Дисертації з теми "Disease programming"
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Erwig, Lars-Peter. "Macrophage programming in inflammatory disease." Thesis, University of Aberdeen, 2004. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU194083.
Повний текст джерелаHansell, J. A. "Oxidative stress and developmental programming of cardiovascular disease." Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.603660.
Повний текст джерелаMartin-Gronert, Malgorzata Sylvia. "Mechanisms underlying the developmental programming of health and disease." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608293.
Повний текст джерелаBlackmore, Heather Louise. "Programming of cardiovascular disease by maternal diet-induced obesity." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648545.
Повний текст джерелаRose, Catherine Margaret. "Programming of cardiovascular disease : an exploration of epigenetic mechanisms." Thesis, University of Edinburgh, 2015. http://hdl.handle.net/1842/21082.
Повний текст джерелаYuan, Ruoxi. "Dynamic Programming of Innate Immunity in Health and Disease." Diss., Virginia Tech, 2016. http://hdl.handle.net/10919/82925.
Повний текст джерелаPh. D.
Marchand, Michael C. "Fetal programming of renal morphology and function." Thesis, University of Northampton, 2004. http://nectar.northampton.ac.uk/2681/.
Повний текст джерелаBlackman, Nicole. "Chronic Disease and Injury Prevention Programming for Canada's Indigenous Population." ScholarWorks, 2018. https://scholarworks.waldenu.edu/dissertations/5165.
Повний текст джерелаWarner, Matthew John. "Mechanisms of post-transcriptional gene regulation in the developmental programming of adulthood disease." Thesis, University of Cambridge, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.610291.
Повний текст джерелаForsén, Tom. "Early growth and adult disease : programming of coronary heart disease, type 2 diabetes and hypertension by fetal and childhood growth." Helsinki : University of Helsinki, 2000. http://ethesis.helsinki.fi/julkaisut/laa/kansa/vk/forsen/.
Повний текст джерелаTegethoff, Marion. "Fetal origins of pediatric disease fetoplacental plasticity and intrauterine programming by stress and glucocorticoids." Göttingen Cuvillier, 2009. http://d-nb.info/999629417/04.
Повний текст джерелаFlanagan, Daniel. "Programming of hormonal axes contributing to the link between fetal growth, diabetes and cardiovascular disease." Thesis, University of Southampton, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298118.
Повний текст джерелаMouralidarane, A. C. "The role of developmental programming in the pathogenesis of non-alcoholic fatty liver disease (NAFLD)." Thesis, University College London (University of London), 2012. http://discovery.ucl.ac.uk/1354935/.
Повний текст джерелаZhao, Ken Kun. "Treatments of Chlamydia Trachomatis and Neisseria Gonorrhoeae." Digital Archive @ GSU, 2008. http://digitalarchive.gsu.edu/math_theses/49.
Повний текст джерелаLow, Kathy A. "Motor programming and learning of complex finger movements in Parkinson's disease : a movement-related potential study /." free to MU campus, to others for purchase, 1997. http://wwwlib.umi.com/cr/mo/fullcit?p9842549.
Повний текст джерелаHamilton, Kristin Marie. "Benefits of Community Research-Based Programming to Improve Freezing of Gait for Individuals with Parkinson Disease." Thesis, The University of Arizona, 2013. http://hdl.handle.net/10150/297620.
Повний текст джерелаJain, Ravi. "Intelligent techniques for the diagnosis of coronary artery disease /." Title page, contents and abstract only, 1998. http://web4.library.adelaide.edu.au/theses/09PH/09phj248.pdf.
Повний текст джерелаSiemienowicz, Katarzyna Joanna. "Fetal programming of adult disease : causes and consequences of metabolic dysregulation in an ovine model of PCOS." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/28977.
Повний текст джерелаAlassadi, Abdulrahman, and Tadas Ivanauskas. "Classification Performance Between Machine Learning and Traditional Programming in Java." Thesis, Högskolan Kristianstad, Fakulteten för naturvetenskap, 2019. http://urn.kb.se/resolve?urn=urn:nbn:se:hkr:diva-20009.
Повний текст джерелаBeeson, Jessica Holly. "An investigation into whether an exercise intervention during pregnancy can prevent the programming of cardiovascular disease in the offspring of obese mothers." Thesis, University of Cambridge, 2019. https://www.repository.cam.ac.uk/handle/1810/289772.
Повний текст джерелаSinclair, Dina. "Incorporating the Centers for Disease Control and Prevention into Vaccine Pricing Models." Scholarship @ Claremont, 2017. http://scholarship.claremont.edu/hmc_theses/111.
Повний текст джерелаWilkinson, Mary Ann. "The impact of neurolinguistic programming rapport skills training for registered nurses on one-on-one teaching of Acquired Immune Deficiency Syndrome prevention." Diss., Virginia Polytechnic Institute and State University, 1988. http://hdl.handle.net/10919/54461.
Повний текст джерелаEd. D.
Paz, Sandro. "Antiviral Resistance and Dynamic Treatment and Chemoprophylaxis of Pandemic Influenza." Scholar Commons, 2014. https://scholarcommons.usf.edu/etd/5097.
Повний текст джерелаCunha, Fábio da Silva. "Similaridades nas desigualdades : um modelo animal para o estudo de vulnerabilidade ao sedentarismo." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2013. http://hdl.handle.net/10183/70421.
Повний текст джерелаIntroduction: We have previously proposed a theoretical model in which extreme unequal social backgrounds coexist in a complex scenario promoting similar health outcomes, named “Similarities in the inequalities”, and had evidence of this effect in humans. Our objective was to propose an animal model to reflect the “Similarities in the inequalities” phenomenon. Methods: Rats were time-mated and randomly allocated to: Control (Adlib), receiving an ad libitum diet of standard laboratory chow, 50% food restricted (FR), receiving 50% of the ad libitum-fed dam’s intake and high fat diet (HF), receiving a diet containing 45.0% fat. These diets were provided from day 10 of pregnancy throughout the 21-day of lactation. Within 24 hours after birth, all pups were cross-fostered to other dams, forming the following groups: Adlib_Adlib, FR_Adlib, FR_FR, Adlib_FR, HF_Adlib, HF_HF, Adlib_HF. Dam’s body weight and show consumption, pup’s birth weight, growth and physical activity in running wheels, was compared between groups through GEE, using different statistical models. Twoway ANOVA was used to evaluate abdominal fat and biochemical outcomes. Results: Body weight of Adlib and HF dams was higher compared to FR dams. Apart from some isolated effects of the exposure to the FR or HF diets during specific perinatal times (gestation and/or lactation), the “Similarities in the inequalities” effect was seen in birth weight (both FR and HF pups were smaller than Adlib pups) and physical activity (the extreme groups FR_Adlib and HF_Adlib were similarly different from the reference group Adlib_Adlib, being less active in males and more active in females). Body weight monitoring throughout life showed that males were heavier than females. None of the three statistical models showed differences between groups in total abdominal fat. Conclusion: Our study contributes to the idea that health inequalities are related to similar health outcomes for both populational extremes, and proposes an animal model to further explore this effect.
