Relevant bibliographies by topics / Usher

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Academic literature on the topic 'Usher'

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Published: 4 June 2021
Last updated: 25 May 2024

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Journal articles on the topic "Usher"

1

Crawford, Doreen. "Usher syndrome." Nursing Children and Young People 30, no. 6 (November 8, 2018): 18. http://dx.doi.org/10.7748/ncyp.30.6.18.s16.

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Castiglione, Alessandro, and Claes Möller. "Usher Syndrome." Audiology Research 12, no. 1 (January 11, 2022): 42–65. http://dx.doi.org/10.3390/audiolres12010005.

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Usher syndrome (USH) is the most common genetic condition responsible for combined loss of hearing and vision. Balance disorders and bilateral vestibular areflexia are also observed in some cases. The syndrome was first described by Albrecht von Graefe in 1858, but later named by Charles Usher, who presented a large number of cases with hearing loss and retinopathy in 1914. USH has been grouped into three main clinical types: 1, 2, and 3, which are caused by mutations in different genes and are further divided into different subtypes. To date, nine causative genes have been identified and confirmed as responsible for the syndrome when mutated: MYO7A, USH1C, CDH23, PCDH15, and USH1G (SANS) for Usher type 1; USH2A, ADGRV1, and WHRN for Usher type 2; CLRN1 for Usher type 3. USH is inherited in an autosomal recessive pattern. Digenic, bi-allelic, and polygenic forms have also been reported, in addition to dominant or nonsyndromic forms of genetic mutations. This narrative review reports the causative forms, diagnosis, prognosis, epidemiology, rehabilitation, research, and new treatments of USH.
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Jatana, Kris R., Denise Thomas, Lisa Weber, Marilyn B. Mets, Josh B. Silverman, and Nancy M. Young. "Usher Syndrome." Otology & Neurotology 34, no. 3 (April 2013): 484–89. http://dx.doi.org/10.1097/mao.0b013e3182877ef2.

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Kimberling, William J., Claes G. Moller, Sandra L. H. Davenport, Gunnar Lund, Timothy J. Grissom, Ira Priluck, Valorie White, Michael D. Weston, Karen Biscone-Halterman, and Patrick E. Brookhouser. "Usher Syndrome." Laryngoscope 99, no. 1 (January 1989): 66???72. http://dx.doi.org/10.1288/00005537-198901000-00013.

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M??ller, Claes G., William J. Kimberling, Sandra L. H. Davenport, Ira Priluck, Valorie White, Karen Biscone-Halterman, Lars M. ??dkvist, Patrick E. Brookhouser, Gunnar Lund, and Timothy J. Grissom. "Usher Syndrome." Laryngoscope 99, no. 1 (January 1989): 73???79. http://dx.doi.org/10.1288/00005537-198901000-00014.

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Yu, Xiaodi, Ganeshram R. Visweswaran, Zoe Duck, Srisailam Marupakula, Sheila MacIntyre, Stefan D. Knight, and Anton V. Zavialov. "Caf1A usher possesses a Caf1 subunit-like domain that is crucial for Caf1 fibre secretion." Biochemical Journal 418, no. 3 (February 25, 2009): 541–51. http://dx.doi.org/10.1042/bj20080992.

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The chaperone/usher pathway controls assembly of fibres of adhesive organelles of Gram-negative bacteria. The final steps of fibre assembly and fibre translocation to the cell surface are co-ordinated by the outer membrane proteins, ushers. Ushers consist of several soluble periplasmic domains and a single transmembrane β-barrel. Here we report isolation and structural/functional characterization of a novel middle domain of the Caf1A usher from Yersinia pestis. The isolated UMD (usher middle domain) is a highly soluble monomeric protein capable of autonomous folding. A 2.8 Å (1 Å=0.1 nm) resolution crystal structure of UMD revealed that this domain has an immunoglobulin-like fold similar to that of donor-strand-complemented Caf1 fibre subunit. Moreover, these proteins displayed significant structural similarity. Although UMD is in the middle of the predicted amphipathic β-barrel of Caf1A, the usher still assembled in the membrane in the absence of this domain. UMD did not bind Caf1M–Caf1 complexes, but its presence was shown to be essential for Caf1 fibre secretion. The study suggests that UMD may play the role of a subunit-substituting protein (dummy subunit), plugging or priming secretion through the channel in the Caf1A usher. Comparison of isolated UMD with the recent structure of the corresponding domain of PapC usher revealed high similarity of the core structures, suggesting a universal structural adaptation of FGL (F1G1 long) and FGS (F1G1 short) chaperone/usher pathways for the secretion of different types of fibres. The functional role of two topologically different states of this plug domain suggested by structural and biochemical results is discussed.
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Moskovitz, Herb. "Review of Usher." Edgar Allan Poe Review 9, no. 2 (2008): 89–90. http://dx.doi.org/10.2307/41506302.

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Verma, Anupam, and O. P. Shukla. "Usher’ S Syndrome." Indian Journal of Otolaryngology and Head and Neck Surgery 56, no. 2 (April 2004): 119–20. http://dx.doi.org/10.1007/bf02974312.

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Norte, Maria Carolina Braga, Antônio José Cortez Juares, José Carlos Nardi, Alfredo Rafael Dell’Aringa, and Kazue Kobari. "Síndrome de Usher." Revista Brasileira de Otorrinolaringologia 73, no. 4 (August 2007): 574. http://dx.doi.org/10.1590/s0034-72992007000400020.

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Kimberling, William, and Ann Lindenmuth. "The Usher Syndromes." Seminars in Hearing 27, no. 3 (August 2006): 182–92. http://dx.doi.org/10.1055/s-2006-947285.

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Dissertations / Theses on the topic "Usher"

1

Wahlqvist, Moa. "Health and People with Usher syndrome." Doctoral thesis, Örebro universitet, Institutionen för hälsovetenskap och medicin, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-46059.

