Relevant bibliographies by topics / Epigenetic Modulations

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  2. Dissertations / Theses
  3. Books
  4. Book chapters
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Academic literature on the topic 'Epigenetic Modulations'

Author: Grafiati
Published: 12 April 2025

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Journal articles on the topic "Epigenetic Modulations"

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Kaur, Jasmine, Abdelkader Daoud, and Scott T. Eblen. "Targeting Chromatin Remodeling for Cancer Therapy." Current Molecular Pharmacology 12, no. 3 (July 29, 2019): 215–29. http://dx.doi.org/10.2174/1874467212666190215112915.

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Background: Epigenetic alterations comprise key regulatory events that dynamically alter gene expression and their deregulation is commonly linked to the pathogenesis of various diseases, including cancer. Unlike DNA mutations, epigenetic alterations involve modifications to proteins and nucleic acids that regulate chromatin structure without affecting the underlying DNA sequence, altering the accessibility of the transcriptional machinery to the DNA, thus modulating gene expression. In cancer cells, this often involves the silencing of tumor suppressor genes or the increased expression of genes involved in oncogenesis. Advances in laboratory medicine have made it possible to map critical epigenetic events, including histone modifications and DNA methylation, on a genome-wide scale. Like the identification of genetic mutations, mapping of changes to the epigenetic landscape has increased our understanding of cancer progression. However, in contrast to irreversible genetic mutations, epigenetic modifications are flexible and dynamic, thereby making them promising therapeutic targets. Ongoing studies are evaluating the use of epigenetic drugs in chemotherapy sensitization and immune system modulation. With the preclinical success of drugs that modify epigenetics, along with the FDA approval of epigenetic drugs including the DNA methyltransferase 1 (DNMT1) inhibitor 5-azacitidine and the histone deacetylase (HDAC) inhibitor vorinostat, there has been a rise in the number of drugs that target epigenetic modulators over recent years. Conclusion: We provide an overview of epigenetic modulations, particularly those involved in cancer, and discuss the recent advances in drug development that target these chromatin-modifying events, primarily focusing on novel strategies to regulate the epigenome.
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Wrede, Dylan, Mika Bordak, Yeabtsega Abraham, and Masfique Mehedi. "Pulmonary Pathogen-Induced Epigenetic Modifications." Epigenomes 7, no. 3 (July 6, 2023): 13. http://dx.doi.org/10.3390/epigenomes7030013.

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Epigenetics generally involves genetic control by factors other than our own DNA sequence. Recent research has focused on delineating the mechanisms of two major epigenetic phenomena: DNA methylation and histone modification. As epigenetics involves many cellular processes, it is no surprise that it can also influence disease-associated gene expression. A direct link between respiratory infections, host cell epigenetic regulations, and chronic lung diseases is still unknown. Recent studies have revealed bacterium- or virus-induced epigenetic changes in the host cells. In this review, we focused on respiratory pathogens (viruses, bacteria, and fungi) induced epigenetic modulations (DNA methylation and histone modification) that may contribute to lung disease pathophysiology by promoting host defense or allowing pathogen persistence.
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Arif, K. M. Taufiqul, Esther K. Elliott, Larisa M. Haupt, and Lyn R. Griffiths. "Regulatory Mechanisms of Epigenetic miRNA Relationships in Human Cancer and Potential as Therapeutic Targets." Cancers 12, no. 10 (October 11, 2020): 2922. http://dx.doi.org/10.3390/cancers12102922.

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Initiation and progression of cancer are under both genetic and epigenetic regulation. Epigenetic modifications including alterations in DNA methylation, RNA and histone modifications can lead to microRNA (miRNA) gene dysregulation and malignant cellular transformation and are hereditary and reversible. miRNAs are small non-coding RNAs which regulate the expression of specific target genes through degradation or inhibition of translation of the target mRNA. miRNAs can target epigenetic modifier enzymes involved in epigenetic modulation, establishing a trilateral regulatory “epi–miR–epi” feedback circuit. The intricate association between miRNAs and the epigenetic architecture is an important feature through which to monitor gene expression profiles in cancer. This review summarises the involvement of epigenetically regulated miRNAs and miRNA-mediated epigenetic modulations in various cancers. In addition, the application of bioinformatics tools to study these networks and the use of therapeutic miRNAs for the treatment of cancer are also reviewed. A comprehensive interpretation of these mechanisms and the interwoven bond between miRNAs and epigenetics is crucial for understanding how the human epigenome is maintained, how aberrant miRNA expression can contribute to tumorigenesis and how knowledge of these factors can be translated into diagnostic and therapeutic tool development.
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Wikumpriya, Gunasekara Chathura, Madhuranga Walawedurage Srinith Prabhatha, Jiye Lee, and Chan-Hee Kim. "Epigenetic Modulations for Prevention of Infectious Diseases in Shrimp Aquaculture." Genes 14, no. 9 (August 25, 2023): 1682. http://dx.doi.org/10.3390/genes14091682.

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Aquaculture assumes a pivotal role in meeting the escalating global food demand, and shrimp farming, in particular, holds a significant role in the global economy and food security, providing a rich source of nutrients for human consumption. Nonetheless, the industry faces formidable challenges, primarily attributed to disease outbreaks and the diminishing efficacy of conventional disease management approaches, such as antibiotic usage. Consequently, there is an urgent imperative to explore alternative strategies to ensure the sustainability of the industry. In this context, the field of epigenetics emerges as a promising avenue for combating infectious diseases in shrimp aquaculture. Epigenetic modulations entail chemical alterations in DNA and proteins, orchestrating gene expression patterns without modifying the underlying DNA sequence through DNA methylation, histone modifications, and non-coding RNA molecules. Utilizing epigenetic mechanisms presents an opportunity to enhance immune gene expression and bolster disease resistance in shrimp, thereby contributing to disease management strategies and optimizing shrimp health and productivity. Additionally, the concept of epigenetic inheritability in marine animals holds immense potential for the future of the shrimp farming industry. To this end, this comprehensive review thoroughly explores the dynamics of epigenetic modulations in shrimp aquaculture, with a particular emphasis on its pivotal role in disease management. It conveys the significance of harnessing advantageous epigenetic changes to ensure the long-term viability of shrimp farming while deliberating on the potential consequences of these interventions. Overall, this appraisal highlights the promising trajectory of epigenetic applications, propelling the field toward strengthening sustainability in shrimp aquaculture.
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Hmood, Qammar Shaker. "Harnessing CRISPR-Cas for Targeted Epigenetic Manipulations: a physiological study of Gene Regulation." European Journal of Medical Genetics and Clinical Biology 1, no. 5 (May 10, 2024): 115–29. http://dx.doi.org/10.61796/jmgcb.v1i5.453.