Mertens, Christophe. "Analysis of vocal tremor in normophonic and dysphonic speakers." Doctoral thesis, Universite Libre de Bruxelles, 2015. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/218423.
Повний текст джерелаDoctorat en Sciences de l'ingénieur et technologie
info:eu-repo/semantics/nonPublished
Schick, Jona Fabian [Verfasser]. "Effizienz von Disease Management Programmen / Jona Fabian Schick." Ulm : Universität Ulm, 2019. http://d-nb.info/1200470087/34.
Повний текст джерелаFerraro, Zachary Michael. "An Examination of Maternal Contributors and Potential Modifiers of Fetal Growth in Pregnancy." Thèse, Université d'Ottawa / University of Ottawa, 2012. http://hdl.handle.net/10393/22817.
Повний текст джерелаArroyo, Juan Pablo. "Exploring Potential Risk Factors of Fetal Origins of Diabetes| Maternal Stressors during Pregnancy and Birth Outcomes among Women in a Hospital in the Municipality of Caguas, Puerto Rico." Thesis, University of South Florida, 2013. http://pqdtopen.proquest.com/#viewpdf?dispub=1543402.
Повний текст джерелаPuerto Rico has the highest prevalence of type 2 diabetes, low birth-weight, and the second highest prevalence of preterm-birth in all the U.S. and its non-incorporated territories. These conditions are related. Birth-weight at both ends of the spectrum and preterm-birth are associated with an increased risk for developing type 2 diabetes and immune-inflammatory dysregulations. Maternal psychosocial stressors during pregnancy have also been recognized as potential risk factors for type 2 diabetes, and have been consistently associated with preterm-birth and low birth-weight across populations. Current evidence points toward epigenetic fetal metabolic-programming as the mechanism that underlies the increased risk for the previously mentioned morbidities. However, the particular psychosocial stressors that may contribute to the high prevalence of low birth-weight and preterm-birth in the population of Puerto Rico have not been well studied.
The present study assesses the relationships between particular psychosocial stressors, socioeconomic status, food insecurity, and birth outcomes. The results of this study show that low-risk pregnancy women were more likely to have babies with a higher ponderal index if they were exposed to stressors during gestation months 5, 6, and 7, or if exposed to "relationship stress" at any time during pregnancy. Women exposed to "financial difficulties" at any time during pregnancy were more likely to deliver babies at an earlier gestational age. Differences in birth outcomes between the exposed and non-exposed women were independent of maternal anthropometric measurements, maternal age at birth, number of previous births, and sex of the baby. Significant differences in birth outcomes were found between categories of father's self-identified and identified by others ethnicity, but sample size within categories was small. Although mothers with children at home had higher levels of food insecurity, and the level of food insecurity was correlated with higher levels of stress, no birth outcome measure was associated with food insecurity.
Some results are atypical in comparison with other populations, and therefore these findings may contribute to the understanding of population differences in the relationship between maternal stress during pregnancy and birth outcomes. The relatively small sample size and strict exclusion criteria of this study may limit the generalizability of the findings. Epidemiological similarities between Puerto Rico and other populations, and the possibility of a higher ponderal index increasing the risk for type 2 diabetes in the population of Puerto Rico need to be examined in future research.
Ribó, Gené Sílvia. "Role of early postnatal nutrition during lactation in offspring metabolic health programming." Doctoral thesis, Universitat de Barcelona, 2017. http://hdl.handle.net/10803/462066.
Повний текст джерелаL'obesitat i el sobrepès infantil poden causar sovint complicacions greus en la salut, incloent hipertensió, dislipèmia, resistència a la insulina, diabetis tipus 2 i esteatosis hepàtica no alcohòlica, entre d’altres. Diversos estudis han demostrat que la nutrició post-natal precoç és de gran importància en la modulació de la salut del nounat. En aquesta tesis, hem estudiat el paper de la nutrició durant les primeres etapes de la vida en la salut metabòlica a llarg termini aplicant dos enfocaments diferents: a) efectes metabòlics de suplementar de la dieta materna durant la lactància amb betaïna sobre la descendència a curt i llarg termini i b) transmissió transgeneracional del fenotip d’intolerància a la glucosa induïda per un augment accelerat de pes en etapes primerenques de la vida, causat per l'excés de nutrició post-natal. La composició de la llet materna és important per modular el creixement i la salut metabòlica de l'infant. Entre els nutrients que conté la llet materna, cal destacar la glicina betaïna (o betaïna). A més de disminuir els nivells de greix en fetge, diverses publicacions demostren que suplementar la dieta materna amb betaïna durant la lactància també millora l'homeòstasi de la glucosa i modula la composició de la microbiota intestinal del nounat. Al suplementar amb betaïna l’aigua de femelles durant la lactància vam observar efectes beneficiosos en la descendència a nivell metabòlic a curt i llarg termini. També vam poder observar que la betaïna protegia contra l'obesitat induïda per una dieta rica en greixos en l’etapa adulta. Se sap que la llet materna també conté bacteris essencials que poden influir en la composició de microbiota intestinal del lactant. S'ha analitzat la microbiota de l’ili i cec de ratolins suplementats amb betaïna, i amb o sense antibiòtics en diferents etapes de la vida. Analitzant el microbioma trobem que la composició de la comunitat microbiana dels ratolins de dues setmanes de vida estava modulada per la suplementació de betaina. Els canvis en el microbioma causats per l'administració d'antibiòtics durant la lactància estan significativament correlacionats amb una major adipositat i risc de desenvolupar obesitat durant l'edat adulta. El tractament amb antibiòtics en els nostres ratolins va anul·lar els efectes induïts per betaïna a llarg termini sobre el pes corporal. A més, la tolerància a la glucosa no estava millorarada quan es combinaven els antibiòtics amb el tractament amb betaïna. L'augment ràpid de pes durant les primeres etapes de la vida s'ha associat a diversos components de la Síndrome Metabòlica en l’adult. Prèviament en aquest laboratori hem desenvolupat un model murí de sobrealimentació neonatal i augment de pes ràpid a partir d’una reducció de la mida de la ventrada. L'excés d'alimentació neonatal (ON) va alterar el metabolisme dels mascles exposats (F0). A més, els fills (F1) i els néts (F2) dels ratolins exposats a la sobrenutrició també van desenvolupar un metabolisme alterat durant l'edat adulta. En acord, s'ha demostrat que l'exposició ambiental sobre els mascles pot afectar la salut de generacions posteriors. Així, ens vam plantejar que les modificacions epigenètiques, incloses la metilació de l'ADN, les modificacions de l'histona i l'ARN no codificant, podrien estar implicades en l'herència del risc de diabetis en el nostre model. Es va analitzar el metilma d’esperma de les generacions F0 i F1, i el metiloma de fetges de ratolins de 8 dies d'edat de les generacions F1 i F2, observant canvis significatius en la metilació de regions específiques d'ADN. Al comparar els ratolins control amb ON de cada generació i teixit, vam trobar 912 sondes diferentment metiladas. Els nostres resultats suggereixen que la metilació de la línia germinal masculina provocada per reptes nutricionals durant etapes primerenques de la vida pot portar informació que influeixi en el metabolisme en les següents generacions.
