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Dissertations / Theses on the topic 'Progerin'

Author: Grafiati
Published: 4 June 2021
Last updated: 24 January 2023

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1

Sabri, Mohammad. "Proximity-Labeling of Near Neighbors of Lamin A and Lamin A-Δ50 (PROGERIN)". Digital Commons @ East Tennessee State University, 2013. https://dc.etsu.edu/honors/100.

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In an attempt to isolate and identify proteins that differentially interact with or locate near lamin A and progerin, we used a previously described method named BioID (proximity-dependent biotin identification). This method is based on fusion of a promiscuous E. coli biotin-protein ligase (BL) to a targeting protein (in this study, lamin A-GFP and progerin-GFP). The biotin ligase biotinylates amino residues in proteins that are near-neighbors of the fusion protein. To create the fusion proteins, BL was sub-cloned from a pcDNA3.1 MCS-BirA(R118G)-HA plasmid donated by Kyle Roux from University
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2

Eisch, Veronika [Verfasser], Karima [Akademischer Betreuer] Djabali, Bertold [Gutachter] Hock, and Karima [Gutachter] Djabali. "Characterizing the spatiotemporal distribution and interaction of the lamin A isoforms progerin and prelamin A during mitosis in the Progeroid Syndromes Hutchinson-Gilford progeria syndrome and Mandibuloacral Dysplasia Type B / Veronika Eisch ; Gutachter: Bertold Hock, Karima Djabali ; Betreuer: Karima Djabali." München : Universitätsbibliothek der TU München, 2020. http://d-nb.info/1227580355/34.

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3

Schwerer, Hélène. "Étude des altérations du programme de réplication lors du vieillissement cellulaire : peuvent-elles être reprogrammées ?" Thesis, Montpellier 1, 2014. http://www.theses.fr/2014MON13524.

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La réplication de l'ADN, qui doit assurer à chaque cycle cellulaire une copie fidèle du génome pour que les cellules filles héritent du même génome, est un processus hautement régulé, faisant intervenir son organisation en chromatine mais aussi sa dynamique au sein de l'architecture nucléaire. Le vieillissement cellulaire, qu'il soit physiologique, pathologique ou induit in vitro par des conditions de culture sub-optimales, est accompagné de modifications de l'organisation du génome en chromatine, susceptibles de modifier la régulation spatiotemporelle du programme de réplication. Dans quelle
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4

Vaissié, Alix. "Alternatives to “native human islets” for research in vitro and in vivo : pseudo-islets and pancreatic endocrine cells from pluripotent stem cells – the role of progerin in differentiation and maturation." Thesis, Lille 2, 2019. http://www.theses.fr/2019LIL2S035.

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Introduction : L'utilisation des îlots humains de Langerhans est la référence pour la recherche, tant physiologique que pour le développement de nouvelles molécules thérapeutiques pour le traitement du diabète de type 2. La demande d'îlots de Langerhans humains pour des projets de recherche est en constante augmentation, cependant, la disponibilité est limitée et les différentes préparations d'îlots de Langerhans révèlent une grande variabilité entre elles.Objectifs : L'objectif principal de cette thèse était de proposer une alternative aux îlots de Langerhans humains natifs qui permettrait d’
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5

Cantecor, Benedicte. "Vieillissement cutané : efficacité de la combinaison statine-aminobiphosphonate." Thesis, Aix-Marseille, 2013. http://www.theses.fr/2013AIXM5504.

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6

Bathula, Kranthidhar. "Nuclear Rupture in Progeria Expressing Cells." VCU Scholars Compass, 2018. https://scholarscompass.vcu.edu/etd/5479.

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Cells regularly take on various types of force in the body. They have structures that are able to mediate, transfer and respond to the forces. A mutation in force regulating proteins such as lamin in the nucleus or the KASH domain which connects the nucleus to the cytoskeleton of the cell can cause catastrophic events to occur. The aims of this study were to better understand the response of the nucleus when structural proteins are mutated or are not present while under force. Progeria, a rare disease where an additional farnesyl group is attached to lamin was used in this study. Different typ
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7

Navarro, Claire. "Etudes génétiques et fonctionnelles de syndromes progéroïdes." Aix-Marseille 2, 2007. http://www.theses.fr/2007AIX20666.