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Genome engineering, epigenome editing, as one of the prominent research techniques, has also become instrumental in discovering the gene expression regulation mechanisms and exploring their physiological correlates in health and pathology. This review summarizes the state-of-the-art CRISPR-Cas strategies that focus on epigenetics modification and projects its utility in molecular physiology of gene regulation. In this course we will delve into how CRISPR-Cas systems interact with epigenetic signals through DNA methylation, histone modifications and accessibility to chromatin. Then we look at the physiological effects of epigenetic modulations in cellular differentiation and development, cellular signal and homeostasis, disease pathogenesis, and therapeutic for application. Issues and perspectives on how epigenome manipulations can revolutionize therapeutics are also emphasized exploring the potential of precision medicine and individualized therapies. Overall, the review stresses the pivotal role of epigenetic modulation in the development of our understanding of gene expressions/mediation and cellular physiology. It also provides some inputs on the potential directions that the field of genetic engineering might take in the future.
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Wong, Belinda Shu Ee, Qidong Hu, and Gyeong Hun Baeg. "Epigenetic modulations in nanoparticle-mediated toxicity." Food and Chemical Toxicology 109 (November 2017): 746–52. http://dx.doi.org/10.1016/j.fct.2017.07.006.

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Stanzione, Rosita, Maria Cotugno, Franca Bianchi, Simona Marchitti, Maurizio Forte, Massimo Volpe, and Speranza Rubattu. "Pathogenesis of Ischemic Stroke: Role of Epigenetic Mechanisms." Genes 11, no. 1 (January 13, 2020): 89. http://dx.doi.org/10.3390/genes11010089.

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Epigenetics is the branch of molecular biology that studies modifications able to change gene expression without altering the DNA sequence. Epigenetic modulations include DNA methylation, histone modifications, and noncoding RNAs. These gene modifications are heritable and modifiable and can be triggered by lifestyle and nutritional factors. In recent years, epigenetic changes have been associated with the pathogenesis of several diseases such as diabetes, obesity, renal pathology, and different types of cancer. They have also been related with the pathogenesis of cardiovascular diseases including ischemic stroke. Importantly, since epigenetic modifications are reversible processes they could assist with the development of new therapeutic approaches for the treatment of human diseases. In the present review article, we aim to collect the most recent evidence concerning the impact of epigenetic modifications on the pathogenesis of ischemic stroke in both animal models and humans.
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Salinas, Irving, Niharika Sinha, and Aritro Sen. "Androgen-induced epigenetic modulations in the ovary." Journal of Endocrinology 249, no. 3 (June 2021): R53—R64. http://dx.doi.org/10.1530/joe-20-0578.

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In recent years, androgens have emerged as critical regulators of female reproduction and women’s health in general. While high levels of androgens in women are associated with polycystic ovary syndrome (PCOS), recent evidence suggests that a certain amount of direct androgen action through androgen receptor is also essential for normal ovarian function. Moreover, prenatal androgen exposure has been reported to cause developmental reprogramming of the fetus that manifests into adult pathologies, supporting the Developmental Origins of Health and Disease (DOHaD) hypothesis. Therefore, it has become imperative to understand the underlying mechanism of androgen actions and its downstream effects under normal and pathophysiological conditions. Over the years, there has been a lot of studies on androgen receptor function as a transcriptional regulator in the nucleus as well as androgen-induced rapid extra-nuclear signaling. Conversely, new evidence suggests that androgen actions may also be mediated through epigenetic modulation involving both the nuclear and extra-nuclear androgen signaling. This review focuses on androgen-induced epigenetic modifications in female reproduction, specifically in the ovary, and discusses emerging concepts, latest perceptions, and highlight the areas that need further investigation.
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Hoffman, Jessie B., Michael C. Petriello, and Bernhard Hennig. "Impact of nutrition on pollutant toxicity: an update with new insights into epigenetic regulation." Reviews on Environmental Health 32, no. 1-2 (March 1, 2017): 65–72. http://dx.doi.org/10.1515/reveh-2016-0041.

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Abstract Exposure to environmental pollutants is a global health problem and is associated with the development of many chronic diseases, including cardiovascular disease, diabetes and metabolic syndrome. There is a growing body of evidence that nutrition can both positively and negatively modulate the toxic effects of pollutant exposure. Diets high in proinflammatory fats, such as linoleic acid, can exacerbate pollutant toxicity, whereas diets rich in bioactive and anti-inflammatory food components, including omega-3 fatty acids and polyphenols, can attenuate toxicant-associated inflammation. Previously, researchers have elucidated direct mechanisms of nutritional modulation, including alteration of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling, but recently, increased focus has been given to the ways in which nutrition and pollutants affect epigenetics. Nutrition has been demonstrated to modulate epigenetic markers that have been linked either to increased disease risks or to protection against diseases. Overnutrition (i.e. obesity) and undernutrition (i.e. famine) have been observed to alter prenatal epigenetic tags that may increase the risk of offspring developing disease later in life. Conversely, bioactive food components, including curcumin, have been shown to alter epigenetic markers that suppress the activation of NF-κB, thus reducing inflammatory responses. Exposure to pollutants also alters epigenetic markers and may contribute to inflammation and disease. It has been demonstrated that pollutants, via epigenetic modulations, can increase the activation of NF-κB and upregulate microRNAs associated with inflammation, cardiac injury and oxidative damage. Importantly, recent evidence suggests that nutritional components, including epigallocatechin gallate (EGCG), can protect against pollutant-induced inflammation through epigenetic regulation of proinflammatory target genes of NF-κB. Further research is needed to better understand how nutrition can modulate pollutant toxicity through epigenetic regulation. Therefore, the objective of this review is to elucidate the current evidence linking epigenetic changes to pollutant-induced diseases and how this regulation may be modulated by nutrients allowing for the development of future personalized lifestyle interventions.
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Pan, Desi, and Xianping Lu. "New therapeutic avenue of epigenetic modulations in cancer." Translational Breast Cancer Research 1 (April 2020): 2. http://dx.doi.org/10.21037/tbcr.2020.03.03.

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Dissertations / Theses on the topic "Epigenetic Modulations"

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Kerbaj, Coline. "Investigating the role of OGT and c-Myc in modulating EZH2 functions in hepatocellular carcinoma." Electronic Thesis or Diss., Lyon 1, 2024. http://www.theses.fr/2024LYO10358.