Kirchberg, Franca [Verfasser], and Berthold [Akademischer Betreuer] Koletzko. "The use of metabolomics to improve our understanding of the early programming of diseases / Franca Kirchberg ; Betreuer: Berthold Koletzko." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2018. http://d-nb.info/1185978844/34.
Повний текст джерелаPadmanabhan, Babu roshan. "Taxano-genomics, a strategy incorporating genomic data into the taxonomic description of human bacteria." Thesis, Aix-Marseille, 2014. http://www.theses.fr/2014AIXM5056.
Повний текст джерелаMy PhD project was to create a pipeline for taxono-genomics for the comparison of multiple bacterial genomes. Secondly I automated the process of assembly (NGS) and annotation using various open source softwares as well as creating in house scripts for the lab. Finally we incorporated the pipeline in describing several bacterial species from out lab. This thesis is subdivided mainly into Taxono-genomics and Microbiogenomics. The reviews in taxono-genomics section, describes about the technological advances in genomics and metagenomics relevant to the field of medical microbiology and describes the strategy taxono-genomics in detail and how polyphasic strategy along with genomic approaches are reformatting the definition of bacterial taxonomy. The articles describes clinically important bacteria, their whole genome sequencing and the genomic, comparative genomic and taxono-genomic studies of these bacteria
Chen, Carla Chia-Ming. "Bayesian methodology for genetics of complex diseases." Thesis, Queensland University of Technology, 2010. https://eprints.qut.edu.au/43357/1/Carla_Chen_Thesis.pdf.
Повний текст джерелаMagliano, D'Angelo Carlo. "Agonista PAN-PPAR (receptores ativadores de proliferação peroxissomal) e alterações hepáticas na prole adulta de camundongos de mães obesas." Universidade do Estado do Rio de Janeiro, 2012. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=6118.
Повний текст джерелаO objetivo do presente estudo foi avaliar se o Bezafibrato, um agonista PAN-PPAR, é capaz de aliviar a doença não alcoólica do fígado gorduroso (NAFLD) na prole de machos de mães C57BL/6 obesas. Fêmeas virgens foram alimentadas com uma dieta HL (hiperlipídica, 49% de lipídios) ou uma dieta C (controle, 10% de lipídios) por oito semanas antes do acasalamento e durante os períodos de gestação e lactação. A prole de machos foi subdividida em quatro grupos: C (dieta controle para as mães e filhotes); C/BZ (dieta controle para as mães e filhotes com tratamento com Bezafibrato[100mg/Kg]); HL (dieta HL para as mães e dieta controle para os filhotes); e HL/BZ (dieta HL para as mães e dieta controle para os filhotes com tratamento com Bezafibrato [100mg/Kg]). O tratamento com Bezafibrato começou na 12 semana e se manteve por três semanas. Análise do metabolismo, bioquímica, estereológica e por western-blotting foram realizadas. A dieta HL causou um fenótipo de sobrepeso nas mães e acarretou em uma intolerância oral à glicose com aumento da glicemia de jejum. A prole HL apresentou hiperfagia, ganho de massa corporal, altos níveis de triglicerídeo hepático e plasmático, esteatose hepática e aumento da expressão de proteínas lipogênicas concomitante com diminuição do receptor ativador de proliferação peroxissomal alfa (PPARα), que é responsável pela β-oxidação e aumento do receptor ativador de proliferação peroxissomal gama (PPARγ) e do elemento regulador de esterol ligante da proteína 1 (SREBP-1c) proteínas envolvidas na lipogênese hepática. Por outro lado, o tratamento com o Bezafibrato reverteu o quadro da programação metabólica no fígado, com uma melhora dos parâmetros morfológicos, bioquímicos e moleculares do fígado dos animais, com um aumento da ativação de PPARα em associação a uma diminuição do PPARγ e não alterando a expressão de SREBP-1c. Em conclusão, nós demonstramos que o tratamento com Bezafibrato melhora a NAFLD causada pela obesidade materna.
The aim of the present study was to evaluate whether Bezafibrate , a PAN-PPAR agonist, could attenuate non-alcoholic fatty liver disease (NAFLD) of male offspring from obese C57BL/6 dams. Dams were fed on a HF (high-fat, 49% lipids) diet or SC (standard chow; 10% lipids) diet for 8 weeks before mating and during gestation and lactation periods. Male offspring were subdivided into 4 groups: SC (standard-chow for dams and offspring); SC/BZ [standard-chow for dams and offspring with treatment with BZ (100mg/Kg)]; HF (high-fat diet for dams and standard-chow for offspring); HF/BZ [high-fat diet for dams and standard-show for offspring with treatment with Bezafibrate (100mg/Kg)]. Treatment with Bezafibrate started at 12th week and was maintained for 3 weeks. Metabolic measurements, biochemical analysis, stereological tools and western-blotting were performed. The HF diet yielded an overweight phenotype and an increase in oral glucose tolerance and fasting glucose of dams. The HF offspring presented hyperphagia, body mass gain, high levels of plasmatic and hepatic triglycerides, impairment of glucose metabolism, hepatic steatosis and high expression of lipogenic proteins concomitant to decreased expression of PPARα, which is responsible for β-oxidation. On the other hand, treatment with Bezafibrate reverted hepatic outcomes of metabolic programming, with an improvement of morphological, biochemical and molecular parameters of animals livers, with an increase of PPARα activation in association with a decrease of PPARγ expression and no changes in SREBP-1c expression. In conclusion, we demonstrated that treatment with Bezafibrate improved NAFLD caused by maternal obesity.
