The impact of selected genetic and environmental factors on length of use of pulawska breed sows / Oddziaływanie wybranych czynników genetycznych i środowiskowych na długość użytkowania loch rasy puławskiej

2013 ◽  
Vol 30 (4) ◽  
pp. 1-8
Author(s):  
Marek Babicz ◽  
Ewa Skrzypczak ◽  
Kinga Kropiwiec ◽  
Robert Cichocki ◽  
Jacek Burdzanowski
Keyword(s):  
Environmental Factors ◽  
Genetic And Environmental Factors ◽  
The Impact

scholarly journals Impact of Genetic and Environmental Factors on hsCRP Concentrations and Response to Therapeutic Agents

2009 ◽  
Vol 55 (2) ◽  
pp. 256-264 ◽  
Author(s):  
Jian Shen ◽  
Jose M Ordovas
Keyword(s):  
Environmental Factors ◽  
Genetic Polymorphisms ◽  
Genetic Variants ◽  
Inflammatory Marker ◽  
Lipid Lowering ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Fenofibrate Treatment ◽  
Genetic And Environmental Factors ◽  
The Impact

Abstract Background: Inflammation plays an instrumental role in all stages of atherosclerosis. High-sensitivity C-reactive protein (hsCRP), a systemic inflammatory marker, has been gaining recognition as an independent risk factor for cardiovascular disease (CVD). Both baseline hsCRP concentrations and drug-induced hsCRP changes are highly variable and potentially subject to genetic regulation. Content: This review summarizes the current studies examining the effect of genetic and environmental factors on baseline plasma hsCRP concentrations, with a main focus on C-reactive protein, pentraxin-related (CRP) genetic polymorphisms and various dietary components that affect hsCRP concentrations. We also address the association of CRP genetic variations with CVD risk, a relationship that may support or refute the causality of CRP in the atherosclerotic process. Moreover, we discuss the impact of CRP genetic polymorphisms on hsCRP changes in response to 3-week fenofibrate treatment in the genetic intervention of the Genetics of Lipid Lowering Drugs and Diet Network study. Summary: Genetic variants on the CRP locus and other loci and dietary and lifestyle factors are responsible for the interindividual variability of plasma hsCRP concentrations. CRP genetic variants further influence differing plasma hsCRP response after 3-week fenofibrate treatment in patients with metabolic syndrome. Future studies focusing on the influence and interaction of genetic variation on the hsCRP response to dietary and other behavior modification as well as drug treatment could have important implications for the development of more personalized preventive and therapeutic approaches to reduce CVD.

scholarly journals Combat exposure severity as a moderator of genetic and environmental liability to post-traumatic stress disorder

2013 ◽  
Vol 44 (7) ◽  
pp. 1499-1509 ◽  
Author(s):  
E. J. Wolf ◽  
K. S. Mitchell ◽  
K. C. Koenen ◽  
M. W. Miller
Keyword(s):  
Environmental Factors ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Combat Exposure ◽  
Shared Environment ◽  
Post Traumatic Stress ◽  
Post Traumatic ◽  
Genetic And Environmental Factors ◽  
The Impact

BackgroundTwin studies of veterans and adults suggest that approximately 30–46% of the variance in post-traumatic stress disorder (PTSD) is attributable to genetic factors. The remaining variance is attributable to the non-shared environment, which, by definition, includes combat exposure. This study used a gene by measured environment twin design to determine whether the effects of genetic and environmental factors that contribute to the etiology of PTSD are dependent on the level of combat exposure.MethodThe sample was drawn from the Vietnam Era Twin Registry (VETR) and included 620 male–male twin pairs who served in the US Military in South East Asia during the Vietnam War era. Analyses were based on data from a clinical diagnostic interview of lifetime PTSD symptoms and a self-report measure of combat exposure.ResultsBiometric modeling revealed that the effects of genetic and non-shared environment factors on PTSD varied as a function of level of combat exposure such that the association between these factors and PTSD was stronger at higher levels of combat exposure.ConclusionsCombat exposure may act as a catalyst that augments the impact of hereditary and environmental contributions to PTSD. Individuals with the greatest exposure to combat trauma were at increased risk for PTSD as a function of both genetic and environmental factors. Additional work is needed to determine the biological and environmental mechanisms driving these associations.

