scholarly journals Future of environmental research in the age of epigenomics and exposomics

2017 ◽  
Vol 32 (1-2) ◽  
pp. 45-54 ◽  
Author(s):  
Nina Holland
Keyword(s):  
Public Health ◽  
Molecular Mechanisms ◽  
Environmental Research ◽  
Whole Body ◽  
Epigenetic Mechanisms ◽  
Multifactorial Diseases ◽  
Adverse Health Outcomes ◽  
Increased Risk ◽  
Susceptible Populations ◽  
Risk Of Cancer

Abstract Environmental research and public health in the 21st century face serious challenges such as increased air pollution and global warming, widespread use of potentially harmful chemicals including pesticides, plasticizers, and other endocrine disruptors, and radical changes in nutrition and lifestyle typical of modern societies. In particular, exposure to environmental and occupational toxicants may contribute to the occurrence of adverse birth outcomes, neurodevelopmental deficits, and increased risk of cancer and other multifactorial diseases such as diabetes and asthma. Rapidly evolving methodologies of exposure assessment and the conceptual framework of the Exposome, first introduced in 2005, are new frontiers of environmental research. Metabolomics and adductomics provide remarkable opportunities for a better understanding of exposure and prediction of potential adverse health outcomes. Metabolomics, the study of metabolism at whole-body level, involves assessment of the total repertoire of small molecules present in a biological sample, shedding light on interactions between gene expression, protein expression, and the environment. Advances in genomics, transcriptomics, and epigenomics are generating multidimensional structures of biomarkers of effect and susceptibility, increasingly important for the understanding of molecular mechanisms and the emergence of personalized medicine. Epigenetic mechanisms, particularly DNA methylation and miRNA expression, attract increasing attention as potential links between the genetic and environmental determinants of health and disease. Unlike genetics, epigenetic mechanisms could be reversible and an understanding of their role may lead to better protection of susceptible populations and improved public health.

scholarly journals Fluoride Exposure Induces Inhibition of Sodium-and Potassium-Activated Adenosine Triphosphatase (Na+, K+-ATPase) Enzyme Activity: Molecular Mechanisms and Implications for Public Health

2019 ◽  
Vol 16 (8) ◽  
pp. 1427 ◽  
Author(s):  
Declan Timothy Waugh
Keyword(s):  
Enzyme Activity ◽  
Atpase Activity ◽  
Molecular Mechanisms ◽  
Chemical Elements ◽  
Biological Pathways ◽  
Normal Brain ◽  
Biological Interface ◽  
Increased Risk ◽  
And Function ◽  
Risk Of Cancer

In this study, several lines of evidence are provided to show that Na + , K + -ATPase activity exerts vital roles in normal brain development and function and that loss of enzyme activity is implicated in neurodevelopmental, neuropsychiatric and neurodegenerative disorders, as well as increased risk of cancer, metabolic, pulmonary and cardiovascular disease. Evidence is presented to show that fluoride (F) inhibits Na + , K + -ATPase activity by altering biological pathways through modifying the expression of genes and the activity of glycolytic enzymes, metalloenzymes, hormones, proteins, neuropeptides and cytokines, as well as biological interface interactions that rely on the bioavailability of chemical elements magnesium and manganese to modulate ATP and Na + , K + -ATPase enzyme activity. Taken together, the findings of this study provide unprecedented insights into the molecular mechanisms and biological pathways by which F inhibits Na + , K + -ATPase activity and contributes to the etiology and pathophysiology of diseases associated with impairment of this essential enzyme. Moreover, the findings of this study further suggest that there are windows of susceptibility over the life course where chronic F exposure in pregnancy and early infancy may impair Na + , K + -ATPase activity with both short- and long-term implications for disease and inequalities in health. These findings would warrant considerable attention and potential intervention, not to mention additional research on the potential effects of F intake in contributing to chronic disease.

scholarly journals Exercise prevents whole-body type 2 diabetes risk factors better than estradiol replacement in rats

2021 ◽  
Author(s):  
Luke J. Fritsch ◽  
Skylar J. McCaulley ◽  
Colton R. Johnson ◽  
Nicholaus J. Lawson ◽  
Brittany K. Gorres-Martens
Keyword(s):  
Type 2 Diabetes ◽  
Weight Gain ◽  
Protein Expression ◽  
Molecular Mechanisms ◽  
Body Weight Gain ◽  
Serum Insulin ◽  
Whole Body ◽  
Body Type ◽  
Increased Risk