Drabik, Anna Izabela [Verfasser]. "Evaluationsmethoden populationsbasierter Programme zur Prävention chronischer Krankheiten am Beispiel von Disease-Management-Programmen : ein Überblick sowie eine Anwendung der Propensity-Score-Matching-Methode auf das Disease- Management-Programm „Typ-II-Diabetes“ der BARMER-Krankenkasse in Deutschland / Anna Izabela Drabik." Köln : Deutsche Zentralbibliothek für Medizin, 2012. http://d-nb.info/1025008189/34.
Повний текст джерелаWeingarten, Marco [Verfasser]. "Effektivität eines Ausdauer- und Krafttrainings bei älteren Menschen mit Diabetes Mellitus Typ 2 und im Rahmen von Disease Management Programmen optimal eingestellten HbA1c-Ausgangswerten / Marco Weingarten." Kiel : Universitätsbibliothek Kiel, 2014. http://d-nb.info/1046832239/34.
Повний текст джерелаMorehouse, Susan Agnes. "Attention, how does it move us? A kinematic analysis of the effects of visual attention and motor programming on manual aiming movements in healthy young and healthy elderly individuals, and those with Alzheimer's and Parkinson's diseases." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape10/PQDD_0019/NQ49282.pdf.
Повний текст джерелаZangoli, Greta Alessandra. "Possono i programmi personalizzati di educazione ed autogestione basati su piattaforme elettroniche avere effetto in termini di qualita della vita e cambiamento delle abitudini nei pazienti con BPCO? Revisione della letteratura." Bachelor's thesis, Alma Mater Studiorum - Università di Bologna, 2018.
Знайти повний текст джерелаEkici, Ali. "Emerging applications of OR/MS emergency response planning and production planning in semiconductor and printing industry /." Diss., Atlanta, Ga. : Georgia Institute of Technology, 2009. http://hdl.handle.net/1853/31746.
Повний текст джерелаCommittee Chair: Keskinocak, Pinar; Committee Member: Ergun, Ozlem; Committee Member: Goldsman, David; Committee Member: Hupert, Nathaniel; Committee Member: Swann, Julie. Part of the SMARTech Electronic Thesis and Dissertation Collection.
Torrens, García Juana María. "Effects of moderate maternal energy restriction on the offspring metabolic health, in terms of obesity and related diseases, and identification of determinant factors and early biomarkers." Doctoral thesis, Universitat de les Illes Balears, 2015. http://hdl.handle.net/10803/288315.
Повний текст джерелаIntroducción Numerosas evidencias, procedentes de estudios epidemiológicos en humanos y de modelos animales, indican que la salud materna y su estado nutricional durante la gestación y la lactancia pueden programar la propensión a desarrollar obesidad en la descendencia. Se están llevando a cabo grandes esfuerzos para entender los mecanismos moleculares responsables de dicha programación metabólica. La identificación de los mecanismos responsables podría dar ciertas pistas para el desarrollo de estrategias que permitan prevenir o revertir dicha propensión a desarrollar obesidad, y también podría ayudarnos en la identificación de biomarcadores tempranos de salud metabólica. Por consiguiente, el principal objetivo de esta tesis doctoral ha sido: Caracterizar en ratas los efectos de una restricción energética materna moderada durante la gestación o la lactancia sobre la salud metabólica de la descendencia, en relación a la obesidad y las alteraciones metabólicas asociadas, así como también identificar nuevas estrategias de prevención frente la programación de la obesidad y nuevos biomarcadores tempranos de salud metabólica. Contenido de la investigación Hemos caracterizado un modelo animal, que previamente se había descrito que presentaba una mayor propensión a desarrollar obesidad y alteraciones metabólicas asociadas – las crías de ratas sometidas a una restricción calórica moderada durante la gestación (CRG) – para identificar algunos de los mecanismos potencialmente responsables de sus efectos negativos. Los niveles de expresión de genes claves relacionados con la homeostasia energética en el hipotálamo y el tejido adiposo, y el análisis de ciertos parámetros circulantes, revelaron que estos animales estaban programados, ya desde edades tempranas, para una menor respuesta a la insulina y a la acción central de la leptina. Esto podría explicar la hiperfagia observada en estos animales y la mayor propensión a la obesidad, que presentan particularmente los machos. Algunas de estas alteraciones programadas, tales como la alteración de la sensibilidad a la insulina y a leptina, y la elevada presión sistólica, característica de los animales CRG, se vieron revertidas al favorecer el incremento de la oxidación hepática de ácidos grasos, en edades tempranas, a través de la transferencia génica, mediada por vectores virales adeno-asociados, del ADNc de la Cpt1am (que codifica para una forma permanentemente activa de la CPT1A, insensible a su inhibidor fisiológico malonil-CoA). A diferencia de la restricción calórica durante la gestación, observamos que la restricción calórica moderada en ratas madre durante la lactancia protege a su descendencia (CRL) frente al desarrollo de obesidad inducida por la dieta y frente al desarrollo de alteraciones metabólicas asociadas, tales como la dislipidemia, la resistencia a la insulina y la hiperleptinemia. Esta condición durante la lactancia determina cambios tempranos a nivel de expresión génica en el tejido adiposo y el hígado, afectando la capacidad lipogénica y oxidativa, e incrementando la sensibilidad a la acción periférica de la insulina y la leptina. Algunas de estas adaptaciones se mantuvieron parcialmente en edad adulta. Los animales CRL adultos mostraron cambios a nivel de expresión génica en el tejido adiposo y en el hipotálamo que fueron dependientes del sexo, sugiriendo que los machos estaban más protegidos frente a la resistencia periférica a la insulina inducida por una dieta hiperlipídica, así como también mostraron una capacidad mejorada para responder a la leptina a nivel central; en cambio, las hembras CRL estaban programadas para una mejor sensibilidad a la acción periférica de la leptina y a la acción central de la insulina. Utilizamos este modelo animal para identificar marcadores tempranos de transcripción indicadores de salud metabólica mejorada mediante el análisis por microarray de células mononucleares de sangre periférica (PBMCs). Con respecto a los factores que podrían estar potencialmente implicados en los efectos beneficiosos de la restricción calórica durante la lactancia sobre las crías, el menor contenido de marcadores de daño proteico por oxidación y glicación hallado en la leche de madres CRL, en comparación con la leche de madres control, podría ser relevante. Conclusión La nutrición materna durante el periodo perinatal puede ser un determinante importante de la sensibilidad a la insulina y la leptina de sus crías. Mientras que la restricción calórica durante la gestación programa a las crías para una menor capacidad de respuesta a la inulina y a la acción central de la leptina, las crías de madres expuestas a una restricción calórica moderada durante la lactancia muestran una sensibilidad mejorada a estas hormonas. Se han identificado un grupo de genes cuyos niveles de expresión en células sanguíneas podrían considerarse como potenciales marcadores tempranos de salud metabólica, pudiendo proporcionar una herramienta biológica válida para el estudio de procesos metabólicos en humanos.
