM 2021 Conference. New York, NY, USA : ACM, 2021. http://dx.doi.org/10.1145/3472716.3472857.

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Steadman, Matt, et Steve Adler. « SCAsat Audio Distribution “Best of Satellite, Best of WAN” ». Dans SMPTE Australia Conference. IEEE, 2015. http://dx.doi.org/10.5594/m001603.

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Kbar, Ghassan, Shady Aly et Bhaa Alhanafi. « Smart and Context Aware Search for University Campus (SCASUC) ». Dans 2012 International Conference on Multimedia Computing and Systems (ICMCS). IEEE, 2012. http://dx.doi.org/10.1109/icmcs.2012.6320141.

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Bandara, Nalin, Kosala Gunawardane et Nihal Kularatna. « Exprimental verification of Supercapacitor Assisted Sub Module Inverter (SCASMI) Technique ». Dans 2020 2nd IEEE International Conference on Industrial Electronics for Sustainable Energy Systems (IESES). IEEE, 2020. http://dx.doi.org/10.1109/ieses45645.2020.9210666.

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Leino, Marina S., Jane A. Warner, Nick Platt et Donna E. Davies. « The Scavenger Receptor SCARA5 Is Expressed In Human Alveolar Epithelial Cells ». Dans American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4975.

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Kelshaw, Patricia, Cook Nathan, Iverson Grant, Terry Douglas, Cortes Nelson, Hacherl Samantha, Erdman Nicholas et Caswell Shane. « 12.12 The test-retest reliability of the child SCAT5 ». Dans 6th International Conference on Concussion in Sport. BMJ Publishing Group Ltd and British Association of Sport and Exercise Medicine, 2024. http://dx.doi.org/10.1136/bjsports-2023-concussion.181.

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Yeshwanth, V., Ankur Deshwal, Sundeep Krishnadasan, Seungwon Lee et Joonho Song. « Sparse CNN Architecture Search (Scas) ». Dans 2020 IEEE International Conference on Multimedia and Expo (ICME). IEEE, 2020. http://dx.doi.org/10.1109/icme46284.2020.9102879.

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Li, Yuanyuan, Zhexin Li, Yu Liu et Yumei Wang. « SCAST : Wireless Video Multicast Scheme Based on Segmentation and Softcast ». Dans 2017 IEEE Wireless Communications and Networking Conference (WCNC). IEEE, 2017. http://dx.doi.org/10.1109/wcnc.2017.7925618.

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Prato, Thomas, Julianne Schmidt et Robert Lynall. « 2.17 The relationship between symptom severity and child SCAT5 performance ». Dans 6th International Conference on Concussion in Sport. BMJ Publishing Group Ltd and British Association of Sport and Exercise Medicine, 2024. http://dx.doi.org/10.1136/bjsports-2023-concussion.208.

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Bruce, Jared, Willem Meeuwisse, Paul Comper, Michael Hutchison, John Rizos, Joanie Thelen, Stephanie Ruppen et Ruben Echemendia. « 3.2 Development of SCAT5 reliable change metrics in professional hockey ». Dans 6th International Conference on Concussion in Sport. BMJ Publishing Group Ltd and British Association of Sport and Exercise Medicine, 2024. http://dx.doi.org/10.1136/bjsports-2023-concussion.42.

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