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Les syndromes progéroïdes (SP) représentent un ensemble de pathologies caractérisées par des signes de vieillissement prématuré. Ce travail de thèse a consisté à tenter d’identifier de nouvelles "laminopathies", ensemble de maladies génétiques dues à des défauts des lamines, associées à des formes de vieillissement prématuré. Du point de vue physiopathologique, les syndromes progéroïdes (SP) peuvent être classés en deux catégories majeures. La première concerne les SP causés par des mutations dans des gènes codants pour des protéines impliquées dans les mécanismes de réparation de l’ADN. La se
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8

Frankel, Diane. "Lamines et microARNs : implication dans un modèle de laminopathie héréditaire, la Progeria de Hutchinson-Gilford et de laminopathie acquise, l'adénocarcinome bronchique." Thesis, Aix-Marseille, 2018. http://www.theses.fr/2018AIXM0761.

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Les laminopathies regroupent des pathologies liées aux lamines. La Progeria est due à une mutation du gène LMNA entrainant la synthèse d’une protéine anormale : la progérine. Elle s’accumule dans le noyau et entraîne des dommages cellulaires aboutissant à une sénescence prématurée, à l’origine d’un vieillissement prématuré et accéléré des patients dont le décès survient vers l’âge de 14 ans. Les microARNs (miRs) sont des petits ARNs non-codants régulant l’expression des gènes. Dans le projet principal de ma Thèse, nous avons identifié par un miRNome en RT-qPCR, 14 miRs différentiellement expri
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9

Decker, Michelle Leanna. "Telomere length and dynamics in Hutchinson-Gilford progeria syndrome." Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/34180.

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Hutchinson-Gilford Progeria Syndrome (HGPS) is a premature aging disorder caused by mutations in the gene LMNA, which encodes the nuclear matrix protein, Lamin A. Lamin A is found predominantly at the nuclear periphery but also throughout the nucleus in a ‘nucleoplasmic veil’. The majority of HGPS patients have a single nucleotide mutation (1824 C→T) which results in the activation of a cryptic donor splice site causing a 150 nucleotide deletion in the mRNA and consequently a 50 amino acid in-frame deletion in the protein. The mutation results in aberrant processing and nuclear localization
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10

Bidault, Guillaume. "Etude cellulaire des syndromes lipodystrophiques et progéroïdes liés aux mutations du gène lmna : résistance à l’insuline et dysfonction endothéliale." Paris 6, 2013. http://www.theses.fr/2013PA066404.

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La lipodystrophie partielle familiale de dunnigan (fpld2) ou la progéria de hutchinson-gilford (hgps), syndrome de vieillissement accéléré, sont dues à des mutations du gène lmna, codant les lamines de type a. Elles partagent certaines atteintes : lipodystrophie, résistance à l’insuline et athérosclérose précoce. Elles mettent en lumière les liens étroits entre atteintes métaboliques, vieillissement et maladies cardiovasculaires. Au cours de ma thèse, je me suis intéressé aux mécanismes cellulaires impliqués dans la résistance à l’insuline et la dysfonction endothéliale, qui participeraient au
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11

Lutomska, Anna. "Werner Syndrom Zellen haben eine veränderte transkriptionelle Regulation nach Wachstumsfaktorstimulation." [S.l. : s.n.], 2008. http://nbn-resolving.de/urn:nbn:de:bsz:289-vts-65317.

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12

Endisha, Helal. "SIRT6 and Premature Aging of Hutchinson-Gilford Progeria Syndrome Fibroblasts." VCU Scholars Compass, 2013. http://scholarscompass.vcu.edu/etd/3238.

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The genetic disease Hutchinson-Gilford Progeria Syndrome (HGPS) arises from a de novo single nucleotide mutation (1824CàT) in the LMNA gene. As a result, the mutated lamin A protein (progerin) remains farnesylated and permanently attached to the nuclear membrane. Progerin accumulates and deforms the nuclear membrane leading to an array of cellular abnormalities driving the cells to enter a state of permanent cell-cycle arrest early on in replicative age i.e. premature cellular senescence. Cellular senescence has been extensively studied as one of the contributing factors to aging in HGPS patie
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13

Stephen, David V. M. "Progenic isonymy among the Chamorro of Guam." Diss., The University of Arizona, 2001. http://hdl.handle.net/10150/289753.