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The present thesis concerns people with Usher syndrome (USH) and their health. People with USH have a congenital hearing loss of various degrees and an eye disease with a progressive course; for some, the balance is also affected. Three clinical groups have been identified 1, 2 and 3, and 13 genes have currently been identified. USH is the most common cause of deafblindness. Clinical knowledge and the limited research that exists have shown that people with deafblindness can experience difficulties in everyday life. Depression, anxiety and social withdrawal have been described. The general aim of the present thesis was to describe the health of people with USH. The empirical material employed was based on an extensive survey in which people with USH answered two questionnaires concerning health, anxiety, depression, social trust, work, health-care, financial situation, and alcohol and drug use. The focus of the present thesis is on general health, physical health and psychological health, social trust and finance. Three studies in the present theses focus on USH1, 2 and 3, respectively; finally, the fourth study provides an in-group comparison of people with USH. The results of studies I and III are compared with a crosssection of the Swedish population. The results revealed poor physical and psychological health, a lack of social trust and a strained financial situation regardless of clinical diagnosis. The discussion stresses the importance of taking a biopsychosocial approach when describing the health of people with USH, in which previous research is lacking. Additional research should focus on the mechanisms at different levels that affect people with USH and their health from a life- course perspective. Furthermore, research should include a salutogenic perspective to explore the resources and strengths of people with USH.
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Saihan, Z. "Clinical and molecular genetics of Usher syndrome." Thesis, University College London (University of London), 2012. http://discovery.ucl.ac.uk/1347966/.

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Usher syndrome (USH) is the name given to a group of recessively inherited disorders characterised by hearing loss, progressive visual loss due to a retinal degeneration termed retinitis pigmentosa (RP) and in some cases vestibular dysfunction. It is the most common form of syndromic RP and is clinically and genetically heterogeneous. There are three clinical subtypes termed USH1, USH2 and USH3, which are defined by the severity of hearing loss and vestibular dysfunction with visual loss due to RP being common to each subtype. To date, mutations in nine genes have been associated with the three clinical subtypes of Usher syndrome as well as non-syndromic hearing loss and RP. This wide spectrum of clinical and genetic variability provides challenges to clinicians in making a diagnosis of Usher syndrome and delivering prognostic information to affected individuals, whilst the genetic heterogeneity presents problems to geneticists attempting to achieve a molecular diagnosis. This study aims to address these issues by determining the distribution of clinical and molecular subtypes of USH in the United Kingdom (UK). This study represents an original contribution to the knowledge of Usher syndrome, as it is the first prospective clinical study to sequence the coding regions of each of the nine genes associated with this disorder in 187 affected families regardless of their clinical subtype. Detailed ophthalmic phenotyping was performed in 219 individuals. This comprehensive strategy of molecular analysis afforded the opportunity to interrogate for the possibility of digenic effects for which no evidence was found. This strategy enabled the discovery of an atypical and novel phenotype associated with the USH1C gene. A molecular diagnosis was achieved in 80% of families with Usher syndrome and the ophthalmic phenotype of a large cohort of affected individuals with Usher syndrome has been further delineated. This study has resulted in a large cohort of UK patients with a confirmed molecular diagnosis and detailed ophthalmic phenotyping, which will provide a framework for subsequent longitudinal studies enabling the characterisation of how visual function progresses over time. Understanding the natural history of this disorder in genotyped individuals will help pave the way for subsequent gene-directed therapy studies in the future.
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Blaydon, Diana Claire. "Molecular genetics of Usher syndrome type 1C." Thesis, University College London (University of London), 2004. http://discovery.ucl.ac.uk/1446499/.

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Usher syndrome type 1C is an autosomal recessive condition in which profound, congenital sensorineural deafness is found in association with vestibular hypofunction and childhood onset retinitis pigmentosa. The gene responsible for Usher type 1C, USH1C, codes for a PDZ domain-containing protein, harmonin, of unknown function. In addition, the locus for a form of non- syndromic autosomal recessive deafness, DFNB18, overlaps with the USH1C gene. In this thesis the USH1C gene is studied in more detail, both at the molecular level and at the protein level. Two cohorts of patients, individuals diagnosed with Usher type 1, and a group of sibs with recessive non-syndromic deafness concordant for markers flanking the DFNB18 locus, were screened for mutations in USH1C. One Usher type 1 patient was homozygous for a recurrent mutation, and the possibility of a founder effect was investigated by analysing intragenic SNPs. Another Usher type 1 patient had two novel coding mutations that were studied in more detail to establish whether they were likely to be disease-causing or represent rare polymorphisms. USH1C is an alternatively spliced gene with evidence for tissue-specific isoforms of the protein. The repertoire of alternative isoforms and their tissue distributions were studied in human foetal tissues using non-quantitative RT- PCR. Particular attention was paid to a putative isoform thought to utilize an alternative start site in the centre of the gene. This isoform may have importance in other tissues when a mutation at the 5' end of USH1C results in a non-functional protein from the usual start site. The sub-cellular localization of harmonin was investigated in individual human epithelial cells using fluorescent immunocytochemistry, and fluorescent immunohistochemistry was used to study the localization in mouse inner ear sections. Finally, to understand more about the possible role of harmonin in the ear and the eye, an in vitro GST pull-down assay was set up to investigate the interaction of harmonin with another Usher type 1 protein, protocadherin 15.
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Roberts, Phillip Christopher. "Madeline Usher: An Opera in One Act." Bowling Green State University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=bgsu1395398280.

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Demontis, Fabio. "Modeling human Usher syndrome during Drosophila melanogaster development." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2006. http://nbn-resolving.de/urn:nbn:de:swb:14-1153400348308-78109.