scholarly journals Atopic dermatitis in children: up to date insight on development and trends in therapy

2020 ◽  
Vol 23 (4) ◽  
pp. 265-270
Author(s):  
Ivan I. Balabolkin
Keyword(s):  
Atopic Dermatitis ◽  
Environmental Factors ◽  
Allergen Immunotherapy ◽  
Calcineurin Inhibitors ◽  
Barrier Dysfunction ◽  
Innate And Adaptive Immunity ◽  
Pathogenetic Therapy ◽  
Ige Mediated ◽  
Genetic And Environmental Factors ◽  
The Impact

The development of atopic dermatitis (AD) in children is determined by the impact of genetic and environmental factors, epidermal barrier dysfunction, and changes in the system of innate and adaptive immunity. 76.3% of patients have IgE-mediated atopic dermatitis. The article elucidates questions of the pathogenesis and treatment of atopic dermatitis using topical corticosteroids, calcineurin inhibitors, emollients, antihistamines, allergen immunotherapy, omalizumab, probiotics. Conducting individualized pathogenetic therapy in ATD allows you to achieve control throughout the disease.

scholarly journals Impact of Gene–Environment Interactions on Cancer Development

2020 ◽  
Vol 17 (21) ◽  
pp. 8089
Author(s):  
Ariane Mbemi ◽  
Sunali Khanna ◽  
Sylvianne Njiki ◽  
Clement G. Yedjou ◽  
Paul B. Tchounwou
Keyword(s):  
Environmental Factors ◽  
Scientific Evidence ◽  
Critical Role ◽  
Experimental Studies ◽  
Joint Effect ◽  
Human Diseases ◽  
Nucleotide Polymorphisms ◽  
Gene Environment ◽  
Genetic And Environmental Factors ◽  
The Impact

Several epidemiological and experimental studies have demonstrated that many human diseases are not only caused by specific genetic and environmental factors but also by gene–environment interactions. Although it has been widely reported that genetic polymorphisms play a critical role in human susceptibility to cancer and other chronic disease conditions, many single nucleotide polymorphisms (SNPs) are caused by somatic mutations resulting from human exposure to environmental stressors. Scientific evidence suggests that the etiology of many chronic illnesses is caused by the joint effect between genetics and the environment. Research has also pointed out that the interactions of environmental factors with specific allelic variants highly modulate the susceptibility to diseases. Hence, many scientific discoveries on gene–environment interactions have elucidated the impact of their combined effect on the incidence and/or prevalence rate of human diseases. In this review, we provide an overview of the nature of gene–environment interactions, and discuss their role in human cancers, with special emphases on lung, colorectal, bladder, breast, ovarian, and prostate cancers.

P-004 Homocysteine levels in preterm neonates – The impact of genetic and environmental factors

2013 ◽  
Vol 131 ◽  
pp. S77
Author(s):  
M.J. Simchen ◽  
A. Maayan-Metzger ◽  
A. Lubetsky ◽  
J. Kuint ◽  
N. Rosenberg ◽  
...  
Keyword(s):  
Environmental Factors ◽  
Preterm Neonates ◽  
Genetic And Environmental Factors ◽  
The Impact

scholarly journals The Impact of Cigarette Smoking on Risk of Rheumatoid Arthritis: A Narrative Review

Cells ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 475 ◽  
Author(s):  
Yuki Ishikawa ◽  
Chikashi Terao
Keyword(s):  
Rheumatoid Arthritis ◽  
Environmental Factors ◽  
Cigarette Smoking ◽  
Cyclic Peptide ◽  
Bone Destruction ◽  
Narrative Review ◽  
Special Focus ◽  
Main Role ◽  
Genetic And Environmental Factors ◽  
The Impact

Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic inflammation and subsequent proliferation of synovial tissues, which eventually leads to cartilage and bone destruction without effective treatments. Anti-citrullinated cyclic peptide/protein antibody (ACPA) and rheumatoid factor (RF) are two main characteristic autoantibodies found in RA patients and are associated with unfavorable disease outcomes. Although etiologies and causes of the disease have not been fully clarified yet, it is likely that interactive contributions of genetic and environmental factors play a main role in RA pathology. Previous works have demonstrated several genetic and environmental factors as risks of RA development and/or autoantibody productions. Among these, cigarette smoking and HLA-DRB1 are the well-established environmental and genetic risks, respectively. In this narrative review, we provide a recent update on genetic contributions to RA and the environmental risks of RA with a special focus on cigarette smoking and its impacts on RA pathology. We also describe gene–environmental interaction in RA pathogenesis with an emphasis on cigarette smoking and HLA-DRB1.

scholarly journals A Comparison of Personality, Life Events, Comorbidity, and Health in Monozygotic Twins Discordant for Anorexia Nervosa

2017 ◽  
Vol 20 (4) ◽  
pp. 310-318 ◽  
Author(s):  
Laura M. Thornton ◽  
Sara E. Trace ◽  
Kimberly A. Brownley ◽  
Monica Ålgars ◽  
Suzanne E. Mazzeo ◽  
...  
Keyword(s):  
Anorexia Nervosa ◽  
Environmental Factors ◽  
Life Events ◽  
Statistical Power ◽  
Monozygotic Twins ◽  
Health And Wellbeing ◽  
Gastrointestinal Problems ◽  
Genetic And Environmental Factors ◽  
The Impact ◽  
Mz Twins

Genetic and environmental factors contribute to the etiology of anorexia nervosa (AN). The co-twin control design is one of the most powerful methods available to evaluate environmental factors that could contribute to differences between monozygotic (MZ) twins who are discordant for AN. Using available data from a unique and rare sample of 22 Swedish female MZ pairs discordant for AN, we compared personality, life events, comorbidity, and health factors. Twins with AN had significantly higher perfectionism scores than unaffected co-twins and reported younger ages at first diet than unaffected co-twins who had dieted. Consistent with previous literature, more twins with AN reported gastrointestinal problems than unaffected co-twins. Although not significant due to low statistical power, more unaffected co-twins reported experiencing emotional neglect than twins with AN. Early dieting may be a harbinger of the development of AN or an early symptom. Higher perfectionism may represent a risk factor, sequela, or both. Sibling perception of neglect is noteworthy given the impact of an ill child with AN on family function and wellbeing. The health and wellbeing of siblings should be addressed clinically when one child in the family suffers from AN.

scholarly journals Potential Role of Fluoride in the Etiopathogenesis of Alzheimer’s Disease

2018 ◽  
Vol 19 (12) ◽  
pp. 3965 ◽  
Author(s):  
Marta Goschorska ◽  
Irena Baranowska-Bosiacka ◽  
Izabela Gutowska ◽  
Emilia Metryka ◽  
Marta Skórka-Majewicz ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Environmental Factors ◽  
Inflammatory Factors ◽  
Genetic Determinants ◽  
The Central Nervous System ◽  
Genetic And Environmental Factors ◽  
Induced Apoptosis ◽  
Apoptosis And Inflammation ◽  
The Impact

The etiopathogenesis of Alzheimer’s disease has not been fully explained. Now, the disease is widely attributed both to genetic and environmental factors. It is believed that only a small percentage of new AD cases result solely from genetic mutations, with most cases attributed to environmental factors or to the interaction of environmental factors with preexistent genetic determinants. Fluoride is widespread in the environment and it easily crosses the blood–brain barrier. In the brain fluoride affects cellular energy metabolism, synthesis of inflammatory factors, neurotransmitter metabolism, microglial activation, and the expression of proteins involved in neuronal maturation. Finally, and of specific importance to its role in Alzheimer’s disease, studies report fluoride-induced apoptosis and inflammation within the central nervous system. This review attempts to elucidate the potential relationship between the effects of fluoride exposure and the pathogenesis of Alzheimer’s disease. We describe the impact of fluoride-induced oxidative stress and inflammation in the pathogenesis of AD and demonstrate a role for apoptosis in disease progression, as well as a mechanism for its initiation by fluoride. The influence of fluoride on processes of AD initiation and progression is complex and warrants further investigation, especially considering growing environmental fluoride pollution.

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