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This study examines several methodological issues pertaining to the application of isonymy techniques to a historical population located on the island of Guam in Micronesia. Since European contact the indigenous Chamorro population of Guam has undergone a series of precipitous population declines. The Spanish colonial administration imposed a dual surname system on the Chamorro. The surname information was compiled into a demographic database representing approximately 39,000 persons traced from late 19th century vital records. Analysis using the methods of isonymy was conducted on lineages es
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14

Seager, Anna L. "Molecular and cytogenetic analysis of premature ageing disease Hutchinson-Gilford Progeria Syndrome." Thesis, Swansea University, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.638787.

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The principal aim of this study was to evaluate the underlying cellular mechanisms causing HGPS by using an in depth cytogenetic and molecular approach. Firstly, the total genome karyotype of HGPS lines and clinically normal cell lines was analysed utilising modified, multi-colour fluorescent <i>in situ</i> hybridisation (FISH), dual colour FISH, locus specific FISH, and DNA banding methods. The combinations of assays disclosed a characteristic cytogenetic mosaicsm in HGPS, with a distinctive pattern of complex, chromosome aberrations. In particular, chromosome 11 and X alterations were observ
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15

Smallwood, Dawn Teresca. "Investigating lamin A mutations in progeroid syndromes and partial lipodystrophy." Thesis, University of Leicester, 2012. http://hdl.handle.net/2381/11070.

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Lamin A/C is a component of the nuclear lamina that contributes to nuclear integrity, chromatin organisation, gene transcription and DNA replication. Mutation of the LMNA gene, encoding lamin A/C, causes a number of diseases affecting different tissues, but the mechanism(s) by which this widely expressed protein causes tissue-specific disease remains unclear. Hutchinson-Gilford progeria syndrome (HGPS) is an early-onset premature aging disorder. The most common LMNA mutation (G608G) prevents complete posttranslational processing of lamin A, resulting in aberrant retention of a farnesyl group.
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16

Delecourt, Valérie. "Progeria de Hutchinson-Gilford : rôle des microARNs dans la régulation du cycle cellulaire et de l’induction de la sénescence." Thesis, Aix-Marseille, 2019. http://theses.univ-amu.fr.lama.univ-amu.fr/191029_DELECOURT_457tp323ndh876rd859pxmm_TH.pdf.

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La Progeria de Hutchinson-Gilford (HGPS) est une maladie génétique rare caractérisée par un vieillissement précoce et accéléré aboutissant au décès des patients vers l'âge de 14 ans. Elle est due à une mutation qui est responsable de la synthèse d’une protéine nucléaire anormale : la progérine. Au cours de la vie des patients, la progérine s’accumule dans le noyau et induit des anomalies cellulaires à l’origine d’un état de sénescence. Parmi ces anomalies, nous avons mis en évidence une dérégulation de l’expression de microARNs (miRs) qui sont de petits ARNs non-codants régulant l’expression d
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17

Kocharyan, Avetik. "Derivation and Characterization of Pax7 Positive Skeletal Muscle Precursor Cells from Control and HGPS-derived induced Pluripotent Stem Cells." Thesis, Université d'Ottawa / University of Ottawa, 2018. http://hdl.handle.net/10393/37517.

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Hutchinson-Gilford Progeria Syndrome (HGPS) is a rare genetic disorder associated with premature aging in various tissues and organs of the afflicted individuals, including accelerated skeletal muscle atrophy. Classical HGPS manifests due to single-base substitution in the LAMNA gene which encodes Lamin A/C proteins. As a result of the mutation, a truncated form of Lamin (known as Progerin) is produced which undergoes persistent farnesylation during post-translational modification. Accumulation of Progerin in the nucleus has been linked to various cellular abnormalities including abnormal nucl
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18

Macedo, Rita da Rocha Lima. "A síndrome progeróide de Hutchinson-Gilford e suas complicações na cavidade oral." Master's thesis, [s.n.], 2015. http://hdl.handle.net/10284/5133.