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Human Usher syndrome is a severe and congenital form of syndromic deafness that affects 1 person in 25,000 people in the world population. Normally the stereocilia, microvillar protrusions of the apical membrane of inner ear hair cells, are organized into coherent bundles. This precise organization is critical for mechanosensing, i.e. for hearing. Mutation in any of the five known Usher syndrome genes is sufficient to alter the precise organization of stereocilia, a condition that results in deafness. To date, however, the molecular mechanisms responsible for the splaying of stereocilia and genesis of the disease are not well understood. Here, I identified Drosophila melanogaster genes related to human Usher syndrome and characterized some of them (Cad99C, DSANS and crinkled) during Drosophila development, in the processes of microvilli morphogenesis in the follicular and wing imaginal disc epithelia. Cadherin Cad99C is a transmembrane protein with putative cell adhesion properties. Similar to its human ortholog Protocadherin 15, Drosophila Cad99C localizes to microvillar protrusions in the follicular epithelium. In this epithelium, Cad99C is required for the proper morphogenesis and organization of microvilli into bundles, similar to human Protocadherin 15. Further, overexpression of the full-length Cad99C or of a deleted version, devoid of the cytoplasmic region, promotes microvilli bundling. This finding suggests that Cad99C establishes adhesive interactions between microvilli via its extracellular region. Interestingly, morphological alteration of follicle cell microvilli associates with defective deposition of the vitelline membrane, an extracellular matrix that protects the embryo from osmotic stresses. These findings suggest that microvilli are normally required for the even deposition of the extracellular matrix. In order to test whether Cad99C is involved in microvilli morphogenesis and bundling in other tissues, I analyzed the function of Cad99C in a larval tissue, the wing imaginal disc. Cad99C overexpression, but not Cad99C removal, is sufficient to alter microvilli morphology and organization in the columnar epithelium of the wing imaginal disc. Likely, other molecules can compensate for Cad99C loss of function in this tissue. To possibly get some insights on the molecular function of other Usher syndrome proteins, I analyzed the function of Drosophila SANS and crinkled in the follicular epithelium, where both these genes are expressed. crinkled is the ortholog of myosinVIIa, that encodes a motor protein of the actin cytoskeleton. DSANS is related to human SANS and encodes a cytoplasmic protein of unknown function. It has been puzzling how removal of SANS, a cytoplasmic protein, could impair adhesion and bundling of stereocilia. To study the function of DSANS, I generated null mutant flies and observed that, in the absence of DSANS, delivery of Cad99C to microvilli is impaired. Cad99C localization is however unperturbed in crinkled mutant follicle cells. By immunostaining, DSANS immunoreactivity was detected diffusively in the cytoplasm and in dot-like structures, possibly corresponding to vesicles. In conclusion, DSANS is a cytoplasmic protein that is required for the efficient delivery of Cad99C to microvilli protrusions. Taken together, the analysis that I here performed of Drosophila Usher syndrome related genes indicates two novel molecular mechanisms of function for the corresponding human Usher syndrome proteins. First, human Protocadherin 15, like Drosophila Cad99C, could be involved in establishing adhesive interactions between microvilli protrusions of the inner ear (stereocilia). Removal of Protocadherin 15 would then cause splaying of stereocilia due to lack of inter-stereocilia adhesive links. Second, the analysis here performed suggests that SANS is involved in the efficient delivery of Protocadherin 15 to stereocilia. Mutations in SANS would then lead to splaying of stereocilia and deafness due to poor localization of Protocadherin 15 to stereocilia.
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Cortese, Matteo. "Cellular and molecular mechanisms of Usher syndrome pathogenesis." Thesis, Paris 6, 2016. http://www.theses.fr/2016PA066390/document.

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Le syndrome d’Usher (USH) cause une surdité-cécité chez l’homme. Au moins neuf gènes responsables ont été identifiés. L’origine de l’atteinte auditive a été dévoilée par l’analyse de souris mutantes, mais les causes de la cécité sont encore obscures. Néanmoins, unes des protéines de Usher, la myosine VIIa, a été impliquée dans le transport intracellulaire dans les photorécepteurs. Pour mieux comprendre le rôle dans la rétine, j’ai étudié l’un de ses partenaires, la spectrine βV. Nous avons conclu que cette spectrine, en collaboration avec les protéines USH1, est impliquée dans le trafic cellulaire: elle couple les moteurs (myosine VIIA, kinesine II et le complexe dynéine/dynactine) à leurs cargos en route vers le segment externe des photorécepteurs. La combinaison d’études comparatives dans les cellules ciliées (CC) de l'oreille interne de grenouille et de souris, de tests biochimiques et d’analyses phylogénétiques indique que le transport vers et depuis la surface apicale des cellules est la fonction ancestrale de cette spectrine. Chez les mammifères, une pression évolutive a engendré le recrutement de la spectrine βV à la paroi latérale des CC externes auditives, probablement pour participer à une nouvelle fonction: l’électromotilité. Enfin, j’ai étudié l’origine de la surdité dans le syndrome d’Usher III. Le seul gène causal connu est CLRN1, qui code pour la clarine-1. Nous avons conclu que la clarine-1 est nécessaire à la maturation et le maintien des touffes ciliaires des CC. De plus, la clarine-1 est essentielle pour le regroupement des canaux calciques voltage-dépendants au voisinage immédiat de la machinerie exocytotique de la synapse à ruban des CC internes
Usher syndrome (USH) causes a combined deafness-blindness in humans. At least nine causative genes are known. While the analysis of USH knockout mice has shed light on the origin of the auditory deficit, the causes of vision loss are still unclear. Nevertheless, USH1B protein, myosin VIIa, appears to contribute to intracellular traffic in photoreceptor cells. To better understand the role of this myosin in the retina, I studied the functions of its interacting partner, spectrin βV. We found that spectrin V, along with USH1 proteins, participates in intracellular transport by coupling motor proteins (myosin VIIa, kinesin II, dynein/dynactin complex) to the cargoes en route towards the outer segment of photoreceptor cells. Evidence from comparative studies in frog and mouse inner ear, biochemical assays and phylogenetic analyses point to cargo trafficking to and from the apical cell region, as the likely ancestral function of this spectrin. Our analyses also suggest that evolutionary pressures in the mammalian lineage drove the recruitment of spectrin βV to the lateral wall of auditory outer hair cells, probably to support a new function: electromotility. Finally, I explored the origin of hearing loss in Usher syndrome of type III (USH3). So far, the only causal gene known is CLRN1, which codes for clarin-1. The comparative characterization of two Clrn1 mouse mutants revealed that clarin-1 is required for the maturation and maintenance of the hair bundle in the hair cells. Moreover, our results indicate that clarin-1 is also essential to cluster the voltage-gated Ca2+ channels in close proximity to the exocytotic machinery of the ribbon synapse of inner hair cells
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Cortese, Matteo. "Cellular and molecular mechanisms of Usher syndrome pathogenesis." Electronic Thesis or Diss., Paris 6, 2016. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2016PA066390.pdf.