Introducció Nombroses evidències, procedents d’estudis epidemiològics en humans i de models animals, indiquen que la salut materna i el seu estatus nutricional durant la gestació i la lactància poden programar la propensió de la descendència a desenvolupar obesitat. S’estan duent a terme grans esforços per entendre els mecanismes moleculars responsables d’aquesta programació metabòlica. La identificació d’aquests mecanismes podria donar-nos certes pistes per al desenvolupament d’estratègies que permetin prevenir o revertir la propensió programada a desenvolupar obesitat, i també podria ajudar-nos en la identificació de biomarcadors primerencs de salut metabòlica. Per això, el principal objectiu d’aquesta tesis doctoral ha estat: Caracteritzar en rates els efectes d’una restricció energètica moderada a les mares durant la gestació o la lactància sobre la salut metabòlica de la descendència, en relació a l’obesitat i les alteracions metabòliques associades, així com també identificar noves estratègies de prevenció enfront a la programació de l’obesitat i nous biomarcadors primerencs de salut metabòlica. Contingut de la investigació Hem caracteritzat un model animal, que prèviament se va veure que exhibia una major propensió a desenvolupar obesitat i alteracions metabòliques associades – les cries de rates sotmeses a una restricció calòrica moderada durant la gestació (CRG) – per identificar alguns dels mecanismes potencialment responsables dels seus efectes negatius. Els nivells d’expressió de gens clau relacionats amb la homeòstasi energètica a l’hipotàlem i al teixit adipós, i l’anàlisi de certs paràmetres circulants, varen mostrar que aquests animals estaven programats, ja des d’etapes primerenques de la vida, per una menor resposta a la insulina i a la acció central de la leptina. Això podria explicar la hiperfàgia observada en aquests animals i la major propensió a l’obesitat, que presenten particularment els mascles. Algunes d’aquestes alteracions programades, com ara l’alteració de la sensibilitat a la insulina i a la leptina, i l’elevada pressió sistòlica, característica dels animals CRG, es van veure revertides en afavorir l’increment de la oxidació hepàtica dels àcids grassos, a edats primerenques, a través de la transferència gènica, mitjançant vectors virals adeno-associats, de l’ADNc de la Cpt1am (que codifica per una forma permanentment activa de la CPT1A, insensible al seu inhibidor fisiològic, el malonil-CoA). A diferència de la restricció calòrica durant la gestació, observarem que la restricció calòrica moderada en rates mare durant la lactància, protegeix a la seva descendència (CRL) enfront del desenvolupament d’obesitat induïda per la dieta i el desenvolupament d’alteracions metabòliques associades a l’adultesa, com ara la dislipèmia, la resistència a la insulina i la hiperleptinèmia. Aquesta condició durant la lactància determina canvis primerencs a nivell d’expressió gènica en el teixit adipós i en el fetge, afectant la capacitat lipogènica i oxidativa, i incrementant la sensibilitat a la acció perifèrica de la insulina i la leptina. Algunes d’aquestes adaptacions se varen mantenir parcialment en edat adulta. Els animals adults CRL varen mostrar canvis en els nivells d’expressió gènica en el teixit adipós i a l’hipotàlem, que varen ser dependents del sexe, suggerint que els mascles estaven més protegits enfront a la resistència perifèrica a la insulina induïda per una dieta hiperlipídica, i també mostraren una capacitat millorada per respondre a la leptina a nivell central; en canvi, les femelles CRL estaven programades per a una millor sensibilitat a l’acció perifèrica de la leptina i a la acció central de la insulina. Utilitzarem aquest model animal per a la identificació de biomarcadors primerencs de transcripció, indicadors de salut metabòlica millorada, mitjançant l’anàlisi per microarray en cèl•lules mononuclears de sang perifèrica (PBMCs). Pel que fa als factors que podrien estar potencialment implicats en els efectes beneficiosos de la restricció calòrica materna durant la lactància sobre la descendència, el menor contingut de marcadors de dany proteic per glicació i d’oxidació trobat a la llet de mares CRL, en comparació amb la llet de mares control, podria ser rellevant. Conclusió La nutrició materna durant el període perinatal pot ser un determinant important de la sensibilitat a la insulina i a la leptina de les seves cries. La restricció calòrica durant la gestació programa a les cries per a una menor resposta a la insulina i a la acció central de la leptina; en canvi, les cries de mares exposades a una restricció calòrica moderada durant la lactància mostren una major sensibilitat a aquestes hormones. S’han identificat un grup de gens, els nivells de expressió dels quals en cèl•lules sanguínies se poden considerar com a potencials marcadors primerencs de salut metabòlica, podent proporcionar una eina biològica vàlida per a l’estudi dels processos metabòlics en humans.
Junior, Geraldo de Oliveira Silva. "Restrição proteica materna e alteração do desenvolvimento das artérias coronárias em camundongos." Universidade do Estado do Rio de Janeiro, 2011. http://www.bdtd.uerj.br/tde_busca/arquivo.php?codArquivo=4785.
Повний текст джерелаO desenvolvimento da programação fetal é considerado um importante fator de risco para doenças não-transmissíveis da vida adulta, incluindo doença cardíaca coronariana. Com o objetivo de investigar a associação entre nutrição materna e o desenvolvimento das artérias coronárias (AC) em embriões de camundongos estadiados; embriões de camundongos C57BL/6 nos estádios de 16-23 foram retirados de mães alimentadas com dietas de proteína normal (NP) ou de baixa proteína (LP), e as AC foram estudadas. Embora os embriões LP possuam massa corporal menor, entretanto tinham taxas de crescimento cardíaco maior, quando comparados com os embriões NP. O Plexo subepicárdico foi observado no início do período pós-somítico (estádio 16) de embriões NP, enquanto que nos embriões LP apenas no estádio 17 (P <0,01), persistindo até o estádio 18 (P <0,01). As artérias coronárias foram detectadas inicialmente no estádio18 dos embriões NP, já nos embriões LP foram encontradas a partir do estádio 19 (P <0,01). Núcleos apoptóticos foram observados em torno do anel aórtico peritruncal no estádio 18 em embriões NP e LP. Células FLK1+ (Fetal Liver Kinase 1 = VEGFr2 = Vascular Endothelial Growth Factor Receptor 2) apresentaram uma distribuição homogênea nos embriões NP já no estádio 18, enquanto uma distribuição semelhante nos embriões LP foi visto apenas nos estádios 22 e 23. A restrição proteica materna em camundongos leva a um atraso no crescimento do coração no período embrionário modificando o desenvolvimento do plexo peritruncal subepicárdica e diminuindo a taxa de apoptose na região do futuro orifício coronariano.