Introduction: The absence of estrogens in postmenopausal women is linked to an increased risk of type 2 diabetes (T2D), and estradiol replacement can decrease this risk. Notably, exercise can also treat and prevent T2D. This study seeks to understand the molecular mechanisms by which estradiol and exercise induce their beneficial effects via assessing whole-body and cellular changes. Methods: Female Wistar rats were ovariectomized and fed a high-fat diet for 10 weeks and divided into the following 4 experimental groups: 1) no treatment (control), 2) exercise (Ex), 3) estradiol replacement, and 4) Ex+estradiol. Results: Both Ex and estradiol decreased the total body weight gain. However, only exercise effectively reduced the white adipose tissue (WAT) weight gain, food intake, blood glucose levels and serum insulin levels. At the molecular level, exercise increased the non-insulin stimulated pAkt levels in the WAT. In the liver, estradiol increased the protein expression of ACC and FAS, and estradiol decreased the hepatic protein expression of LPL. In the WAT, estradiol and exercise increased the protein expression of ATGL. Conclusion: Exercise provides better protection against T2D when considering whole body measurements, which may be due to increased non-insulin stimulated pAkt in the WAT. However, at the cellular level, several molecular changes in fat metabolism and fat storage occurred in the liver and WAT with estradiol treatment.

scholarly journals Hormone-Related Cancer and Autoimmune Diseases: A Complex Interplay to be Discovered

2022 ◽  
Vol 12 ◽  
Author(s):  
A Losada-García ◽  
SA Cortés-Ramírez ◽  
M Cruz-Burgos ◽  
M Morales-Pacheco ◽  
Carlos D Cruz-Hernández ◽  
...  
Keyword(s):  
Immune System ◽  
Autoimmune Diseases ◽  
Molecular Mechanisms ◽  
Continuous Process ◽  
Clinical Signs ◽  
The Body ◽  
Future Research ◽  
Adaptive Immune ◽  
Increased Risk ◽  
Risk Of Cancer

Neoplasic transformation is a continuous process that occurs in the body. Even before clinical signs, the immune system is capable of recognizing these aberrant cells and reacting to suppress them. However, transformed cells acquire the ability to evade innate and adaptive immune defenses through the secretion of molecules that inhibit immune effector functions, resulting in tumor progression. Hormones have the ability to modulate the immune system and are involved in the pathogenesis of autoimmune diseases, and cancer. Hormones can control both the innate and adaptive immune systems in men and women. For example androgens reduce immunity through modulating the production of pro-inflammatory and anti-inflammatory mediators. Women are more prone than men to suffer from autoimmune diseases such as systemic lupus erythematosus, psoriasis and others. This is linked to female hormones modulating the immune system. Patients with autoimmune diseases consistently have an increased risk of cancer, either as a result of underlying immune system dysregulation or as a side effect of pharmaceutical treatments. Epidemiological data on cancer incidence emphasize the link between the immune system and cancer. We outline and illustrate the occurrence of hormone-related cancer and its relationship to the immune system or autoimmune diseases in this review. It is obvious that some observations are contentious and require explanation of molecular mechanisms and validation. As a result, future research should clarify the molecular pathways involved, including any causal relationships, in order to eventually allocate information that will aid in the treatment of hormone-sensitive cancer and autoimmune illness.

scholarly journals Germline Structural Variations in Cancer Predisposition Genes

2021 ◽  
Vol 12 ◽  
Author(s):  
Tímea Pócza ◽  
Vince Kornél Grolmusz ◽  
János Papp ◽  
Henriett Butz ◽  
Attila Patócs ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Current Knowledge ◽  
Cancer Predisposition ◽  
Detection Methods ◽  
Small Scale ◽  
Structural Variations ◽  
Increased Risk ◽  
Predisposition Genes ◽  
Cancer Syndromes ◽  
Risk Of Cancer

In addition to single nucleotide variations and small-scale indels, structural variations (SVs) also contribute to the genetic diversity of the genome. SVs, such as deletions, duplications, amplifications, or inversions may also affect coding regions of cancer-predisposing genes. These rearrangements may abrogate the open reading frame of these genes or adversely affect their expression and may thus act as germline mutations in hereditary cancer syndromes. With the capacity of disrupting the function of tumor suppressors, structural variations confer an increased risk of cancer and account for a remarkable fraction of heritability. The development of sequencing techniques enables the discovery of a constantly growing number of SVs of various types in cancer predisposition genes (CPGs). Here, we provide a comprehensive review of the landscape of germline SV types, detection methods, pathomechanisms, and frequency in CPGs, focusing on the two most common cancer syndromes: hereditary breast- and ovarian cancer and gastrointestinal cancers. Current knowledge about the possible molecular mechanisms driving to SVs is also summarized.

scholarly journals Rethinking the Paradigm and Practice of Occupational Health in a World Without Decent Work: A Perspective From East and Southern Africa