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Le syndrome d’Usher (USH) cause une surdité-cécité chez l’homme. Au moins neuf gènes responsables ont été identifiés. L’origine de l’atteinte auditive a été dévoilée par l’analyse de souris mutantes, mais les causes de la cécité sont encore obscures. Néanmoins, unes des protéines de Usher, la myosine VIIa, a été impliquée dans le transport intracellulaire dans les photorécepteurs. Pour mieux comprendre le rôle dans la rétine, j’ai étudié l’un de ses partenaires, la spectrine βV. Nous avons conclu que cette spectrine, en collaboration avec les protéines USH1, est impliquée dans le trafic cellulaire: elle couple les moteurs (myosine VIIA, kinesine II et le complexe dynéine/dynactine) à leurs cargos en route vers le segment externe des photorécepteurs. La combinaison d’études comparatives dans les cellules ciliées (CC) de l'oreille interne de grenouille et de souris, de tests biochimiques et d’analyses phylogénétiques indique que le transport vers et depuis la surface apicale des cellules est la fonction ancestrale de cette spectrine. Chez les mammifères, une pression évolutive a engendré le recrutement de la spectrine βV à la paroi latérale des CC externes auditives, probablement pour participer à une nouvelle fonction: l’électromotilité. Enfin, j’ai étudié l’origine de la surdité dans le syndrome d’Usher III. Le seul gène causal connu est CLRN1, qui code pour la clarine-1. Nous avons conclu que la clarine-1 est nécessaire à la maturation et le maintien des touffes ciliaires des CC. De plus, la clarine-1 est essentielle pour le regroupement des canaux calciques voltage-dépendants au voisinage immédiat de la machinerie exocytotique de la synapse à ruban des CC internes
Usher syndrome (USH) causes a combined deafness-blindness in humans. At least nine causative genes are known. While the analysis of USH knockout mice has shed light on the origin of the auditory deficit, the causes of vision loss are still unclear. Nevertheless, USH1B protein, myosin VIIa, appears to contribute to intracellular traffic in photoreceptor cells. To better understand the role of this myosin in the retina, I studied the functions of its interacting partner, spectrin βV. We found that spectrin V, along with USH1 proteins, participates in intracellular transport by coupling motor proteins (myosin VIIa, kinesin II, dynein/dynactin complex) to the cargoes en route towards the outer segment of photoreceptor cells. Evidence from comparative studies in frog and mouse inner ear, biochemical assays and phylogenetic analyses point to cargo trafficking to and from the apical cell region, as the likely ancestral function of this spectrin. Our analyses also suggest that evolutionary pressures in the mammalian lineage drove the recruitment of spectrin βV to the lateral wall of auditory outer hair cells, probably to support a new function: electromotility. Finally, I explored the origin of hearing loss in Usher syndrome of type III (USH3). So far, the only causal gene known is CLRN1, which codes for clarin-1. The comparative characterization of two Clrn1 mouse mutants revealed that clarin-1 is required for the maturation and maintenance of the hair bundle in the hair cells. Moreover, our results indicate that clarin-1 is also essential to cluster the voltage-gated Ca2+ channels in close proximity to the exocytotic machinery of the ribbon synapse of inner hair cells
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Larsonneur, Fanny. "Characterisation of new chaperone-usher fimbriae : the Yad fimbriae." Sorbonne Paris Cité, 2015. http://www.theses.fr/2015USPCC122.