Programming of fetal development is considered to be an important risk factor for non-communicable diseases of adulthood, including coronary heart disease (CHD). Aiming to investigate the association between maternal nutrition and the development of the coronary arteries (CA) in staged mice embryos, C57BL/6 mice embryos from stages 16 to 23 were taken from mothers fed a normal protein (NP) or low protein (LP) diet, and the CA were studied. Although the LP embryos had lower masses, they had faster heart growth rates when compared to the NP embryos. The subepicardial plexuses were observed earlier in the NP embryos (stage 20) than in the LP ones (stage 22) (P<0.01). Apoptotic nuclei were seen around the aortic peritruncal ring beginning at stage 18 in the NP and LP embryos. FLK1+ (fetal liver kinase 1 = VEGFr2 or vascular endothelial growth factor receptor 2) cells had a homogeneous distribution in the NP embryos as early as stage 18, whereas a similar distribution in the LP embryos was only seen at stages 22 and 23. Maternal protein restriction in mice leads to a delay in the growth of the heart in the embryonic period modifying the development of the subepicardial peritruncal plexus and the apoptosis in the future coronary orifice region.
Grover, Sanita. "Role of hypothalamic pituitary adrenal axis in prenatal programming of adult disease." 2008. http://hdl.handle.net/2440/48490.
Повний текст джерелаThesis (Ph.D.) -- University of Adelaide, School of Paediatrics and Reproductive Health, 2008
Parvin, Hoda. "Modeling and analyzing spread of epidemic diseases: case study based on cervical cancer." 2007. http://hdl.handle.net/1969.1/ETD-TAMU-1331.
Повний текст джерелаPereira, Susana Patrícia da Silva. "Programming of fetal cardio-renal mitochondria by maternal nutrition." Doctoral thesis, 2016. http://hdl.handle.net/10316/29635.
Повний текст джерелаEarly-life malnutrition results in structural alterations to fetal kidney and heart, predisposing offspring to later life cardio-renal dysfunction. Epidemiologic studies link low birth weight to predisposition to cardiovascular disease (CVD) later in life with both sex and diet impacting the incidence of CVD. Kidneys of adults who suffered from growth restriction at birth have substantial variation in nephron endowment. Animal models suggest cardio-renal structural and functional consequences in the offspring exposed to sub-optimal intrauterine nutrition. Mitochondrial bioenergetics plays a key role in cardiac and renal energy metabolism, growth and function. In this relevant work, we hypothesized that moderate maternal nutrient reduction (MNR) would adversely impact fetal cardio-renal mitochondrial metabolism in a well-established non-human primate model which produces intra-uterine growth reduction at term. Female pregnant baboons were fed normal chow diet or 70% of control diet (maternal nutrient reduction, MNR). Cesarean sections were performed at 0.9 gestation (165 days gestation) under anesthesia. Maternal fasting blood was drawn from the femoral vein in the morning before cesarean section and before the fetus was exteriorized from the uterine cavity. Umbilical vein blood was also sampled. The mother, the placenta and the fetus were analyzed for morphometric measurements and tissue sampling. Fetal kidneys and heart were rapidly harvested and appropriately processed, flash frozen or fixed, for posterior analyses. Biochemical and amino acid analyses were performed in the maternal and fetal blood samples. Analysis of mitochondrial DNA was performed by quantitative real-time PCR, and Human Mitochondrial Energy Metabolism and Human Mitochondria Pathway PCR Arrays were used to analyze mitochondrial relevant mRNA. In situ protein content was detected by immunohistochemistry and semi-quantification was performed by Western blot. Enzymatic activity of mitochondrial proteins was determined by alterations in the absorbance of specific substrates or products. Adenine nucleotide levels and energy charge were determined by HPLC, as well determination of vitamin E and reduced and oxidized glutathione contents. Other indicators of oxidative state, as malondialdehyde content (MDA), glutathione peroxidase and glutathione reductase activities were determined spectrophotometrically. Ultimately, transmission electron microscopy was use to assess mitochondrial morphology. MNR until 0.9 gestation decreases maternal weight gain and placental weight, being the effects more severe in MNR mothers carrying a male fetuses. Despite the smaller overall fetal size, fetal kidney weight-to-body weight or the heart weight-to-body weight ratios were not affected. MNR caused adjustments in the protein metabolism reflected in altered maternal amino acids concentrations and impaired glucose metabolism, with MNR mothers displaying higher levels of cortisol and glucose in blood circulation. Regarding the fetal kidney, we demonstrated fetal gender-specific differential mRNA expression encoding mitochondrial metabolite transport and dynamics proteins. MNR-related differential gene expression was more evident in female fetuses, with 16 transcripts significantly altered, including 14 downregulated and 2 upregulated. MNR impacted 10 transcripts in male fetuses, with 7 downregulated and 3 upregulated. Alteration in mRNA levels was accompanied by a decrease in mitochondrial protein cytochrome c oxidase subunit VIc. In conclusion, transcripts encoding fetal renal mitochondrial energy metabolism proteins are nutrition sensitive in a gender-dependent manner. For the fetal cardiac left ventricle, we found that MNR increased mtDNA content and the transcription of key mitochondrial genes involved in mitochondrial dynamics and oxidative phosphorylation (OXPHOS), resulting in increased content of several mitochondrial proteins, namely components of the mitochondrial respiratory chain (NDUFB8, UQCRC1 and cytochrome c) and ATP synthase. However, the activity of OXPHOS enzymes was significantly decreased in MNR fetuses, possibly contributing to a decreased ATP content and an increased oxidative stress in the cardiac left ventricle tissues reported by augmented levels of the lipid peroxidation marker, MDA. Microscopy of the fetal cardiac left ventricles reflected the disturbance induced by MNR, revealing mitochondria with sparse and disarranged cristae. These checkpoints suggest that MNR orchestrated a serial of events that ultimately resulted in an impaired capacity of fetal cardiac left ventricle tissue to produce energy through the OXPHOS system. The present study provides for the first time evidence of an association between MNR and mitochondrial remodeling in the fetus. Although the MNR fetal manifestation were tissue and gender specific, the overall scenario point to and impairment in mitochondrial function in the fetal tissues analyzed. We speculate that these differences lead to decreased mitochondrial fitness that contributes to cardio-renal dysfunction in later life. Our work has a translational application in human health, showing that control of maternal health during pregnancy may reduce long term disease risk in the offspring with greatest benefit for the individual and for national health care systems.