2021 ◽  
pp. 104829112110171
Author(s):  
Rene Loewenson
Keyword(s):  
Public Health ◽  
Occupational Health ◽  
Decent Work ◽  
Science Practice ◽  
Political Factors ◽  
The Public ◽  
Adverse Health Outcomes ◽  
Increased Risk ◽  
Precarious Labor ◽  
Work And Employment

The global political economy is generating new forms and growing shares of informal, insecure, and precarious labor, adding to histories of insecure work and an externalization of social costs. The COVID-19 pandemic has highlighted the consequences of ignoring such signals in terms of the increased risk and vulnerability of insecure labor. This paper explores how such trends are generating intersecting adverse health outcomes for workers, communities, and environments and the implications for breaking siloes and building links between the paradigms, science, practice, and tools for occupational health, public health, and eco-health. Applying the principle of controlling hazards at the source is argued in this context to call for an understanding of the upstream production and socio-political factors that are jointly affecting the nature of work and employment and their impact on the health of workers, the public, and the planet.

scholarly journals Using Mouse and Drosophila Models to Investigate the Mechanistic Links between Diet, Obesity, Type II Diabetes, and Cancer

2018 ◽  
Vol 19 (12) ◽  
pp. 4110 ◽  
Author(s):  
Coral Warr ◽  
Katherine Shaw ◽  
Arani Azim ◽  
Matthew Piper ◽  
Linda Parsons
Keyword(s):  
Cancer Progression ◽  
Type Ii Diabetes ◽  
Molecular Mechanisms ◽  
Genetic Manipulation ◽  
Growth Factor Signaling ◽  
Type Ii ◽  
Cancer Models ◽  
Increased Risk ◽  
Diet And Cancer ◽  
Risk Of Cancer

Many of the links between diet and cancer are controversial and over simplified. To date, human epidemiological studies consistently reveal that patients who suffer diet-related obesity and/or type II diabetes have an increased risk of cancer, suffer more aggressive cancers, and respond poorly to current therapies. However, the underlying molecular mechanisms that increase cancer risk and decrease the response to cancer therapies in these patients remain largely unknown. Here, we review studies in mouse cancer models in which either dietary or genetic manipulation has been used to model obesity and/or type II diabetes. These studies demonstrate an emerging role for the conserved insulin and insulin-like growth factor signaling pathways as links between diet and cancer progression. However, these models are time consuming to develop and expensive to maintain. As the world faces an epidemic of obesity and type II diabetes we argue that the development of novel animal models is urgently required. We make the case for Drosophila as providing an unparalleled opportunity to combine dietary manipulation with models of human metabolic disease and cancer. Thus, combining diet and cancer models in Drosophila can rapidly and significantly advance our understanding of the conserved molecular mechanisms that link diet and diet-related metabolic disorders to poor cancer patient prognosis.

scholarly journals Epigenetic Influences in the Obesity/Colorectal Cancer Axis: A Novel Theragnostic Avenue

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Duncan Ayers ◽  
Hatim Boughanem ◽  
Manuel Macías-González
Keyword(s):  
Colorectal Cancer ◽  
Epigenetic Mechanism ◽  
World Health ◽  
Biomedical Science ◽  
Epigenetic Mechanisms ◽  
Rna Methylation ◽  
Health Lifestyle ◽  
Increased Risk ◽  
Risk Of Cancer ◽  
The Impact

The World Health Organization (WHO) considers that obesity has reached proportions of pandemic. Experts also insist on the importance of considering obesity as a chronic disease and one of the main contributors to the worldwide burden of other nontransmissible chronic diseases, which have a great impact on health, lifestyle, and economic cost. One of the most current challenges of biomedical science faces is to understand the origin of the chronic nontransmissible diseases, such as obesity and cancer. There is a large evidence, both in epidemiological studies in humans and in animal models, of the association between obesity and an increased risk of cancer incidence. In the last years, the initial discovery of epigenetic mechanisms represents the most relevant finding to explain how the genome interacts with environmental factors and the ripple effects on disease pathogeneses. Since then, all epigenetic process has been investigated by the scientific communities for nearly two decades to determine which components are involved in this process. DNA/RNA methylation and miRNA are classified as two of the most important representative classes of such epigenetic mechanisms and dysregulated activity of such mechanism can certainly contribute to disease pathogenesis and/or progression especially in tumors. This review article serves to highlight the impact of DNA/RNA methylation and miRNA-based epigenetic mechanism activities in the interplay between obesity and the development and clinical significance of colorectal cancer.

scholarly journals Risk Of Cancer And Radiation Dose Received By Patients From Common Diagnostic Radiological Examinations