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Très répandus dans la nature, les biofilms sont fréquemment des perturbateurs des processus industriels et peuvent également remettre en cause la sécurité sanitaire dans le domaine médical. La formation de biofilms débute par une étape d'adhésion associée à une importante variété de facteurs extracellulaires qui vont permettre la reconnaissance d'un grand nombre de ligands différents. Parmi ces adhésines, la famille des chaperone-usher constitue un groupe hétérogène et abondant de structures extracellulaires qui participent à la colonisation bactérienne de nombreux environnements. Un des axes de recherche de notre laboratoire vise à identifier et caractériser les acteurs moléculaires permettant à la bactérie modèle E. Coli d'adhérer aux surfaces et de former des biofilms. Cette bactérie possède une dizaine de chaperone-usher "cryptiques" en conditions classiques de laboratoire, mais fonctionnelles lorsqu'elles sont exprimées. Nous nous sommes concentrés sur un fimbriae formant des « fagot» lorsqu'il est exprimé chez E. Cou K-12 : le fimbriae Yad. Notre travail a débuté par une caractérisation structurale de Yad permettant d'identifier YadN comme la piline majeure formant la structure principale du fimbriae et YadC comme la lectine reconnaissant un sucre : le xylose. Un second axe d'étude a permis de mieux comprendre la complexité du réseau de régulation de yad mettant en jeux de nombreux régulateurs ainsi que des facteurs environnementaux tels que l'oxygène ou la température. Le xylose étant un des constituants principal de la biomasse végétale et l'expression de yad étant maximale en condition anaérobie et à des températures inférieures à 37°C, une étude dans la rhizosphère des plantes a été réalisée. Des expériences de compétitions de colonisations bactériennes dans la rhizosphère de graines de maïs germées ont ainsi démontré que les bactéries exprimant Yad colonisent mieux que la souche sauvage. Ces résultats suggèrent donc que le fimbriae Yad participe à la survie d' E. Coli à l'extérieur de son hôte, dans son habitat secondaire
Bacterial cell surface proteins and appendages mediate adhesion to surfaces or host tissues. Initial adhesion is thus a key step in colonization and biofilm formation pro cesses leading to infection. The chaperone-usher family includes many fimbriae promoting interaction with host specific epithelial cell surfaces as well as colonisation of secondary habitats such as plants. Our laboratory objective is to characterize E. Coli arsenal of adhesins since they allow certain microorganisms to survive in the host or on surfaces, to understand their role in E. Cou biology. We recently identified seven E. Cou K-12 chaperone-usher fimbriae silenced under classical laboratory conditions but functional when constitutively expressed. One of these fimbriae is produced upon the expression of the yad operon and forms a network of surfaces appendages forming bundles connecting bacteria. This structural organisation is responsible for the capacity of the Yad fimbriae to induce adhesion to abiotic and biotic surfaces. We undertook a functional characterisation of these fimbriae, thus identifying their structural components. We demonstrate that they promote adhesion of E. Coli to xylose through the lectin, YadC, located at die tip of the fimbriae. The study of yad regulation showed that it is strongly repressed by the nucleoid-associated protein H-NS. Additionally, we demonstrated that a complex regulatory network involving multiple regulators and environmental factors such as temperature and oxygenation also participate in the control of yad expression. Indeed, yad expression is highly increased in anaerobic conditions and at 30°C. Those results and Yad affinity for xylose prompt us to assay Yad involvement in rhizosphere colonization. Yad expressing bacteria colonize the rhizosphere more efficiently in competition experiments with the wild¬type strain. Those results show that E. Con possesses a large arsenal of adhesion factors, which expression is controlled by environmental conditions that could modulate its ability to colonize and persist
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Liquori, Alessandro. "Deciphering molecular mechanisms of unusual variants in Usher Syndrome." Thesis, Montpellier, 2015. http://www.theses.fr/2015MONTT016.

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Le syndrome de Usher (USH) est une maladie transmise selon le mode autosomique récessif caractérisée par l’association d’une surdité congénitale (HL) et d’une rétinite pigmentaire (RP), et dans certains cas, d’une aréflexie vestibulaire. Une hétérogénéité clinique et génétique est reconnue. Environ 10 % des cas USH restent non résolus après analyse moléculaire exhaustive des différents gènes. Ces cas incluent les patients qui ne portent aucune mutation dans un des gènes USH connus ainsi que les patients porteurs d’une seule mutation dans un gène USH. Au cours de cette thèse, nous nous sommes intéressés à l’étude des patients porteurs d’une seule mutation dans les gènes USH2A et PCDH15.Dans la première partie de la thèse, nous avons analysé une cohorte de patients avec un phénotype USH2A bien défini : 5 patients pour lesquels une seule mutation à l’état hétérozygote avait été identifiée dans le gène USH2A et un patient porteur d’un variant silencieux en trans d’une mutation non-sens.Pour les 5 patients, nous avons émis l’hypothèse que la seconde mutation, restant à être identifiée, pourrait se trouver dans des régions introniques profondes. Pour cela, nous avons développé une approche de séquençage à haut débit (NGS) de l’ADN pour identifier les variants introniques profonds dans le gène USH2A et évaluer leurs conséquences sur l’épissage. Comme preuve de concept et pour valider l’approche, y compris le pipeline bio-informatique et l’évaluation des outils de prédiction de l’épissage, nous avons analysé un patient porteur d’un pseudoexon (PE) connu dans le gène USH2A. Ensuite, les 5 patients ont été étudiés en utilisant le pipeline défini, ce qui a conduit à l’identification de 3 nouveaux variants introniques profonds chez 4 d’entre eux. Tous les variants ont été prédits comme pouvant avoir un impact sur l’épissage et aboutir à l’insertion de PE. Ces prédictions ont été validées par les essais minigènes. Grâce à cette étude, nous présentons une stratégie innovante pour identifier les mutations introniques profondes, lorsque l’analyse des transcrits n’est pas possible. Par ailleurs, le pipeline bio-informatique développé fonctionne indépendamment de la taille du gène analysé, ce qui permet l’application possible de cette approche à n’importe quel gène. Par ailleurs, un oligonucléotide antisens de type morpholino (AMO) a été évalué in vitro afin de rétablir l’altération d’épissage induite par une des mutations identifiées. Les résultats ont montré un taux d’exclusion élevé du transcrit aberrant et suggèrent une application possible en thérapie moléculaire. Nous avons ensuite effectué des études sur le variant USH2A c.1377T>A, un variant silencieux afin d’évaluer son effet sur l’épissage. L’analyse de l’ARN issu de cellules nasales du patient a montré que ce variant conduit au saut de l’exon 8 dans les transcrits USH2A. Ceci a été confirmé par un essai minigène. En outre, des études préliminaires ont été réalisées en utilisant des outils de prédictions et des essais minigènes pour évaluer l’implication des éléments cis-régulateurs dans le défaut d’épissage observé chez le patient. Dans la deuxième partie de la thèse, nous avons analysé une patiente USH1, pour laquelle une seule mutation avait été identifiée dans le gène PCDH15. Dans ce cas, nous avons combiné la culture des cellules épithéliales nasales avec l’analyse des transcrits PCDH15. Celle-ci a été réalisée par séquençage de cinq RT-PCR chevauchantes. Grâce à cette analyse, nous avons réussi à délimiter une région d’intérêt dans le transcrit, dont l’amplification a échoué exclusivement pour l’allèle porteur de la mutation non identifiée. D’autres analyses ont été effectuées dans la région génomique correspondante par capture ciblée couplée au séquençage NGS et LongRange PCR suivi de séquençage Sanger. Cependant, aucun variant candidat n’a été identifié à ce jour. Nous suggérons l’implication de mécanismes moléculaires complexes qui restent à être caractérisés
Usher syndrome (USH) is an autosomal recessive disorder characterized by the association of sensorineural hearing loss (HL) and retinitis pigmentosa (RP), and in some cases, vestibular areflexia. Clinical and genetic heterogeneity are recognised. Indeed, three clinical types can be caused by mutations in one of the 10 known genes and USH2A represents the most frequently involved gene.Approximately 10 % of the USH cases remain genetically unsolved after extensive molecular analysis of the different genes, which includes sequencing of the exons and their intronic boundaries, combined to large rearrangements screening by array CGH. These unsolved cases include patients who do not carry any mutation in any of the known USH genes and patients who carry a single USH mutation. During this thesis we focalised on the study of patients carrying a single mutation in USH2A and PCDH15 gene.First, we have analysed a cohort of well-defined USH2A patients: five patients, for whom a single USH2A heterozygous mutation had been identified and one patient carrying a silent variant in trans to a nonsense mutation. For the 5 patients, we supposed that the second mutation remaining to be found could be localised deep in the introns. Indeed, a deep intronic mutation resulting in the inclusion of a pseudoexon (PE 40) in USH2A transcripts had been identified, following RNA analysis from nasal cells. Unfortunately, analysing USH2A transcripts still represent a challenging approach in a diagnostic settings and it is not always possible. To circumvent this issue, we have developed a DNA-Next Generation Sequencing (NGS) approach to identify deep intronic variants in USH2A and evaluate their consequences on splicing. As a proof of concept and to validate this approach, including the bioinformatics pipeline and the assessment of splicing predictor tools, the patient carrying the PE 40 was analysed at first. Then, the 5 patients were studied using the defined pipeline, which led to the identification of 3 distinct novel deep intronic variants in 4 of them. All were predicted to affect splicing and resulted in the insertion of PEs, as shown by minigene assays. Through this study, we present a new and attractive strategy to identify deep intronic mutations, when RNA analyses are not possible. In addition, the bioinformatics pipeline developed is independent of the gene size, implying the possible application of this approach to any disease-linked gene. Moreover, an antisense morpholino oligonucleotide (AMO) tested in vitro for its ability to restore the splicing alterations caused by one of the identified mutation provided high inhibition rates. These results are indicative of a potential application for molecular therapy.In the second case, we have performed studies on the USH2A c.1377T>A silent variant to investigate its effect on splicing. Analysis of RNA from nasal cells of patients showed that this variant led to the skipping of exon 8 in USH2A transcripts. This was confirmed by minigene assay. Moreover, preliminary studies have been performed using prediction tools and minigene assays to assess the involvement of cis-acting elements in causing the aberrant splicing.In the second part of the thesis, we have analysed an USH1 patient, for whom only one mutation had been identified in the PCDH15 gene. In this case, we combined nasal epithelial cells culture with the analysis of the PCDH15 transcripts. This was performed by sequencing five overlapping RT-PCRs. Through this analysis, we were able to delimit a region within the transcript, which failed to be amplified exclusively in the allele carrying the unidentified mutation. Further analyses have been performed in the corresponding genomic region by NGS-target capture and LongRange PCR associated with Sanger sequencing. However, no evident mutation has been identified so far. Therefore, we suggest the involvement of complex molecular mechanisms that remain to be characterised
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Delhommel, Florent. "Etude structurale de la Whirline, protéine modulaire cruciale dans les mécanismes de la vision et de l'audition." Thesis, Paris 6, 2017. http://www.theses.fr/2017PA066151/document.