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Le carcinome hépatocellulaire (CHC) est le plus fréquent des cancers du foie et une importante cause de mortalité. Les modifications épigénétiques jouent un rôle essentiel dans ce cancer et sont des cibles thérapeutiques intéressantes. Au cours de ma thèse, je me suis intéressée à l‘histone méthyltransférase (HMT) EZH2, qui augmente dans le CHC et est liée à la résistance au traitement. En tant que sous-unité catalytique du complexe PRC2, EZH2 est responsable de la marque H3K27me3 et la répression de gènes (rôle canonique). Dans le cancer, EZH2 a d’autres fonctions indépendantes de PRC2 et peut contribuer à l’expression de gènes (rôle non canonique). Les inhibiteurs enzymatiques d’EZH2 ne sont pas efficaces sur les tumeurs solides, suggérant que l’activité non catalytique d’EZH2 joue un rôle dans ces cancers. EZH2 est régulé par des modifications post-traductionnelles, telle la O-GlcNAcylation par l’O-GlcNAc transférase (OGT) qui augmente dans le CHC. Nous avons montré que dans le CHC la fraction d’EZH2 associée à OGT est surtout impliquée dans l’expression de gènes. Notre but était de caractériser les mécanismes sous-tendant l’activation de gènes par EZH2/OGT et de déterminer le rôle du complexe PRC2 et c-Myc, qui peut être modulé par OGT et joue un rôle important dans le CHC, dans ces processus. Nous avons montré que EZH2 et c-Myc sont O-GlcNAcylés dans les cellules hépatocytaires et que l’O-GlcNAcylation de EZH2 est importante pour son recrutement aux gènes cibles. Nos données indiquent que c-Myc joue un rôle important dans la régulation de gènes par EZH2/OGT. De manière intéressante, nos résultats suggèrent qu’une partie des fonctions non canoniques d’EZH2 dans les cellules hépatocytaires humaines pourrait être dépendante du complexe PRC2. L’ensemble de nos résultats indiquent qu’OGT et c-Myc contribuent aux fonctions non canoniques d’EZH2 dans des cellules hépatocytaires humaines et apportent de nouvelles connaissances quant au potentiel des régulations épigénétiques comme cible thérapeutique dans le CHC. Une meilleure connaissance des mécanismes moléculaires sous-tendant les dérégulations de gènes dans le CHC ouvrira des perspectives pour de nouvelles stratégies thérapeutiques
Hepatocellular carcinoma (HCC), the most common form of liver cancer and leading cause of death, is a heterogeneous disease with no unique driver mutation. Up to 50% of HCCs harbor alterations in epigenetic machineries that represent promising therapeutic targets. During my PhD, I focused on the histone methyltransferase (HMT) EZH2 that is upregulated in HCC and related to therapy resistance. EZH2 is the catalytic subunit of the PRC2 complex responsible for H3K27me3, a repressive epigenetic mark (canonical function). In cancer, EZH2/PRC2 represses the expression of tumor suppressor genes but EZH2 can also activate oncogenes and cell cycle genes in a mostly PRC2-independent manner (non-canonical function). EZH2 HMT inhibitors have demonstrated low efficacy in solid tumors suggesting that HMT independent functions of EZH2 are key in these cancers. EZH2 can be regulated by post-translational modifications, including O-GlcNAcylation by O-GlcNAc transferase (OGT) whose expression is increased in HCC. Our data show that EZH2 and OGT are co-recruited to defined gene promoters in HCC and predominantly promote gene expression. To decipher the molecular mechanisms underlying EZH2/OGT-mediated gene activation in HCC, we assessed the roles of PRC2 and c-Myc that plays an important role in HCC and can be modulated by OGT. We showed that EZH2 and c-Myc are O-GlcNAcylated by OGT in human hepatoma cells and that EZH2 O-GlcNAcylation plays a role in EZH2 target promoter recruitment. Our data also indicate that c-Myc plays an important role in EZH2/OGT-mediated gene regulation. Interestingly, our results suggest that part of the non-canonical functions of EZH2 in human hepatoma cells may be PRC2 dependent. Collectively, our data uncover that OGT and c-Myc promote non-canonical functions of EZH2 in transformed liver cells and provide important insights for epigenetic strategies as potential future anti-HCC therapies. A better understanding of the regulatory networks controlling gene expression in HCC will open perspectives for the design of novel therapeutic strategies for HCC
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Lones, John. "Hormonal modulation of developmental plasticity in an epigenetic robot." Thesis, University of Hertfordshire, 2017. http://hdl.handle.net/2299/17859.

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In autonomous robotics, there is still a trend to develop and tune controllers with highly explicit goals and environments in mind. However, this tuning means that these robotic models often lack the developmental and behavioral flexibility seen in biological organisms. The lack of flexibility in these controllers leaves the robot vulnerable to changes in environmental condition. Whereby any environmental change may lead to the behaviors of the robots becoming unsuitable or even dangerous. In this manuscript we look at a potential biologically plausible mechanism which may be used in robotic controllers in order to allow them to adapt to different environments. This mechanism consists of a hormone driven epigenetic mechanism which regulates a robot's internal environment in relation to its current environmental conditions. As we will show in our early chapters, this epigenetic mechanism allows an autonomous robot to rapidly adapt to a range of different environmental conditions. This adaption is achieved without the need for any explicit knowledge of the environment. Allowing a single architecture to adapt to a range of challenges and develop unique behaviors. In later chapters however, we find that this mechanism not only allows for regulation of short term behavior, but also long development. Here we show how this system permits a robot to develop in a way that is suitable for its current environment. Further during this developmental process we notice similarities to infant development, along with acquisition of unplanned skills and abilities. The unplanned developments appears to leads to the emergence of unplanned potential cognitive abilities such as object permanence, which we assess using a range of different real world tests.
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Phipps, Sharla Marion Ostein. "Genetic and epigenetic modulation of telomerase activity in development and disease." Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2008r/phipps.pdf.

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Thesis (Ph. D.)--University of Alabama at Birmingham, 2007.
Additional advisors: Vithal K. Ghanta, J. Michael Ruppert, Theresa V. Strong, R. Douglas Watson. Description based on contents viewed Oct. 3, 2008; title from PDF t.p. Includes bibliographical references.
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Wright, Stephanie D. "Epigenetic modulation of the UL97 gene product in CMV-associated central nervous system tumors." Connect to resource, 2005. http://hdl.handle.net/1811/438.