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Projeto de Pós-Graduação/Dissertação apresentado à Universidade Fernando Pessoa como parte dos requisitos para obtenção do grau de Mestre em Medicina Dentária<br>A Síndrome Progeróide de Hutchinson-Gilford (HGPS) é uma doença genética muito rara que apresenta uma incidência de 1 por cada 4 a 8 milhões de nascidos-vivos. Caracteriza-se pelo envelhecimento precoce cerca de 7 vezes superior ao normal. É causada por uma alteração genética no gene LMNA localizado no cromossoma 1 (um). Os portadores desta doença possuem uma esperança média de vida de 13 anos. Ao nascimento as crianças estão dentro d
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19

Mehta, Ishita Shailesh. "Chromosome territory position and active relocation in normal and Hutchinson-Gilford progeria fibroblasts." Thesis, Brunel University, 2009. http://bura.brunel.ac.uk/handle/2438/4261.

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Radial chromosome positioning in interphase nuclei is non-random and can alter according to developmental, differentiation, proliferation or disease status. The aim of this thesis is to understand how chromosome re-positioning is elicited and to identify the nuclear structures that assist this re-localisation event. By positioning all human chromosomes in primary fibroblasts that have left the proliferative cell cycle, the study within this thesis has demonstrated that in cells made quiescent by reversible growth arrest, chromosome positioning is altered considerably. Upon removal of serum fro
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20

Levy, Anita Rochelle. "Progestin receptor heterogeneity in a breast cancer cell line." Thesis, Rhodes University, 1995. http://hdl.handle.net/10962/d1004100.

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Anti-oestrogens act via the oestrogen receptor whether they compete with the hormone for binding to the receptor and therefore interfere with DNA binding or inhibit transcriptional activity. These receptors exist as a large 85 complex and/or a small 45 form on sucrose density gradients. High performance ion-exchange chromatography has confirmed that the oestrogen and progestin complex is present in various isoforms. Progestin receptor heterogeneity could be influenced by the presence of oestrogens and anti-oestrogens in the culture media of hormone-dependent neoplastic cells. Cell culture meth
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21

Holzhausen, C. E. "Effects of progestin exposure on physiological development of the rat." Thesis, Open University, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.380068.

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22

Schulz, Vera [Verfasser]. "Identifizierung von Kandidatengenen für einen "Telomer-Positions-Effekt" beim Hutchinson-Gilford-Progerie Syndrom / Vera Schulz." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2013. http://d-nb.info/1043196927/34.

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23

Delbarre, Erwan. "Etude comparative de l' assemblage en cellules vivantes des lamines sauvages et mutées." Paris 6, 2005. http://www.theses.fr/2005PA066398.

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24

Santo, Julien. "Caractérisation de composés chimiques agissant sur le phénomène d'épissage alternatif du gène LMNA responsable du vieillissement précoce : applications dans l'obésité." Thesis, Montpellier 2, 2013. http://www.theses.fr/2013MON20154.

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L'épissage alternatif des ARNs pré-messagers est le mécanisme majeur de diversification de l'information génétique chez les eucaryotes supérieurs. Près de 70% des gènes sont concernés par ce mécanisme. Il arrive malgré tout que l'épissage alternatif soit dérégulé ce qui conduit à des défauts d'épissage qui provoquent des maladies telles que le syndrome progérique de Hutchinson-Gilford (HGPS). Cette maladie se caractérise notamment par une apparition précoce des signes distinctifs de la vieillesse ainsi que de défauts métaboliques majeurs. Mon travail de thèse a consisté à sélectionner et à car
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25

Festa, Anna. "Controlli di qualità e rappresentazione 3D delle microtomografie a raggi X applicate allo studio dei modelli murini per la progeria." Master's thesis, Alma Mater Studiorum - Università di Bologna, 2018. http://amslaurea.unibo.it/15565/.