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La vue et l'ouïe font intervenir des cellules capables de rapidement traduire une onde, lumineuse ou sonore, en un message électrochimique transmissible au cerveau. La fonction de ces cellules sensitives repose sur leurs morphologies uniques. Les mutations de onze gènes sont la cause des syndromes Usher, associant cécité et surdité. Les protéines Usher sont indispensables à l'architecture de ces deux types cellulaires ; elles forment des complexes dont les interactions clés sont maintenues principalement par des domaines PDZ. L'une des protéines centrales de ce réseau est la Whirline, une protéine multi-domaine contenant trois domaines PDZ. Pour comprendre les bases moléculaires des syndromes Usher, nous nous sommes concentrés sur la caractérisation biochimique et biophysique de la Whirline. Nous avons identifié un nouveau domaine HHD2 de la Whirline dont nous avons obtenue la structure à haute résolution et déterminé le comportement en solution, isolé et avec les domaines adjacents. Nous avons ensuite caractérisé un supramodule transitoire entre deux domaines PDZ, maintenu par des extensions structurées de chacun des domaines. Nous avons résolu la structure de la conformation compacte unique de ce complexe et étudié son équilibre avec un ensemble de conformations étendues. Nous avons enfin caractérisé in vitro le réseau d'interaction des domaines PDZ de la Whirline avec les protéines Usher. L'ensemble de nos résultats sur la structure modulaire et l'interactome de la Whirline permet de mieux comprendre le rôle de la Whirline dans les différents complexes Usher et d'expliquer les conséquences de ses mutations sur les mécanismes moléculaires de l'audition et de la vision
Vision and hearing rely on the capacity of cells to rapidly transduce electromagnetic waves or sound waves into chemical messages that are transmissible to the brain. The function of these sensory cells requires unique morphologies. The mutations of eleven genes are responsible for Usher syndromes, associating blindness and deafness. The Usher proteins are pivotal to the architecture of the photoreceptor and hearing cells. They form complexes in which the critical interactions are mainly maintained by PDZ domains. One of these central proteins is Whirlin, a multi-domain protein encompassing three PDZ domains. To understand the molecular basis of the Usher syndromes, we focused our project on the biochemical and biophysical characterization of Whirlin. We identified a new HHD2 domain on Whirlin, for which we solved the structure at high resolution and determined the behavior in solution, isolated or with adjacent domains. We then identified a transient supramodule between two PDZ domains, maintained by PDZ structured extensions. We determined the structure of the compact and unique conformation of this tandem and we characterized its equilibrium with an ensemble of more extended conformations. Finally, we characterized in vitro the network of interaction of the PDZ domains of Whirlin, with the majority of the Usher proteins. Our results on the modular structure and the interactome of Whirlin get insight into the role of Whirlin in the numerous complexes formed by the Usher proteins and allow to better explain the consequences of its mutation on the molecular mechanisms of hearing and vision
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Books on the topic "Usher"

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Usher. Milwaukee: G. Stevens Pub., 2006.