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Thesis (Honors)--Ohio State University, 2005.
Title from first page of PDF file. Document formattted into pages: contains 51 p.; also includes graphics. Includes bibliographical references (p. 29-33). Available online via Ohio State University's Knowledge Bank.
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Azoulay, Nelson. "Epigenetic modulation of glucocorticoid receptors in posttraumatic stress disorder: examining child vs. adult trauma." Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=104876.

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PTSD is a devastating disorder that affects 7-12% of individuals who experience a traumatic event in their lives. Individuals suffering from the disorder show a dysfunctional HPA axis with decreased basal cortisol release and increased glucocorticoid receptor sensitivity. Recently, epigenetic studies have shown associations between trauma and the subsequent effects on the HPA axis in abused participants who committed suicide. Importantly, findings also showed child trauma as being a significant factor in DNA methylation levels in promoter region 1F in the hippocampus. This thesis shows the possible role of epigenetic programming of glucocorticoid receptors in PTSD while examining the effects of different timing of trauma. Methods included the measurements of salivary basal cortisol levels, the expression of glucocorticoid receptors in whole blood and the DNA methylation levels in two promoter regions of the glucocorticoid receptors by sequenome epityper. Results showed that individuals suffering from PTSD have decreased salivary cortisol release in the morning, increased glucocorticoid receptors and increased total methylation levels in promoter region 1C in whole blood. Additionally, adulthood trauma seemed to be of greater importance with regards to HPA axis activity while childhood trauma showed to be more significant with regards to epigenetics. These results indicate that 1) individuals suffering from a lifetime PTSD have a dampened HPA axis activity, 2) epigenetics play a different role in PTSD compared to abused individuals who have committed suicide and 3) timing of trauma has a significant effect on both the HPA axis activity and the epigenetic modifications.
Le TSPT est un syndrome dévastateur qui touche entre 7 et 12% de gens qui vivent un événement traumatique. Les personnes qui souffrent du syndrome ont un axe HPA dysfonctionnel avec moins de cortisol salivaire et une augmentation de sensitivité des récepteurs glucocorticoïdes. Il y a récemment eu des études épigénétiques qui ont montré une association entre les traumas et les effets sur l'axe HPA chez des patients abusés qui ont commis un suicide. De plus, les résultats indiquent qu'un trauma durant l'enfance est un facteur significatif pour la méthylation d'ADN dans la région promoteur 1F de l'hippocampe. Cette thèse présente le possible rôle modulateur de l'épigénétique des récepteurs glucocorticoïdes chez les personnes touchées du TSPT tout en examinant les effets du temps du trauma. Les résultats montrent que les individus qui souffrent du TSPT ont moins de cortisol salivaire le matin, une augmentation des récepteurs glucocorticoïdes et une augmentation de niveaux de méthylation totale dans la région promoteur 1C du sang. Il semblerait aussi qu'un trauma vécu durant l'âge adulte soit plus significatif pour l'axe HPA, alors qu'un trauma durant l'enfance semblerait prendre le dessus pour les modifications épigénétiques. Ces résultats montrent que 1) les personnes souffrant du TSPT ont une activité HPA atténuée, 2) l'épigénétique joue un rôle différent chez les TSPT comparés aux patients abusés qui ont commis un suicide et 3) le temps du trauma a des effets significatifs pour l'axe HPA et les modifications épigénétiques.
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Krzystyniak, Joanna. "Epigenetic modulation of intestinal homeostasis and tumorigenesis by Brm SWI/SNF chromatin remodelling factor." Thesis, Cardiff University, 2014. http://orca.cf.ac.uk/73083/.

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SWI/SNF chromatin remodelling complexes are one of the well-characterized cellular machineries capable of regulation of gene expression. Numerous lines of evidence indicate that SWI/SNF complexes are involved in a wide range of cellular processes and the maintenance of homeostasis whereas aberrant expression of those proteins contributes towards cancer development. Colorectal cancer remains one of the most clinically significant cancers due to its high incidence in developed countries and previous studies have demonstrated that SWI/SNF complexes are aberrantly regulated in a significant proportion of patients with this disease. However, whilst the sequence of molecular events leading to CRC has been well-established, the role of SWI/SNF chromatin remodelling complex ATPase subunits Brm and its paralogue Brg1 in the colorectal tumorigenesis remains elusive. The chromatin remodelling catalytic subunit Brm has been found to interact with the Notch pathway effectors ICD-22 and CBF-1 and also to be necessary for expression of the Wnt target gene CD44 and for Rb-mediated cell cycle arrest. In this PhD thesis, the potential of Brm to modulate Wnt-driven intestinal tumorigenesis was addressed. Initially, a murine model carrying constitutively deleted Brm was used to assess the consequences of this loss on homeostasis of the small intestinal and colonic epithelia. The effects of Brm deficiency were also examined in the context of Wnt-activated epithelium via conditional loss of Apc. Additionally, the effect of concomitant loss of Brm and Brg1 was addressed in the contexts of both normal homeostasis and aberrant Wnt signalling. The results presented here demonstrate that Brm plays an important role in the small intestine by regulating the distribution of proliferating cells and cell fate decisions mediated through Notch pathway effectors. Furthermore, Brm deficiency was found to modulate intestinal phenotype of Wnt activation through the attenuation of the Wnt transcriptional programme and the suppressed expression of the intestinal stem cell marker Olfm4. Thus while Brg1 has been widely characterized as a bone fide tumour suppressor, the function of Brm continues to remain elusive especially in the light of contrasting effects co-mediated by Brm on proliferation, differentiation and gene expression. Taken together, these results elucidate the tissue-specific role of Brm, the catalytic subunit of SWI/SNF chromatin remodelling complex, on both normal intestinal homeostasis and acute activation of Wnt pathway while the extent of these Brm-dependent effects depend upon the gradient of Wnt signalling throughout the epithelium of small and large intestine.
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Zha, Lisha [Verfasser], and Susanne [Akademischer Betreuer] Engelmann. "Epigenetic modulation of Doxcycline controlled transgene expression in cells and mice / Lisha Zha ; Betreuer: Susanne Engelmann." Braunschweig : Technische Universität Braunschweig, 2015. http://d-nb.info/1175819328/34.

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Pikulkaew, Surachai. "ROLE OF LIPOSOLUBLE HORMONES AND MATERNAL mRNAs IN THE EPIGENETIC LONG-TERM MODULATION OF ZEBRAFISH DEVELOPMENT." Doctoral thesis, Università degli studi di Padova, 2010. http://hdl.handle.net/11577/3422368.