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La progeria è una malattia genetica rarissima che genera un invecchiamento precoce, con una incidenza di 1 caso su 4 milioni di nascite e circa 100 casi noti attualmente in tutto il mondo. L’età media di sopravvivenza è di circa 13.5 anni, con una aspettativa di vita tra gli 8 e i 21 anni. La massa ossea ridotta e le anomalie scheletriche sono tra i principali disordini dell’invecchiamento precoce. Al fine di sviluppare una migliore comprensione della patogenesi e della progressione della sindrome, oltre che per progredire nelle possibili terapie, sono stati sviluppati modelli animali che r
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Köhler, Florian [Verfasser], and Frank [Akademischer Betreuer] Lyko. "Epigenetic deregulation of lamina-associated domains in Hutchinson-Gilford Progeria Syndrome / Florian Köhler ; Betreuer: Frank Lyko." Heidelberg : Universitätsbibliothek Heidelberg, 2019. http://d-nb.info/1197692789/34.

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27

Turotszy, Alicja [Verfasser]. "The role of NARF and other novel progeria-associated genes/proteins in ageing processes. / Alicja Turotszy." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2021. http://d-nb.info/1227707258/34.

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28

Chen, Zhaoyi. "Modeling Defective Epigenetic Inheritance in Vascular Aging Using Hutchinson-Gilford Progeria Syndrome Vascular Smooth Muscle Cells." Thesis, Université d'Ottawa / University of Ottawa, 2020. http://hdl.handle.net/10393/41096.

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Cardiovascular disease (CVD) is the leading cause of death due to its prevalence in tandem with the propensity of atherosclerosis to worsen and cause myocardial infarction and stroke. The greatest risk factor for CVD development is age. The multifactorial etiology of atherosclerosis has made CVD difficult to model and consequently little is known about CVD onset and progression. Hutchinson-Gilford Progeria Syndrome (HGPS) is a severe human premature aging disorder caused by a mutation in Lamin A that leads to the accumulation of an aberrant Lamin A protein termed progerin. Patients who har
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29

Lopez, Mejia Isabel Cristina. "Alternative splicing of LMNA gene : lessons from a new mouse model of Hutchinson-Gilfort progeria syndrome." Thesis, Montpellier 2, 2011. http://www.theses.fr/2011MON20077.

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Le vieillissement est un processus complexe qui peut être influencé par des facteurs environnementaux et génétiques. Le syndrome progéroïde de Hutchinson-Gilford (HGPS ou progéria) fourni une preuve irréfutable de l'implication de l'épissage dans le processus de vieillissement. La progéria est une maladie due à une mutation hétérozygote silencieuse qui renforce l'utilisation d'un site 5' d'épissage interne dans l'exon 11 de l'ARN pré-messager LMNA, ce qui entraîne la production d'une protéine tronquée appelée «progérine». Le défaut d'épissage du gène LMNA a aussi lieu dans les cellules de pers
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30

Toribio, Calero Jessica Beatriz. "Medición de la progenie del radón en muestras de polvo ambiental." Master's thesis, Pontificia Universidad Católica del Perú, 2018. http://tesis.pucp.edu.pe/repositorio/handle/123456789/12135.

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El gas radón (Rn 222) decae a polonio (Po 218) y este a su vez decae en otros elementos radiactivos llamados progenie del radón, que son sólidas. Durante el decaimiento se emiten partículas radioactivas ionizantes alfa o beta, las que pueden causar efectos en la salud, estas causan daños a nivel de ADN, ARN, etc. El poder de penetración de las partículas alfa es pequeño no, pueden ser detenidas por la epidermis de la piel que actúa como blindaje para el cuerpo, pero si ingresan al organismo por inhalación de aire con progenie adherida al polvo, pueden causar problemas, al ser retenidas en el t
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31

Turner, Rachel. "Relationships between nuclear lamins and telomere biology in progeroid laminopathies and cancer." Thesis, University of Leicester, 2015. http://hdl.handle.net/2381/32257.

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Telomeres are essential for maintaining the integrity of the genome. Shortening and dysfunction of telomeres initiates cellular senescence, halting further cell division, and instigating alterations in biological processes which contribute to ageing. Progeroid syndromes are disorders of ageing. Patients exhibit not only an early external appearance of old age, but several age-related diseases including osteoporosis, muscle wasting and cancer. Laminopathies are diseases caused by mutations in LMNA, the gene encoding the key nuclear matrix component lamin A. Some mutations result in progeroid ph
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32

Morash, Taryn May. "Investigating the regenerative effects of adipose-derived mesenchymal stem cell conditioned media on sarcopenic and progeric skeletal muscle." Thesis, University of Reading, 2018. http://centaur.reading.ac.uk/80706/.