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Usher. Qld., Australia: University of Queensland Press, 1991.

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Usher. Hockessin, Del: Mitchell Lane Publishers, 2005.

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Hill, Z. B. Usher. Philadelphia: Mason Crest, 2012.

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Condon, Matthew. Usher. London: Picador, 1993.

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Usher. Edina, MN: ABDO Pub., 2009.

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Usher. Oxford: Raintree, 2006.

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Loon, Ralph R. Van. Usher handbook. Minneapolis: Augsburg Fortress, 1990.

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Council, Edinburgh (Scotland) City, ed. Usher Hall. [S.l.]: [s.n.], 2000.

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Usher: Poems. New York: W.W. Norton & Co., 2009.

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Book chapters on the topic "Usher"

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Schell, Jonathan. "Usher Syndrome." In Encyclopedia of Ophthalmology, 1–3. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-35951-4_135-3.

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Leroy, Bart P. "Usher Syndromes." In Inherited Chorioretinal Dystrophies, 143–49. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-540-69466-3_12.

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Schell, Jonathan. "Usher Syndrome." In Encyclopedia of Ophthalmology, 1870–72. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-540-69000-9_135.

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Rappold, Gudrun, John-John B. Schnog, Victor E. A. Gerdes, Yvonne G. Weber, Jose M. Serratosa, Anna-Elina Lehesjoki, Alessandra Baumer, et al. "Usher Syndrome." In Encyclopedia of Molecular Mechanisms of Disease, 2154–55. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_1811.

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Ranka, Sumeet, Vishal Singh, and Mainak Choudhury. "USHEr: User Separation in Home Environment." In Lecture Notes in Computer Science, 215–24. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-94523-1_19.

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Plewig, Gerd. "Barney David Usher." In Pantheon of Dermatology, 1150–52. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-33224-1_194.

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Tsang, Stephen H., Alicia R. P. Aycinena, and Tarun Sharma. "Ciliopathy: Usher Syndrome." In Advances in Experimental Medicine and Biology, 167–70. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-95046-4_32.

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Ayyagari, Radha, Anren Li, Ann Nestorowicz, Yan Li, Richard J. H. Smith, M. Alan Permutt, and J. Fielding Hejtmancik. "Usher Syndrome Type 1C." In Degenerative Retinal Diseases, 303–12. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5933-7_33.

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Perry, Dennis R., and Carl H. Sederholm. "Introduction: The “Usher” Formula." In Poe, "The House of Usher," and the American Gothic, 1–18. New York: Palgrave Macmillan US, 2009. http://dx.doi.org/10.1057/9780230620827_1.

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Plewig, Gerd. "Barney David Usher (1899–1978)." In Pantheon der Dermatologie, 1059–62. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-34093-5_187.

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Conference papers on the topic "Usher"

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Toshniwal, Shubham, Parikshit Sharma, Saurabh Srivastava, and Richa Sehgal. "USHER." In the 20th International Conference. New York, New York, USA: ACM Press, 2015. http://dx.doi.org/10.1145/2732158.2732187.

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Tarrant, Patrick. "Planet usher." In the 12th annual ACM international conference. New York, New York, USA: ACM Press, 2004. http://dx.doi.org/10.1145/1027527.1027763.

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Back, D., D. Ehrmann-Müller, M. Hofrichter, J. Schröder, T. Haaf, R. Hagen, and W. Shehata-Dieler. "Audiologische Phänotypisierung des Usher-Syndroms." In Abstract- und Posterband – 90. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Digitalisierung in der HNO-Heilkunde. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1686114.

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Back, D., D. Ehrmann-Müller, M. Hofrichter, J. Schröder, T. Haaf, R. Hagen, and W. Shehata-Dieler. "Audiological phenotypic characterization of Usher-syndrome." In Abstract- und Posterband – 90. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Digitalisierung in der HNO-Heilkunde. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1686336.

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Chen, Kuang, Harr Chen, Neil Conway, Joseph M. Hellerstein, and Tapan S. Parikh. "USHER: Improving data quality with dynamic forms." In 2010 IEEE 26th International Conference on Data Engineering (ICDE 2010). IEEE, 2010. http://dx.doi.org/10.1109/icde.2010.5447832.

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Oliveira, Priscylla de, and Igor Fontoura Baganha. "Síndrome de Usher e disfunções no equilíbrio." In IV Congresso Online de Atualização em Neurologia. Congresse.me, 2023. http://dx.doi.org/10.54265/jnif2274.

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Wright, Kwame-Lante, Fan Bai, and Bhaskar Krishnamachari. "Usher: Utility-based Scheduling Algorithms for Polymorphic Applications." In 2023 IEEE 20th International Conference on Mobile Ad Hoc and Smart Systems (MASS). IEEE, 2023. http://dx.doi.org/10.1109/mass58611.2023.00047.

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Warnecke, Athanasia, Juliane Schott, Peixin Huang, Michael Morgan, Jennifer Nelson-Brantley, Hildegard Büning, Axel Schambach, and Hinrich Staecker. "Third-generation lentiviral gene therapy rescues function in a mouse model of Usher 1BThird-generation lentiviral gene therapy rescues function in a mouse model of Usher 1B." In 94th Annual Meeting German Society of Oto-Rhino-Laryngology, Head and Neck Surgery e.V., Bonn. Georg Thieme Verlag, 2023. http://dx.doi.org/10.1055/s-0043-1767456.