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PART I: Expression analysis of maternal and zygotic steroid hormone receptor mRNAs during zebrafish (Danio rerio) embryogenesis. I have analyzed by qRT-PCR and/or RT-PCR the abundance and degradation rates of maternal mRNAs for nine steroid hormone receptors and their possible replacement by corresponding embryonic transcripts in both ovulated oocytes and embryos of zebrafish collected at 0, 1, 2, 4, 8, 12, 24 and 48 h post-fertilization (hpf). The mRNAs encoded the nuclear receptors for progesterone (Pr), androgen (Ar), estrogen (Erα, Erβ1 and Erβ2), glucocorticoids (Gr), mineralocorticoids (Mr) and the membrane progestin receptor-α and β (mPrα and β). Gr mRNA was the most abundant maternal transcript in oocytes and early embryos, followed by erβ2 and ar mRNAs. They declined during the first 8 hpf, being replaced, thereafter, by the embryonic messengers. Erβ1 and mr transcript levels were low until 8 hpf, but increased steadily during embryonic transcription from 24 to 48 hpf. Pr transcripts were detectable only in ovulated oocytes and at 24 and 48 hpf. At these stages, there was a slight increase of erα mRNA that initially was very low. Mprα and β mRNAs were expressed in ovulated oocytes and faintly persisted during the first 4 hpf. There was no subsequent embryonic expression of these transcripts. The possible involvement of maternal mRNAs for glucocorticoid and sex hormone receptors in the programming of early zebrafish development is intriguing, since they mainly occur at stages in which gene replication predominates over transcription. PART II: Morpholino knockdown of glucocorticoid receptor in zebrafish during embryogenesis The glucocorticoid receptor (Gr) is involved in various physiological processes, including growth, osmoregulation and reproduction in various species of vertebrates. In this study, I have investigated the function of Gr during zebrafish embryogenesis using antisense Morpholino (MO) technology approach in order to block gr mRNA translation. I observed that Gr-morphants were characterized by small head and eyes, short body, pericardial edema, disrupted melanophore patterning, failure to inflate the swim bladder, tail curling, and abnormal swimming behaviour. The effectiveness of Gr knockdown was further verified by Western blotting and in vitro transcription and translation system, which showed marked reduction of the Gr protein in morphant embryos. Microarray analysis revealed that Gr functions prevalently as a negative regulator of gene transcription. Three genes found to be up-regulated following MO knockdown by microarray analysis, including caspase-8, igf2α and centaurin-1α, were evaluated by semiquantitative RT-PCR throughout the embryonic development. Furthermore, whole mount in situ hybridizations indicated that, whereas marker expression pattern was mostly unchanged in morphant embryos, three markers involved in neurogenesis, egr2b, emx1 and six3.1, were up-regulated. In conclusion, the knockdown of Gr in zebrafish revealed a requirement of both maternal and zygotic gr in multiple developmental processes involved in neurogenesis and gut and accessory organs formation. There are indications that the maternal receptor is critical in early embryogenesis, but more work is needed to elucidate the functional transition from the maternal to the zygotic gr and whether they affect distinctive components of the genetic machinery.
PARTE I: Analisi dell’espressione degli mRNA materni e zigotici per recettori di ormoni steroidei durante lo sviluppo nel pesce zebrato (Danio rerio). Ho analizzato mediante qRT-PCR e/o RT-PCR la presenza ed il grado di degradazione degli mRNA materni codificanti per nove recettori di ormoni steroidei, e la loro possibile sostituzione da parte dei trascritti embrionali corrispondenti, sia negli ovociti ovulati che in embrioni di pesce zebrato raccolti a 0, 1, 2, 4, 8, 12, 24 e 48 ore dopo la fecondazione (hpf). Gli mRNA studiati sono quelli codificanti i recettori nucleari per il progesterone (Pr), gli androgeni (Ar), gli estrogeni (Erα, Erβ1 ed Erβ2), i glucocorticoidi (Gr), i mineralcorticoidi (Mr) ed i recettori di membrana α e β per i progestinici (mPrα e mPrβ). L’mRNA codificante la proteina Gr costituisce il trascritto materno maggiormente presente negli ovociti e nei primi stadi di sviluppo embrionale, seguito dagli mRNA codificanti i recettori Erβ2 ed Ar. Tutti questi trascritti diminuiscono durante le prime 8 ore di sviluppo, e vengono poi sostituiti dai rispettivi messaggeri embrionali. I livelli dei trascritti per erβ1 e mr sono bassi prima delle 8 hpf, ed aumentano costantemente, dopo l’inizio della trascrizione embrionale, passando dalle 24 alle 48 hpf. L’mRNA codificante il recettore Pr è stato rilevato soltanto negli ovociti ovulati e nei campioni corrispondenti a 24 e 48 hpf. A questi stadi di sviluppo c’è anche un leggero aumento dell’mRNA codificante la proteina Erα. I trascritti per i recettori mPrα e mPrβ sono presenti negli ovociti ovulati e persistono, a basse concentrazioni, fino alle 4 hpf. Non è stata evidenziata la presenza di trascritti embrionali codificanti per questi due geni. E’ interessante il possibile coinvolgimento degli mRNA codificanti Gr e i recettori degli ormoni sessuali nella programmazione dello sviluppo embrionale precoce del pesce zebrato, dal momento che sono presenti principalmente negli stadi di sviluppo in cui la replicazione genica predomina sulla trascrizione. PARTE II: Inattivazione genica del recettore dei glucocorticoidi di pesce zebrato mediante morfolino Il recettore dei glucocorticoidi (Gr) è coinvolto in numerosi processi fisiologici, tra cui la crescita, l’osmoregolazione e la riproduzione in molte specie di vertebrati. In questo studio, ho analizzato la funzione del Gr durante l’embriogenesi di pesce zebrato utilizzando la tecnologia degli oligonucleotidi antisenso morfolino per inibire la traduzione dell’mRNA codificante Gr. Ho osservato che i morfanti di Gr presentano occhi e testa di dimensioni ridotte, corpo corto, edema pericardico, riduzione della pigmentazione, mancata insufflazione della vescica natatoria, coda incurvata e comportamento natatorio anormale. L’efficacia dell’inattivazione genica del Gr sono stati verificati mediante Western blotting ed utilizzando un sistema di trascrizione e traduzione in vitro, che hanno dimostrato una riduzione della traduzione del Gr negli embrioni morfanti. Analisi di microarray hanno messo in evidenza che questa proteina funziona prevalentemente come repressore della trascrizione genica. I geni caspase-8, igf2α e centaurina-1α risultati sovraespressi mediante microarray dopo trattamento con morfolino, sono stati analizzati mediante RT-PCR semiquantitativa durante tutto il corso dello sviluppo embrionale. Inoltre, esperimenti di ibridazione in situ in toto indicano che, mentre in generale il modello di espressione dei marcatori utilizzati non cambia nei morfanti, tre marcatori coinvolti nel processo di neurogenesi, e cioè egr2b, emx1 e six3.1, sono risultati sovraespressi. In conclusione, i risultati ottenuti dall’inattivazione genica del gr di pesce zebrato rivelano la necessità dei trascritti di origine materna in molteplici processi di sviluppo, quali neurogenesi e formazione di intestino ed organi accessori. Si dovrà comunque analizzare più in dettaglio la transizione funzionale dai trascritti materni a quelli zigotici e stabilire se essi influenzino componenti distinti dei meccanismi a livello genomico.
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Górniak, Joanna Paulina. "Age-related epigenetic changes at base excision repair genes and their modulation by dietary restriction in mice." Thesis, University of Newcastle upon Tyne, 2015. http://hdl.handle.net/10443/2932.