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Ferguson, Angela. "The role of early life infection on the programming of CD4+ T-cells." Thesis, 2013. http://hdl.handle.net/1959.13/938480.
Повний текст джерелаAsthma is a chronic inflammatory disease of the airways that is characterised by activation of CD4+ T-helper 2 type (Th) cells and eosinophils. The cause of this aberrant Th2 response is unknown but lack of early life infection is thought to play a significant role. The timing of infection and the type of pathogen may be critical to programming the immune response to a protective Th1, or destructive Th2, phenotype. The immune responses to infection with Salmonella typhimurium and Mycobacterium bovis Bacille Calmette Guerin (BCG) have been identified as targets for reprogramming or preventing the development of asthma. However, the role of these infections in contributing to a Th2-Th1switch or suppression of this response remains limited. In this investigation ovalbumin (OVA) T-cell receptor (TCR) transgenic (Tg) mice in combination with these bacterial strains expressing OVA have been used to specifically track the affects of each infection as well as OVA exposure on the T-cell response and the development of allergic airways disease (AAD) in the mouse model. BCG infection as an adult and a neonate prior to OVA challenge induced significant reductions in eosinophils in broncho-alveolar lavage fluid (BALF) and lung tissue compared to sham-infected mice that received OVA challenge. However, high levels of both Th1 (interferon gamma (IFN-γ)) and Th2 (interleukin (IL)-4, IL-5, IL-13) cytokines from supernatants of cultured peri-bronchial lymph node (PBLN) cells and splenocytes were found in all groups examined. Further studies tracking the development of the immune system after BCG infection at birth without OVA exposure revealed significant decreases in lung tissue eosinophils and decreased immunoglobulin (Ig) G1, IgG2a and IgE levels from serum compared to sham-infected controls. This coincided with decreased numbers of CD4+ and CD8+ T-cells in the spleens and PBLN cells. Levels of cytokines in splenocytes and PBLN cell cultures failed to show significant trends toward either a polarised Th1 or Th2, leaving a mixed Th1/Th2 phenotype. Infection with S.typhimurium lowered eosinophil levels in BALF, and mucous secreting cell (MSC) and eosinophil number in lung tissue after challenge with 23 OVA, compared to sham-infected mice challenged with OVA. In mice infected as neonates and adults prior to OVA challenge increased levels of IFN-γ from splenocyte culture supernatants were found, compared to sham-infected OVA challenged controls. Decreased levels of IL-5 from splenocyte culture supernatants was found in neonates but not adult mice infected with S.typhimurium prior to OVA challenged compared to sham-infected OVA challenged controls. High levels of both Th1 and Th2 cytokines were present in splenocyte and PBLN culture supernatants from all groups tested, indicating a mixed Th1/Th2 phenotype rather than a profound switch to Th1 immune response. Further studies showed that infection with S.typhimurium at birth without OVA exposure causes changes to the development of the neonatal immune system resulting in decreased eosinophil numbers in BALF and lung tissue, decreased levels of serum IgG1 and IgG2a, and a shift from Th2 to a mixed Th1/Th2 cytokine profile. These changes were found in samples examined up to 9-weeks post infection. This investigation demonstrates that infection with BCG or S.typhimurium can alter the immune system resulting in attenuation of various immunological and patho-physiological features of asthma. Infection with BCG or S.typhimurium as a neonate appears to produce the most pronounced modification in the subsequent immune responses to OVA. These findings provide important insights into possible modified vaccination regimes at birth and during childhood, which may have the potential to prevent the development of asthma and allergic inflammatory disorders in adulthood.
"Developmental programming of adulthood obesity and cardiovascular disease in the mouse by maternal nutritional imbalance." Université catholique de Louvain, 2008. http://edoc.bib.ucl.ac.be:81/ETD-db/collection/available/BelnUcetd-11032008-192928/.
Повний текст джерелаDraycott, Sally Anne Victoria. "The Effects of Varying Maternal Dietary Fat Quantity and Composition on Disease Programming in the Offspring: a Focus on Essential Fatty Acids." Thesis, 2019. http://hdl.handle.net/2440/126951.
Повний текст джерелаThesis (Ph.D.) -- University of Adelaide, School of Agriculture, Food & Wine, 2020
Diniz, Mariana Filipa Simões. "Made in the Womb: Maternal Programming of Offspring Cardiovascular Function." Master's thesis, 2021. http://hdl.handle.net/10316/98058.
Повний текст джерелаO constante aumento da incidência de obesidade, especialmente em mulheres em idade fértil, tem sido um forte motivo de alarme. É estimado que 50% das grávidas têm excesso de peso ou são obesas. A obesidade materna predispõe o descendente para um risco acrescido de desenvolver inúmeras doenças crónicas, tais como obesidade, diabetes tipo 2 ou doença cardiovascular. A doença cardiovascular é, globalmente, a principal causa de morte para homens e mulheres. Não obstante, o risco de desenvolvimento de doença cardiovascular é diferente de acordo com o sexo. A obesidade e nutrição materna durante a gestação podem desencadear o desenvolvimento de doença cardiovascular na descendência, através de adaptações do sistema cardiovascular no útero. Isto pode levar à programação de mecanismos epigenéticos e de vias metabólicas, incluindo a função mitocondrial cardíaca. Atualmente, apesar de alternativas de suplementação serem indicadas nestes casos clínicos de modo a prevenir os efeitos deletérios da obesidade materna na função cardíaca dos descendentes, a falta de estratégias terapêuticas eficazes é notória. Este trabalho engloba uma estratégia inovadora propondo investigar de que forma é que o sistema cardiovascular de um descendente reage à prática materna de exercício físico durante uma gravidez obesogénica, a qual foi induzida através de uma dieta rica em açúcares e gorduras, em específico, como é que a prática de exercício físico materno durante uma gravidez obesogénica pode modular a função cardíaca dos descendentes. Ratos machos e fêmeas com 32 semanas de idade, descendentes de fêmeas rato da estirpe Sprague-Dawley, foram utilizados neste trabalho. Foi avaliado o efeito, a longo termo, da prática de exercício físico materno durante uma gravidez obesogénica na prevenção dos efeitos deletérios induzidos pela obesidade materna durante a gravidez na função cardíaca, em importantes vias metabólicas e na função mitocondrial de descendentes jovens-adultos. Apesar da evidente resposta dimórfica na fisiologia inata dos descendentes, a prática de exercício físico materno durante uma gravidez obesogénica induziu a modulação de parâmetros bioquímicos nos descendentes, traduzida em níveis alterados dos seguintes metabolitos no sangue: triglicerídeos, HDL e LDL, tendo esta resposta um evidente dimorfismo sexual. Estas alterações foram acompanhadas por uma remodelação metabólica do tecido cardíaco, que foi apreciada pelos níveis de proteínas-chave na via de sinalização da insulina, assim como por alteração nos níveis do transportador de ácidos gordos de cadeia curta, o CD36. Isto pode indicar que o transporte de ácidos gordos para o cardiomiócito encontrasse comprometido e, em conjunto com alterados níveis de metabolitos de lípidos, pode modular a função cardíaca mitocondrial de descendentes de mães obesas e exercitadas. De facto, a função cardíaca mitocondrial destes descendentes foi melhorada pela prática de exercício físico durante uma gestação obesogénica, com uma modulação positiva da bioenergética mitocondrial, em conjunto com uma possível modulação da dinâmica mitocondrial, através da observação de níveis alterados de proteínas envolvidas em eventos de fusão (MFN-1 e OPA1) e biogénese (PGC1α e TFAM) mitocondrial. Para além disso, resultados preliminares indicaram que o exercício materno praticado durante uma gravidez obesogénica pode prevenir o stress nitrosativo no tecido cardíaco. Concluindo, a prática de exercício físico durante uma gravidez obesogénica levou a uma modulação dos parâmetros bioquímicos, cardiometabólicos e da função mitocondrial cardíaca dos descendentes em idade jovem, com uma resposta específica de acordo com o sexo do descendente. Estas alterações podem ser benéficas o suficiente para melhorar a saúde cardiovascular dos descendentes, o que poderá levar à atenuação ou até mesmo à prevenção do desenvolvimento de doença cardiovascular numa fase mais tardia da vida.