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Ageing, defined as the progressive deterioration of molecular, cellular, tissue and whole organism function, is a primary risk factor for numerous diseases, such as cardiovasculature disease, neurodegeneration and cancer. In recent years, advances in our knowledge of key determinant mechanisms that underpin ageing decline, drives the notion that these features can be attenuated and targeted therapeutically, enabling elderly individuals to experience an enhanced quality of life into advanced old age. Sarcopenia comprises the age-related loss of muscle mass, quality and function and contributes
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Blondel, Sophie. "Utilisation des cellules souches induites à la pluripotence pour la modélisation pathologique du syndrome de Hutchinson Gilford." Thesis, Evry-Val d'Essonne, 2013. http://www.theses.fr/2013EVRY0014/document.

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La progéria est une maladie génétique rare caractérisée par un vieillissement global, prématuré et accéléré entrainant le décès des enfants atteints aux alentours de l’âge de 13 ans. La compréhension des mécanismes moléculaires à l’origine de ce syndrome ont récemment permis de démarrer deux protocoles d’essai clinique, avec un objectif commun : ralentir la progression de la maladie en bloquant la maturation de la protéine mutée. Cependant, l’identification de nouvelles voies thérapeutiques reste encore, pour cette pathologie, un défi à relever. L’objectif de ce travail de thèse a consisté à u
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34

Barth, Caroline [Verfasser], and Angelika [Gutachter] Stellzig-Eisenhauer. "Anomalien des progenen Formenkreises - eine vergleichende Untersuchung / Caroline Barth. Gutachter: Angelika Stellzig-Eisenhauer." Würzburg : Universität Würzburg, 2014. http://d-nb.info/1102827681/34.

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35

Mallory, Daniel A. Patterson David J. "Comparison of long-term progestin-based protocols to synchronize estrus in beef heifers." Diss., Columbia, Mo. : University of Missouri--Columbia, 2009. http://hdl.handle.net/10355/6647.

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Title from PDF of title page (University of Missouri--Columbia, viewed on March 10, 2010). The entire thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file; a non-technical public abstract appears in the public.pdf file. Thesis advisor: Dr. David J. Patterson. Includes bibliographical references.
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36

Gianini, Rubio Angela Pía. "Hipotiroxinemia materna en ratas Sprague-dawley: Secuelas en la sinapsis glutamatérgica de la progenie." Tesis, Universidad de Chile, 2006. http://repositorio.uchile.cl/handle/2250/130834.

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Memoria para optar al Título Profesional de Médico Veterinario<br>Las hormonas tiroideas T3 y T4 son fundamentales para el desarrollo del SNC del feto y del recién nacido. La hipotiroxinemia materna es una patología asintomática caracterizada por la reducción de los niveles plasmáticos de T4 de la madre. Se ha demostrado en los humanos que cuando la hipotiroxinemia materna ocurre durante los primeros 5 meses de gestación conduce posteriormente a daño cognitivo irreversible en su hijo. Este daño es observado como déficit atencional hasta retardo mental severo. Existe abundante evidencia en la
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Paulos, Peter M. "Reproductive and Growth Responses of the Fathead Minnow (Pimephales Promelas) and Japanese Medaka (Oryzias Latipes) to the Synthetic Progestin, Norethindrone." Thesis, University of North Texas, 2011. https://digital.library.unt.edu/ark:/67531/metadc68029/.

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A commonly prescribed contraceptive, the synthetic progestin norethindrone (NET) inhibits ovulation in humans. However, ecotoxicological data are lacking. Preliminary tests produced an LC50 for NET of > 1.0 mg/L (96-hour, fathead minnow (FHM) and medaka) and a NOEC of 242.0 µg/L, a LOEC of 485.0 µg/L (7-day, growth for FHM and medaka). Reproductive testing revealed a LOEC for fecundity of 24.1 ng/L (21 days, medaka). Further testing confirmed the LOEC of 24.1 ng/L while defining a NOEC of 4.7 ng/L (28 days, medaka). Effect of NET in medaka life-cycle exposure at concentrations exceeding 4.7 ng
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Utt, Matthew Douglas. "The effects of varying the interval from follicular wave emergence to progestin withdrawal on follicular dynamics and the synchrony of estrus in beef cattle." Thesis, Virginia Tech, 2002. http://hdl.handle.net/10919/33769.