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Accumulation of damage in DNA is a characteristic feature of ageing which may result from a decline in DNA repair efficiency. Base excision repair (BER) is the primary mechanism used to repair small-scale DNA damage such as that caused by oxidation. I hypothesised that epigenetic events contribute to the ageing process through deregulation of BER gene expression and that these adverse effects of ageing may be modulated by dietary restriction (DR). To test these hypotheses, I quantified DNA methylation and histone post-translational modifications at BER-gene (Ogg1 and Apex) promoters, together with expression of these genes, in tissues from ageing mice and from mice exposed to DR. Phenotypic changes in DNA incision activity and oxidative damage were also quantified. Cytosine methylation was measured by pyrosequencing at the Ogg1 promoter in brain and livers from ad libitum (AL) and 40% DR mice at 3, 12, 24 and 30 months of age (n=5/group). Ogg1 promoter methylation decreased with age in the liver (p=0.018) and brain (p=0.016) and DR significantly reduced Ogg1 promoter methylation (p=0.014) in the brain. Additionally, in the brain there was a 2 fold enrichment in histone 4 acetylation (H4Ac) and histone 3 lysine 27 tri-methylation (H3K27Me3) as measured by the ChIP assay at Ogg1 and Apex promoters in 30 month old AL animals compared with 3 month old animals (p<0.05). H4Ac was 2.5-fold higher in the Ogg1 promoter in liver in 30 month old DR versus 30 month old AL animals (p=0.004). Furthermore H4K27Me3 was significantly (p=0.023) lower at the liver Ogg1 promoter in 30 month old compared with 3 month old animals. Ogg1 gene expression decreased with age in the brain (n.s.) and liver (p=0.005). Perhaps surprisingly, Ogg1 and Apex expression levels were higher in the brain (p=0.034) but lower in the liver (p=0.003) of DR compared with AL animals. I used a comet-based in vitro assay to quantify BER-related incision activity but did not observe any significant changes in the liver or in whole brain in response to ageing or to DR. However DNA incision activity varied considerably between different brain regions and DR enhanced incision 2 fold in the cortex (p=0.031) and subcortical regions (p=0.019). 8-oxoguanine lesions measured by HPLC-ECD decreased with age (AL and DR) (p<0.001) in the liver but no effect of age was detected in the brain. ii This study revealed for the first time that tissue-specific epigenetic changes at BER genes occur during ageing and the data presented here suggest that epigenetic changes at BER-related gene promoters may affect BER activity in some tissues. Furthermore, I have shown that DR influences the epigenetic and transcription changes in BER-related genes observed during ageing.
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Heddleston, John Michael. "The Role of Hypoxia in Modulating Glioma Cell Tumorigenic Potential." Case Western Reserve University School of Graduate Studies / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=case1310043767.

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Books on the topic "Epigenetic Modulations"

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Jacob, Esther Margarete. Modulation des microRNA-Profils in Hepatomzellen und primären humanen Hepatozyten durch epigenetisch aktive Therapeutika. [S.l: s.n.], 2013.

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Odyssey of Humanity's Diseases Volume 1: Epigenetic and Ecogenetic Modulations from Ancestry Through Inheritance, Environment, Culture, and Behavior. Tellwell Talent, 2020.

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The Odyssey of Humanity's Diseases Volume 3: Epigenetic and Ecogenetic Modulations from Ancestry through Inheritance, Environment, Culture, and Behavior. Tellwell Talent, 2020.

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The Odyssey of Humanity's Diseases Volume 2: Epigenetic and Ecogenetic Modulations from Ancestry through Inheritance, Environment, Culture, and Behavior. Tellwell Talent, 2020.

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The Odyssey of Humanity's Diseases Volume 3: Epigenetic and Ecogenetic Modulations from Ancestry through Inheritance, Environment, Culture, and Behavior. Tellwell Talent, 2020.

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The Odyssey of Humanity's Diseases Volume 1: Epigenetic and Ecogenetic Modulations from Ancestry through Inheritance, Environment, Culture, and Behavior. Tellwell Talent, 2020.

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The Odyssey of Humanity's Diseases Volume 2: Epigenetic and Ecogenetic Modulations from Ancestry through Inheritance, Environment, Culture, and Behavior. Tellwell Talent, 2020.

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Issa, Jean-Pierre J. Epigenetic Modulation and Hematologic Malignancies (Contemporary Hematology). Humana Press, 2008.

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Genetic and Epigenetic Modulation of Cell Functions by Physical Exercise. MDPI, 2020. http://dx.doi.org/10.3390/books978-3-03928-481-8.

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Lusardi, Theresa A., and Detlev Boison. Ketogenic Diet, Adenosine, Epigenetics, and Antiepileptogenesis. Edited by Detlev Boison. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0023.

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Epilepsy is common, affecting about 1% of the population. Conventional treatments are ineffective in about one third of patients, and current therapies do not prevent epilepsy or its progression. For individuals with drug-refractory epilepsy the ketogenic diet (KD) can provide seizure relief in approximately fifty percent of patients, with complete and permanent remission in some cases, suggesting possible antiepileptogenic effects of the diet. Whereas mechanisms underlying antiseizure effects of KD have been identified, mechanistic links between KD therapy and antiepileptogenesis constitute a novel area of research. An adenosine receptor-mediated role of KD therapy in seizure suppression is well established, and recent evidence demonstrates that the KD regulates adenosine homeostasis in the brain. Adenosine in turn has previously unappreciated epigenetic functions as a regulator of DNA methylation. This chapter discusses recent evidence that KD influences the epigenome through modulation of adenosine metabolism as a plausible antiepileptogenic mechanism of the diet.
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Book chapters on the topic "Epigenetic Modulations"

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Zhao, Yuanji, and Sanchita Bhatnagar. "Epigenetic Modulations by Microbiome in Breast Cancer." In Advances in Experimental Medicine and Biology, 55–69. Cham: Springer Nature Switzerland, 2024. http://dx.doi.org/10.1007/978-3-031-66686-5_4.