2019 ◽  
Vol 13 (1) ◽  
pp. 66-69
Author(s):  
Ridha Jawad Al-Basri
Keyword(s):  
Radiation Dose ◽  
Prospective Study ◽  
Atomic Bomb ◽  
Whole Body ◽  
X Ray ◽  
Increased Risk ◽  
Knowledge Of Cancer ◽  
A Prospective Study ◽  
Risk Of Cancer ◽  
Radiological Examinations

Background: Although radiological diagnostic studies (RDS) are an important and acceptable part of medical practice, it is not without hazards. It is associated with increased risk of cancer. Unfortunately the typical and safe dose of each radiological examination is not known. Most of our knowledge of cancer risk comes from studies of survivors of those exposed to whole body radiation from atomic bomb in Hiroshima & Nagasaki, jobs associated with radiation exposure, Chernobyl survivors & patients treated with radiation therapy for cancer and other diseases.  Objectives   To estimate radiation dose received by patients from diagnostic radiological examinations and lifetime attributable risk of cancer (LTARC). Type of the study: A prospective study.  Methods   A prospective study was conducted in Al-Kindi Teaching Hospital (KTH) during the period from 1st June to 31st august 2016. The study was performed on 910 adult patients. There were 595 males (65.38%) and 315 females (34.62%); mean age was 41.5 years (range 20-63).Different RDS were considered including chest-x ray (CXR), skull x-ray(SXR),    x-ray of limbs and pelvis (LPXR) for orthopedic causes , computed tomography scan (CTS) and mammography (MG) . Results   CXR was performed for 260 (28.57%) patients which delivers 0.12 mSv. SXR was done for 160 (17.58%) patients which delivers 0.3 mSv. LPXR was performed for 220 (24.175%) which delivers 0.3-0.6 mSv. MG exposes 150 (16.48%) to 3 mSv. While CTS ,which         delivers 6.2-16 mSv according to anatomic area being scanned, was done for 120(13.19%) patients.  Conclusion    There is great abuse for using RDS from both patients and doctors, without realizing their danger and association with cancer development. It was proved that RDS expos patients to different kinds of tissues injury including cancer.

scholarly journals Radionuclide Imaging of the Molecular Mechanisms Linking Heart and Brain in Ischemic Syndromes

2020 ◽  
Vol 13 (8) ◽  
Author(s):  
Frank M. Bengel ◽  
Nele Hermanns ◽  
James T. Thackeray
Keyword(s):  
Molecular Mechanisms ◽  
Temporal Dynamics ◽  
Systemic Disease ◽  
Nuclear Imaging ◽  
Whole Body ◽  
Ischemic Event ◽  
Clinical Observations ◽  
Increased Risk ◽  
Imaging Markers ◽  
The Brain

For the heart and the brain, clinical observations suggest that an acute ischemic event experienced by one organ is associated with an increased risk for future acute events and chronic dysfunction of the reciprocal organ. Beyond atherosclerosis as a common systemic disease, various molecular mechanisms are thought to be involved in this interaction. Molecular-targeted nuclear imaging may identify the contribution of factors, such as the neurohumoral, circulatory, or especially the immune system, by combining specific radiotracers with whole-body acquisition and global as well as regional multiorgan analysis. This may be integrated with complementary functional imaging markers and systemic biomarkers for comprehensive network interrogation. Such systems-based strategies go beyond the traditional organ-centered approach and provide novel mechanistic insights, information about temporal dynamics, and a foundation for future interventions aiming at optimal preservation of function of both organs.

scholarly journals Molecular Mechanisms Leading from Periodontal Disease to Cancer

2022 ◽  
Vol 23 (2) ◽  
pp. 970
Author(s):  
Bartosz Kamil Sobocki ◽  
Charbel A. Basset ◽  
Bożena Bruhn-Olszewska ◽  
Paweł Olszewski ◽  
Olga Szot ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Adult Population ◽  
Fusobacterium Nucleatum ◽  
Present Evidence ◽  
Health Concerns ◽  
Increased Risk ◽  
Signaling Axis ◽  
Oral Pathogens ◽  
Rank Signaling ◽  
Risk Of Cancer

Periodontitis is prevalent in half of the adult population and raises critical health concerns as it has been recently associated with an increased risk of cancer. While information about the topic remains somewhat scarce, a deeper understanding of the underlying mechanistic pathways promoting neoplasia in periodontitis patients is of fundamental importance. This manuscript presents the literature as well as a panel of tables and figures on the molecular mechanisms of Porphyromonas gingivalis and Fusobacterium nucleatum, two main oral pathogens in periodontitis pathology, involved in instigating tumorigenesis. We also present evidence for potential links between the RANKL–RANK signaling axis as well as circulating cytokines/leukocytes and carcinogenesis. Due to the nonconclusive data associating periodontitis and cancer reported in the case and cohort studies, we examine clinical trials relevant to the topic and summarize their outcome.

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