Obesity incidence has been increasing at an alarming rate, especially in women of reproductive age. It is estimated that 50% of the total number of pregnancies occur in overweight or obese women. Maternal obesity (MO) predisposes the offspring to an increased risk of developing many chronic diseases in an early stage of life, including obesity, type 2 diabetes, and cardiovascular disease (CVD). CVD is the main cause of death worldwide among men and women. Despite this, CVD risk exhibits sexual dimorphism. Maternal diet and MO during gestation could prompt the offspring for CVD development through adaptations of the offspring’s cardiovascular system in the womb. This could lead to cardiac epigenetic and persistent metabolic programming of signalling pathways, including mitochondrial metabolic function, culminating in offspring’s increased predisposition to CVD development. Currently, despite diet supplementation alternatives being provided, effective therapeutical solutions to prevent the deleterious cardiac offspring function programming by obesogenic womb are lacking. This innovative work involves a novel approach to unravel how the offspring’s cardiovascular system reacts to maternal physical exercise practice during an obesogenic pregnancy, which was induced with a high fat/high sugar (HFHS) diet, and whether exercising during an obesogenic pregnancy (MOEx) can modulate the offspring cardiac function programming. Thirty-two-week-old offspring Sprague-Dawley rats exposed to MO and MOEx were used. The long-term therapeutic effect of maternal physical exercise during pregnancy in reversing the MO-induced effects on the cardiac function of young-adult offspring was evaluated by measuring hallmarks of cardiac metabolic impairment and mitochondrial dysfunction. Although the innate sex-specific response in the offspring’s cardiovascular physiology, MOEx induced biochemical modulation in the offspring, as indicated by the altered circulating levels of relevant molecules such as triglycerides, high-density lipoprotein (HDL), and low-density lipoprotein (LDL), despite the evident sexual dimorphism. These alterations were accompanied by cardiac metabolic remodelling, which was evaluated by measuring key-proteins involved in the insulin signalling pathway, along with alterations in the short-chain fatty acid transporter, CD36. This could indicate that MOEx affected cardiomyocyte fatty-acid uptake, and, along with the observed altered lipid metabolites levels, the MOEx offspring’s cardiac mitochondrial function could be modulated. Indeed, the offspring’s cardiac mitochondrial function seemed to be improved by MOEx comparing to MO, exhibiting a positive modulation of mitochondrial bioenergetics, along with possible mitochondrial dynamics modulation, which was observed through altered mitochondrial fusion- (MFN-1 and OPA1) and mitochondrial biogenesis-related proteins (PGC1α and TFAM). In addition, preliminary data indicated that MOEx prevents MO-induced nitrosative stress. Overall, maternal physical exercise practice during an obesogenic pregnancy leads to the modulation of the offspring’s biochemical, cardiac metabolic parameters and cardiac mitochondrial function, in a sex-specific way. These alterations may be favorable enough for the MO offspring’s cardiovascular health, which might result in the attenuation or even prevention of the development of CVD in MOEx offspring early life.
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Jain, Ravi 1967. "Intelligent techniques for the diagnosis of coronary artery disease / Ravi Jain." 1998. http://hdl.handle.net/2440/19356.
Повний текст джерелаxii, 189 leaves : ill. ; 30 cm.
Title page, contents and abstract only. The complete thesis in print form is available from the University Library.
This thesis proposes a genetic-programming-based classifier system for the diagnosis of coronary artery disease. Based on genetic programming, a software system called Evolutionary Pre-Processor has been developed as a new method for the automatic extraction of non-linear features for supervised classification. Two different hybrid intelligent system techniques are presented; fuzzy systems integrated with genetic algorithms and genetic algorithms combined with back-propagation algorithms. All approaches were tested on a real-world problem of coronary artery disease data.
Thesis (Ph.D.)--University of Adelaide, Dept. of Applied Mathematics, 1998
Jain, Ravi 1967. "Intelligent techniques for the diagnosis of coronary artery disease / Ravi Jain." Thesis, 1998. http://hdl.handle.net/2440/19356.
Повний текст джерелаxii, 189 leaves : ill. ; 30 cm.
This thesis proposes a genetic-programming-based classifier system for the diagnosis of coronary artery disease. Based on genetic programming, a software system called Evolutionary Pre-Processor has been developed as a new method for the automatic extraction of non-linear features for supervised classification. Two different hybrid intelligent system techniques are presented; fuzzy systems integrated with genetic algorithms and genetic algorithms combined with back-propagation algorithms. All approaches were tested on a real-world problem of coronary artery disease data.
Thesis (Ph.D.)--University of Adelaide, Dept. of Applied Mathematics, 1998
Smith, Valerie. "Locating gender within HIV/AIDS education in Tanzania : stepping stones to gender equity in HIV/AIDS programming \." 2005. http://link.library.utoronto.ca/eir/EIRdetail.cfm?Resources__ID=370497&T=F.
Повний текст джерела