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Kerbel, Robert S., Robert G. Liteplo, and Phil Frost. "Implications of Therapy-Induced Genetic/Epigenetic Modulations of Tumor Progression and Tumor Cell Heterogeneity for the Treatment of Cancer." In Cancer Biology and Therapeutics, 95–104. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4757-9564-6_6.

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Ross, Ivan A. "Epigenetic Modulation by Isothiocyanates." In Plant-Based Therapeutics, Volume 2, 315–41. Cham: Springer Nature Switzerland, 2024. http://dx.doi.org/10.1007/978-3-031-63681-3_7.

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Montanari, Micaela, Antonio Giordano, Marcella Cintorino, and Marcella Macaluso. "Epigenetic Modulation of Cell Cycle: An Overview." In Cancer Epigenetics, 1–14. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9781118005743.ch1.

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Mancino, Mario, Claudia Esposito, Raffaella Pasquale, Immacolata Vocca, and Francesca Pentimalli. "Epigenetic Modulation in Cell Development and Differentiation." In Cancer Epigenetics, 45–55. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9781118005743.ch4.

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Goto, Sataro, Kyojiro Kawakami, Hisashi Naito, Shizuo Katamoto, and Zsolt Radak. "Epigenetic Modulation of Gene Expression by Exercise." In Healthy Ageing and Longevity, 85–100. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-14830-4_5.

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Lippi, Giuseppe, Elisa Danese, and Fabian Sanchis-Gomar. "Stress, Exercise, and Epigenetic Modulation of Cancer." In Energy Balance and Cancer, 147–66. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-41610-6_6.

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Roy, Madhumita, and Amitava Datta. "Phytochemicals in ROS Mediated Epigenetic Modulation of Cancer." In Handbook of Oxidative Stress in Cancer: Mechanistic Aspects, 1–18. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-15-4501-6_108-1.

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Roy, Madhumita, and Amitava Datta. "Phytochemicals in ROS-Mediated Epigenetic Modulation of Cancer." In Handbook of Oxidative Stress in Cancer: Mechanistic Aspects, 1583–600. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-15-9411-3_108.

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Brand, Marjorie, and F. J. Dilworth. "Modulation of Developmentally Regulated Gene Expression Programs through Targeting of Polycomb and Trithorax Group Proteins." In Toxicology and Epigenetics, 511–38. Chichester, UK: John Wiley & Sons, Ltd, 2012. http://dx.doi.org/10.1002/9781118349045.ch26.

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Conference papers on the topic "Epigenetic Modulations"

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Cabello, Jade Carolina, Marcella Victoria Ras, Katelyn Thy Nhung Tran, and Athit Voytas. "An Investigation on the Intricacies of Epigenetic Modulations in the Pathogenesis of Human Papillomavirus-Associated Cervical Cancer: A Comprehensive Meta-Narrative Synthesis." In 2024 Research Methods Poster Session School of Health Professions. The University of Texas MD Anderson Cancer Center, 2024. http://dx.doi.org/10.52519/00121.

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Lones, John, and Lola Canamero. "Epigenetic adaptation through hormone modulation in autonomous robots." In 2013 IEEE International Conference on Development and Learning and Epigenetic Robotics (ICDL). IEEE, 2013. http://dx.doi.org/10.1109/devlrn.2013.6652561.

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Santos, Jephesson Alex Alex dos, Carolina Nunes Santo, and Luiza Cherobini Pereira. "Abstract 2445: Epigenetic modulation of tumor cell tolerance to chemotherapy." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-2445.

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Luo, N., VM Estrada, ME Sanders, and JM Balko. "Abstract P1-04-02: Improving immunotherapy response by epigenetic modulation." In Abstracts: 2016 San Antonio Breast Cancer Symposium; December 6-10, 2016; San Antonio, Texas. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.sabcs16-p1-04-02.

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Azad, Nilofer S. "Abstract I13: Modulating the immune response with epigenetic agents." In Abstracts: AACR Special Conference on Pancreatic Cancer: Advances in Science and Clinical Care; September 6-9, 2019; Boston, MA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.panca19-i13.

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Sun, Y., B. H. Y. Yeung-Luk, S. E. Wenzel, and W. W. Y. Tang. "Epigenetic Modulation of Airway Smooth Muscle Cell Function Via Glutamate Metabolism." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a2349.

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Jha, Akhilesh, Inmaculada Rioja, Rab Prinjha, and Clare Bryant. "Epigenetic modulation of TLR-driven inflammatory responses in airway epithelial cells." In ERS Lung Science Conference 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/23120541.lsc-2022.30.

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Lones, John, Matthew Lewis, and Lola Canamero. "Hormonal modulation of interaction between autonomous agents." In 2014 Joint IEEE International Conferences on Development and Learning and Epigenetic Robotics (ICDL-Epirob). IEEE, 2014. http://dx.doi.org/10.1109/devlrn.2014.6983015.

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Yang, Shujie, Xue Xiao, Yuping Zhang, Xiangbing Meng, and Kimberly K. Leslie. "Abstract 4711: Epigenetic modulation restores expression of functional progesterone receptor in endometrial cancer cells." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-4711.

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Lai, Ssu-Chuan, Te-Sheng Chang, Yu-Ting Su, Yu-Chih Wu, Yung-Che Kuo, Pei-Chi Lan, and Yen-Hua Huang. "Abstract 5223: IL-6 regulates the OCT4 expression by epigenetic modulation in hepatocellular carcinoma." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-5223.

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Reports on the topic "Epigenetic Modulations"

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Liao, Jianhua, Jingting Liu, Baoqing Liu, Chunyan Meng, and Peiwen Yuan. Effect of OIP5-AS1 on clinicopathological characteristics and prognosis of cancer patients: a meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2022. http://dx.doi.org/10.37766/inplasy2022.10.0118.