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McCormick, M. Patrick. "Lidar In-space Technology Experiment - Overview and Early Results." In Optical Remote Sensing of the Atmosphere. Washington, D.C.: Optica Publishing Group, 1995. http://dx.doi.org/10.1364/orsa.1995.mb1.

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The September 1994 Shuttle flight of the Lidar In-space Technology Experiment (LITE) brought to fruition 10 years of effort at NASA's Langley Research Center where it was built. Being the first flight of a spaceborne lidar to measure atmospheric constituents and parameters and surface properties, it culminates the efforts of many worldwide over the last 20 years to usher in this new remote sensing technique from space.
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Cloft, Thomas G., and Patricia L. Muldoon. "Ultra High Bypass (UHB) Engine Critical Component Technology." In ASME 1989 International Gas Turbine and Aeroengine Congress and Exposition. American Society of Mechanical Engineers, 1989. http://dx.doi.org/10.1115/89-gt-229.

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The commercial air transport industry is on the threshold of the Ultra High Bypass (UHB) engine era, which will usher in another leap forward in fuel efficient, low noise gas turbine engines. Anticipation of propulsion system requirements has led to implementation of advanced technology development supporting both the Counter Rotation Propfan (CRP) and the Advanced Ducted Prop (ADP) concepts. The paper will review the advanced cycles for these concepts, definition of critical component technology and the technology readiness programs underway at Pratt & Whitney (P&W).
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Reports on the topic "Usher"

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Crafts, Nicholas, Emma Duchini, Roland Rathelot, Giulia Vattuone, David Chambers, Andrew Oswald, Max Nathan, and Carmen Villa Llera. Economic challenges and success in the post-COVID era: A CAGE Policy Report. Edited by Mirko Draca. CAGE Research Centre, November 2021. http://dx.doi.org/10.31273/978-1-911675-01-3.

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In 2008 there was an expectation of major reform to social and economic structures following the financial crisis. The European Union (EU) referendum of 2016, and the UK’s subsequent exit from the EU in 2020, was also signalled as a turning point that would bring about epochal change. Now, in the waning of the coronavirus pandemic, we are experiencing a similar rhetoric. There is widespread agreement that the pandemic will usher in big changes for the economy and society, with the potential for major policy reform. But what will be the long-term impacts of the pandemic on the UK economy? Is the right response a “new settlement” or is some alternative approach likely to be more beneficial? This report puts forward a new perspective on the pandemic-related changes that could be ahead. The central theme is assessing the viability of epochal reform in policymaking. There seems to be a relentless desire for making big changes; however, there is arguably not enough recognition of how current settings and history can hold back these efforts. Foreword by: Dame Frances Cairncross, CBE, FRSE.
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Unzeta, Bruno Bueno, Jan de Boer, Ruben Delvaeye, Nikodem Dernegowski, Bertrand Deroisy, Bertrand Deroisy, Marc Fontoynont, Bruce Norman, and Daniel Neves Pimenta. User Interfaces. Edited by Marc Fontoynont. IEA SHC Task 61, February 2021. http://dx.doi.org/10.18777/ieashc-task61-2021-0004.

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This report shows, that the impact of a good User Interfaces (UI) is not only affecting the usability and comfort for the user, but is also a major key to save energy. At least as important for effectiveness to the quality of individual interfaces is consistency in the meaning of individual user interface elements (visual, conceptual, auditory, etc.)
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Naves, Claudia, David Amorim, David Geisler-Moroder, Thorbjörn Laike, Justyna Martyniuk-Peczek, Barbara Szybinska Matusiak, Wilfried Pohl, and Natalia Sokol. Literature review of user needs, toward user requirements. Edited by Barbara Szybinska Matusiak. IEA SHC Task 61, September 2020. http://dx.doi.org/10.18777/ieashc-task61-2020-0001.

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This report has been developed in the frame of the IEA SHC Task 61 Subtask A “User requirements”. The main objective was to rethink and reformulate user requirements to lighting (daylighting and electric lighting) in public buildings on the basis of a thorough literature study. The work is a joint effort of a number of scientists and represents collective knowledge in this topic. The concept of Lighting quality is the one, among many lighting concepts, which expresses the user perspective best. Lighting quality is the important goal of lighting designers and planners; however, it is difficult to define and to measure.
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Lady, James, Peter Westhagen, and John Skalski. USER 2.1; User Specified Estimation Routine, Techncial Manual 2003. Office of Scientific and Technical Information (OSTI), July 2003. http://dx.doi.org/10.2172/962975.

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Glen R. Longhurst. TMAP7 User Manual. Office of Scientific and Technical Information (OSTI), September 2006. http://dx.doi.org/10.2172/910958.

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Howard, Andrew. Mezzanine User Manual. Fort Belvoir, VA: Defense Technical Information Center, May 2002. http://dx.doi.org/10.21236/ada440009.

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Alfonsi, Andrea, Cristian Rabiti, Diego Mandelli, Joshua Cogliati, Congjian Wang, Paul W. Talbot, and Daniel P. Maljovec. RAVEN User Guide. Office of Scientific and Technical Information (OSTI), June 2018. http://dx.doi.org/10.2172/1467401.

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Wang, Yaqi, Sebastian Schunert, and Benjamin A. Baker. Rattlesnake: User Manual. Office of Scientific and Technical Information (OSTI), December 2015. http://dx.doi.org/10.2172/1483595.

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Carnes, Brian, and Stephen Ray Kennon. Percept User Manual. Office of Scientific and Technical Information (OSTI), October 2016. http://dx.doi.org/10.2172/1494324.

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Lutes, Robert G., Srinivas Katipamula, Bora A. Akyol, Nathan D. Tenney, Jereme N. Haack, Kyle E. Monson, and Brandon J. Carpenter. VOLTTRON: User Guide. Office of Scientific and Technical Information (OSTI), April 2014. http://dx.doi.org/10.2172/1130247.

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