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Periodontal diseases are multidimensional and complex. Bacterial content is the initiator, but disease progression depends on genetic and environmental parameters related to the host. Although bone loss magnitude is the common resulting outcome, the biologic process likely represents a unique inflammatory response characteristic to every individual. Therefore, it is obvious that practitioners must take into account the influence of these parameters and tailor a treatment accordingly. New, emerging deoxyribonucleotide‐based technologies allow integration of the biologic impact of the environment, and periodontists should be prepared to incorporate these technologies into their practice to advance personalized medicine. This commentary provides updated insights on the distinctiveness of inflammation per individual in terms of microbiome and genome specificity and cites some educational resources helpful for implementing individualized therapy. 相似文献
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Evy Cleeren Johan Van der Heyden Angela Brand Herman Van Oyen 《Archives of Public Health》2011,69(1):8
The completion of the Human Genome Project triggered a whole new field of genomic research which is likely to lead to new
opportunities for the promotion of population health. As a result, the distinction between genetic and environmental diseases
has faded. Presently, genomics and knowledge deriving from systems biology, epigenomics, integrative genomics or genome-environmental
interactions give a better insight on the pathophysiology of common diseases. However, it is barely used in the prevention
and management of diseases. Together with the boost in the amount of genetic association studies, this demands for appropriate
public health actions. The field of Public Health Genomics analyses how genome-based knowledge and technologies can responsibly
and effectively be integrated into health services and public policy for the benefit of population health. Environmental exposures
interact with the genome to produce health information which may help explain inter-individual differences in health, or disease
risk. However today, prospects for concrete applications remain distant. In addition, this information has not been translated
into health practice yet. Therefore, evidence-based recommendations are few. The lack of population-based research hampers
the evaluation of the impact of genomic applications. Public Health Genomics also evaluates the benefits and risks on a larger
scale, including normative, legal, economic and social issues. These new developments are likely to affect all domains of
public health and require rethinking the role of genomics in every condition of public health interest. This article aims
at providing an introduction to the field of and the ideas behind Public Health Genomics. 相似文献
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背景:随着科学技术的快速发展,表观遗传修饰成为研究热点,其在炎症性肠病中的调控机制部分被揭示,而艾灸能明显改善克罗恩病和溃疡性结肠炎的症状,减轻药物治疗的不良反应,目前其机制尚未阐明。
目的:探讨对可能影响炎症性肠病发病的表观遗传学机制,综述艾灸调节对炎症性肠病的效应机制,探讨表观遗传修饰在艾灸对炎症性肠病中的调节作用。
方法:电子检索PubMed数据库、中国知网和维普网,英文数据库检索时限2000年1月至2014年12月;中文数据库检索时限1999年1月至2014年12月,检索关键词“epigenetic;inflammatory bowel disease;crohn’s disease;ulcerative colitis; DNA methylation;histone modification;miRNA;艾灸;炎症性肠病;克罗恩病;溃疡性结肠炎”。
结果与结论:详细阐述了表观遗传修饰与炎症性肠病的发生、发展等方面的相关性,从DNA甲基化、组蛋白修饰和miRNA等方面对炎症性肠病的相关作用靶点及调控机制。艾灸对炎症性肠病的效应机制主要与调节机体免疫相关,而其抗炎的作用机制可能受表观遗传修饰的调节,参与抑炎细胞因子和促炎细胞因子的调控,使机体从慢性炎症状态向免疫保护与耐受转化。
中国组织工程研究杂志出版内容重点:组织构建;骨细胞;软骨细胞;细胞培养;成纤维细胞;血管内皮细胞;骨质疏松;组织工程全文链接: 相似文献
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Veronica Massey Austin Parrish Josepmaria Argemi Montserrat Moreno Aline Mello Mar García-Rocha Jose Altamirano Gemma Odena Laurent Dubuquoy Alexandre Louvet Carlos Martinez Anna Adrover Silvia Affò Oriol Morales-Ibanez Pau Sancho-Bru Cristina Millán Edilmar Alvarado-Tapias Dalia Morales-Arraez Ramon Bataller 《Gastroenterology》2021,160(5):1725-1740.e2
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It is becoming widely accepted that epigenetic alterations are universally present in human malignancies and that cancer is as much a disease of abnormal epigenetics as it is a genetic disease. The potential utility of epigenetics and epigenomics in cancer research and cancer control is highlighted by the fact that many funding agencies put cancer epigenetics on the priority list. The goal of this meeting, held at the offices of the International Agency for Research on Cancer in Lyon, France, 6 and 7 December 2007, was to discuss recent conceptual and technological advances in cancer epigenetics and epigenomics, the future research needs in the field, and their implications for early detection, risk assessment and prevention of cancer.While epigenetics has been historically linked to phenomena that do not follow normal genetic principles of heritability, recent mechanistic advances have begun to change our understanding of complex diseases including cancer, traditionally viewed as genetic in origin. It is now known that epigenetic mechanisms play critical roles in regulation of many cellular functions and their deregulation may disrupt the control of fundamental processes leading to tumour formation. A flurry of screening and functional studies revealed that most key processes found in cancer cells, such as silencing of tumour suppressor genes, activation of oncogenes, aberrant cell cycle processes, defects in DNA repair, and deregulation of cell death, can be triggered by epigenetic deregulation. Two important features that distinguish epigenetic changes from genetic alterations are the gradual appearance and reversibility of epigenetic events. These features make epigenetic alterations an attractive target for therapeutic intervention and the development of preventive strategies. For example, aberrant patterns of DNA methylation and histone acetylation and methylation can be targeted by drugs aiming to re‐activate epigenetically silenced genes. Until now, most studies on epigenetic changes in cancer were generally focused on specific genes. However, this meeting also stressed the need to take advantage of recent progress in epigenomics and emergence of powerful technologies for detection of epigenetic changes in high throughput and genome‐wide settings. This may further advance our capacity to evaluate the contribution of epigenetic changes induced by environmental epimutagens to human cancer. This information may prove critical for the design of efficient strategies for early diagnosis, therapy, and prevention of cancer. 相似文献
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