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The objective of this experiment was to examine the effects of varying the interval from follicular wave emergence to progestin removal on follicular dynamics and the synchrony of estrus. The experimental design was a 2x2x2 factorial with GnRH or estradiol-17 beta (E2) + progesterone (P4), controlled internal drug-releasing device (CIDR) treatment duration, and PG or saline treatment as main effects. Cycling, Angus cows (n=49), on d 6 to 8 of the estrous cycle, were randomly assigned to receive a CIDR treatment for 7 or 9 d. Approximately half of the cows from each CIDR group received eithe
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39

Bikkul, Mehmet Ural. "Using drug treatments to control genome behaviour in normal and Hutchinson-Gilford Progeria Syndrome fibroblasts, with and without hTERT immortalisation." Thesis, Brunel University, 2016. http://bura.brunel.ac.uk/handle/2438/12774.

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Hutchinson-Gilford Progeria Syndrome (HGPS) is an exceedingly rare genetic condition with striking features reminiscent of marked premature ageing. HGPS is commonly caused by a ‘classic’ mutation in the A-type lamin gene, LMNA (G608G). This leads to the expression of an aberrant truncated lamin A protein, progerin. The nuclear lamina is known to anchor chromosomes, stabilising and regulating the genome. Interphase chromosomes are non-randomly positioned in the nuclei of cells and they occupy specific locations with respect to a radial distribution, gene-poor chromosomes are positioned at the n
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Apte, Ketaki [Verfasser], Reimer [Akademischer Betreuer] Stick, and Manfred [Akademischer Betreuer] Radmacher. "Influence of Lamin A E145K progeria mutation on nuclear mechanics / Ketaki Apte. Gutachter: Reimer Stick ; Manfred Radmacher. Betreuer: Reimer Stick." Bremen : Staats- und Universitätsbibliothek Bremen, 2014. http://d-nb.info/1072079313/34.

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41

Johnson, McKayla. "The Effect of Ultraviolet Light on Cell Viability, DNA Damage and Repair in Hutchinson-Gilford Progeria Syndrome and BJ Fibroblasts." Digital Commons @ East Tennessee State University, 2011. https://dc.etsu.edu/honors/90.

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Patients of Hutchinson-Gilford Progeria Syndrome (HGPS) display a rate of aging up to ten times that of normal human populations. It might be expected that HGPS cells would have a decreased ability to repair DNA damage through the cell cycle as compared to normal cells such as those of the BJ cell line since DNA damage accumulation is a hallmark phenotype of aging. On earth, we are exposed to far more ultraviolet-B (UV-B, 280-315 nm) and UV-A (315-400 nm) than UV-C (100-280 nm) radiation, since the latter is filtered-out by the atmospheric ozone layer. The relative sensitivity of prematurel
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SILVA, Josenice Oliveira da. "Avaliação do PROGER Urbano/99: o caso de Vicência em Pernambuco." Universidade Federal de Pernambuco, 2003. https://repositorio.ufpe.br/handle/123456789/9989.

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Made available in DSpace on 2014-06-12T23:17:12Z (GMT). No. of bitstreams: 2 arquivo9307_1.pdf: 413004 bytes, checksum: ded0b50908b742d59f05c40d6d19a633 (MD5) license.txt: 1748 bytes, checksum: 8a4605be74aa9ea9d79846c1fba20a33 (MD5) Previous issue date: 2003<br>O estudo ora apresentado consiste em uma análise sistemática das mudanças duradouras ou significativas na vida dos beneficiários do PROGER Urbano no ano de 1999 no município. Trata-se de um estudo de avaliação de impactos. A partir da observação de resultados positivos obtidos quando da implementação do PROGER Urbano no ano de
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Henríquez, Leiva Carolina Andrea. "El dilema de la Lapageria Rosea en bosques fragmentados : ¿cantidad o calidad de la progenie?" Tesis, Universidad de Chile, 2002. http://www.repositorio.uchile.cl/handle/2250/106691.