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Review question / Objective: According to recent studies, long non-coding RNA (lncRNAs) i.e., OPA-interacting protein 5 antisense RNA 1 (OIP5-AS1) has an important role in various carcinomas. However, its role in the cancer is contradictory. Therefore, we aimed to evaluate the link between OIP5-AS1 and cancer patients' clinicopathological characteristics and prognosis to better understand OIP5-AS1's role in cancer. Condition being studied: Reported studies have revealed that long non-coding RNA (lncRNAs) are considerably involved in crucial physiological events in several carcinomas, it can inhibit or promote the occurrence and development of tumors by changing the sequence and spatial structure, modulating epigenetic, regulating the expression level and interacting with binding proteins. However, the mechanism of cancer regulation via lncRNAs was incompletely understood. Hence, clarifying the application value of lncRNAs in preclinical and clinical disease diagnosis and treatment was therefore the prime objective in the field of cancer research at the time.
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Yu, Mei, Pengyu Wang, Binbin Li, Qiaoling Ruan, Jingzi ZhangBao, Lei Wu, Xiaoshuang Zhang, Zhaolin Liu, and Fang Huang. NRSF Negatively Regulates Microglial Pro-Inflammatory Activation. Progress in Neurobiology, May 2024. http://dx.doi.org/10.60124/j.pneuro.2024.20.02.

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Microglial activation contributes to neurological disorders like Parkinson’s disease (PD), and modulating this activation is a potential therapeutic approach. The neuron-restrictive silencer factor (NRSF) functions as a negative regulator of gene transcription through epigenetic modifications. While previous research has primarily examined the role of NRSF in neuronal differentiation and injury, emerging evidence indicates that NRSF also plays a significant role in maintaining the phenotype of glial cells. In this study, we explored the role and underlying mechanisms of NRSF in lipopolysaccharide (LPS)-induced pro-inflammatory or interleukin-4 (IL4)-induced anti-inflammatory phenotype of microglial activation. Following LPS stimulation, the nuclear localization of NRSF increased in BV2 microglial cells, primary mouse microglia, and microglia within the substantia nigra of PD mice. Knockdown of NRSF enhanced the expression of inflammation-related factors induced by LPS via the mitogen-activated protein kinase-extracellular signal-regulated kinase (MAPK-ERK) and nuclear factor-κB (NF-κB) p65 signalling pathways in BV2 cells. Moreover, the culture medium from LPS-treated NRSF knockdown BV2 cells exerted greater toxic effects on human neuroblastoma SH-SY5Y cells compared to the control. However, NRSF knockdown exerted inconsistent effects on the expression of anti-inflammatory-related genes in IL4-treated BV2 cells. Our findings suggest that NRSF knockdown promotes microglial pro-inflammatory activation.
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Yahav, Shlomo, John Brake, and Noam Meiri. Development of Strategic Pre-Natal Cycling Thermal Treatments to Improve Livability and Productivity of Heavy Broilers. United States Department of Agriculture, December 2013. http://dx.doi.org/10.32747/2013.7593395.bard.

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The necessity to improve broiler thermotolerance and live performance led to the following hypothesis: Appropriate comprehensive incubation treatments that include significant temperature management changes will promote angiogenesis and will improve acquisition of thermotolerance and carcass quality of heavy broilers through epigenetic adaptation. It was based on the following questions: 1. Can TM during embryogenesis of broilers induce a longer-lasting thermoregulatory memory (up to marketing age of 10 wk) that will improve acquisition of thermotolerance as well as increased breast meat yield in heavy broilers? 2. The improved sensible heat loss (SHL) suggests an improved peripheral vasodilation process. Does elevated temperature during incubation affect vasculogenesis and angiogenesis processes in the chick embryo? Will such create subsequent advantages for heavy broilers coping with adverse hot conditions? 3. What are the changes that occur in the PO/AH that induce the changes in the threshold response for heat production/heat loss based on the concept of epigenetic temperature adaptation? The original objectives of this study were as follow: a. to assess the improvement of thermotolerance efficiency and carcass quality of heavy broilers (~4 kg); b. toimproveperipheral vascularization and angiogenesis that improve sensible heat loss (SHL); c. to study the changes in the PO/AH thermoregulatory response for heat production/losscaused by modulating incubation temperature. To reach the goals: a. the effect of TM on performance and thermotolerance of broilers reared to 10 wk of age was studied. b. the effect of preincubation heating with an elevated temperature during the 1ˢᵗ 3 to 5 d of incubation in the presence of modified fresh air flow coupled with changes in turning frequency was elucidated; c.the effect of elevated temperature on vasculogenesis and angiogenesis was determined using in ovo and whole embryo chick culture as well as HIF-1α VEGF-α2 VEGF-R, FGF-2, and Gelatinase A (MMP2) gene expression. The effects on peripheral blood system of post-hatch chicks was determined with an infrared thermal imaging technique; c. the expression of BDNF was determined during the development of the thermal control set-point in the preoptic anterior hypothalamus (PO/AH). Background to the topic: Rapid growth rate has presented broiler chickens with seriousdifficulties when called upon to efficiently thermoregulate in hot environmental conditions. Being homeotherms, birds are able to maintain their body temperature (Tb) within a narrow range. An increase in Tb above the regulated range, as a result of exposure to environmental conditions and/or excessive metabolic heat production that often characterize broiler chickens, may lead to a potentially lethal cascade of irreversible thermoregulatory events. Exposure to temperature fluctuations during the perinatal period has been shown to lead to epigenetic temperature adaptation. The mechanism for this adaptation was based on the assumption that environmental factors, especially ambient temperature, have a strong influence on the determination of the “set-point” for physiological control systems during “critical developmental phases.” Recently, Piestunet al. (2008) demonstrated for the first time that TM (an elevated incubation temperature of 39.5°C for 12 h/d from E7 to E16) during the development/maturation of the hypothalamic-hypophyseal-thyroid axis (thermoregulation) and the hypothalamic-hypophyseal-adrenal axis (stress) significantly improved the thermotolerance and performance of broilers at 35 d of age. These phenomena raised two questions that were addressed in this project: 1. was it possible to detect changes leading to the determination of the “set point”; 2. Did TM have a similar long lasting effect (up to 70 d of age)? 3. Did other TM combinations (pre-heating and heating during the 1ˢᵗ 3 to 5 d of incubation) coupled with changes in turning frequency have any performance effect? The improved thermotolerance resulted mainly from an efficient capacity to reduce heat production and the level of stress that coincided with an increase in SHL (Piestunet al., 2008; 2009). The increase in SHL (Piestunet al., 2009) suggested an additional positive effect of TM on vasculogenesis and angiogensis. 4. In order to sustain or even improve broiler performance, TM during the period of the chorioallantoic membrane development was thought to increase vasculogenesis and angiogenesis providing better vasodilatation and by that SHL post-hatch.
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