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La fragmentación del hábitat puede afectar a las plantas al modificar su éxito reproductivo. Poblaciones más pequeñas y aisladas podrían experimentar reducción en la cantidad y calidad de semillas producidas, por cambios en la interacción con polinizadores, reducción en la variabilidad genética y modificación de condiciones abióticas. Dado que procesos como la germinación de semillas y el establecimiento de plántulas dependen de la cantidad y calidad de las semillas generadas, y de factores abióticos, la sobrevivencia de las poblaciones en fragmentos se ve amenzada. El objetivo de esta tesis
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Bauer, Rosemary Aileen. "Priming with oral progestin before ovulation induction facilitates ovarian function in the cat (Felis catus)." College Park, Md.: University of Maryland, 2007. http://hdl.handle.net/1903/7667.

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Thesis (Ph. D.) -- University of Maryland, College Park, 2007.<br>Thesis research directed by: Dept. of Animal and Avian Sciences. Title from t.p. of PDF. Includes bibliographical references. Published by UMI Dissertation Services, Ann Arbor, Mich. Also available in paper.
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45

Kortüm, F., M. Chyrek, S. Fuchs, et al. "Hallermann-Streiff Syndrome: No Evidence for a Link to Laminopathies." Karger, 2011. https://tud.qucosa.de/id/qucosa%3A71623.

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Hallermann-Streiff syndrome (HSS) is a rare inherited disorder characterized by malformations of the cranium and facial bones, congenital cataracts, microphthalmia, skin atrophy, hypotrichosis, proportionate short stature, teeth abnormalities, and a typical facial appearance with prominent forehead, small pointed nose, and micrognathia. The genetic cause of this developmental disorder is presently unknown. Here we describe 8 new patients with a phenotype of HSS. Individuals with HSS present with clinical features overlapping with some progeroid syndromes that belong to the laminopathies, such
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De, Sandre-Giovannoli Annachiara. "Implication du gène LMNA, codant pour les Lamines A/C, dans les neuropathies périphériques héréditaires et la progeria de Hutchinson-Gilford." Aix-Marseille 2, 2003. http://www.theses.fr/2003AIX20698.

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Matias, Karla Cristinne de Oliveira. "Politícas públicas para a geração de empregos: considerações sobre o PROGER Turismo." Universidade Federal da Paraí­ba, 2008. http://tede.biblioteca.ufpb.br:8080/handle/tede/3786.

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Made available in DSpace on 2015-04-16T14:48:44Z (GMT). No. of bitstreams: 1 arquivototal.pdf: 548578 bytes, checksum: d7b6f97548c4da787a2eb327037b7b77 (MD5) Previous issue date: 2008-04-14<br>Conselho Nacional de Pesquisa e Desenvolvimento Científico e Tecnológico - CNPq<br>The present work aims to discuss the proposal of the Job and Income Generation Program (PROGER) by the Brazilian Labour Ministry, in its category dedicated to the Tourism sector, instituted in 2003. Beyond the discussion about the main characteristics of PROGER Turismo, this study tries to observe the evolution of t
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Busch, Albert Franz Jakob [Verfasser], and Stefan [Akademischer Betreuer] Hübner. "Prälamin A und Progerie–verursachende Mutanten im Kontext nukleärer Transportprozesse, der Kernlaminaintegrität und CaaX–Prozessierung / Albert Franz Jakob Busch. Betreuer: Stefan Hübner." Würzburg : Universitätsbibliothek der Universität Würzburg, 2012. http://d-nb.info/1024243222/34.

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Albarran, Gutierrez Sara Ruth [Verfasser], Aleksandra [Gutachter] Trifunovic, and Rudolf [Gutachter] Wiesner. "Molecular mechanisms underlying the rate of progeria onset in mtDNA mutator mouse strains / Sara Ruth Albarran Gutierrez ; Gutachter: Aleksandra Trifunovic, Rudolf Wiesner." Köln : Universitäts- und Stadtbibliothek Köln, 2020. http://d-nb.info/1217782877/34.

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Merschhemke, Marianne [Verfasser]. "Die gastroösophageale Refluxkrankheit und extraösophageale Erkrankungen : eine Langzeitbeobachtung im Rahmen der ProGERD-Studie / Marianne Merschhemke." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2008. http://d-nb.info/102326191X/34.

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