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[PMID]: 29339914
[Au] Autor:Hocaloski S; Elliott S; Hodge K; McBride K; Hamilton L; McBride CB; Basso M
[Ad] Address:GF Strong Rehabilitation Centre, Vancouver, British Columbia.
[Ti] Title:Perinatal Care for Women with Spinal Cord Injuries: A Collaborative Workshop for Consensus on Care in Canada.
[So] Source:Top Spinal Cord Inj Rehabil;23(4):386-396, 2017.
[Is] ISSN:1945-5763
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:In North America, there are currently no clearly defined standards of care for women with spinal cord injury (SCI) during the perinatal periods of preconception, pregnancy, labour/delivery, and postpartum. Women with SCI and their partners say resources specific to their needs are hard to find. Little evidence-informed research exists to guide clinicians in the care of women with SCI during pregnancy. To further explore these gaps in knowledge and practices for perinatal care for women with SCI, a 1-day workshop was held in Vancouver, British Columbia (BC), Canada in November 2013. Twenty-nine attendees included women with SCI, SCI-community service providers, researchers, and health care providers from maternal/fetal medicine, rehabilitation, anesthesiology, and psychiatry. A pre-meeting online survey of stakeholders elucidated 3 themes: lack of knowledge for both consumers and care providers, gaps in access to services and information, and a need for collaboration throughout the perinatal journey. The workshop addressed issues of care providers' lack of knowledge of nonmedical issues during the perinatal period, physical and attitudinal barriers to access to care for women with SCI, and the need for better collaboration and communication between care providers, the latter potentially initiated by providing information to care providers through the women with SCI themselves. Content experts attending the workshop collectively made recommendations for knowledge generation and research priorities, clinical application priorities, and the need for policy and guideline development in this field. Two information sources for women have since been developed and are available online.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180119
[Lr] Last revision date:180119
[St] Status:In-Process
[do] DOI:10.1310/sci16-00036

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[PMID]: 28523543
[Au] Autor:Brown AN; Feng J
[Ad] Address:Department of Biological Science, Florida State University, 319 Stadium Drive, Tallahassee, FL, 32306, USA.
[Ti] Title:Drug Addiction and DNA Modifications.
[So] Source:Adv Exp Med Biol;978:105-125, 2017.
[Is] ISSN:0065-2598
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Drug addiction is a complex disorder which can be influenced by both genetic and environmental factors. Research has shown that epigenetic modifications can translate environmental signals into changes in gene expression, suggesting that epigenetic changes may underlie the causes and possibly treatment of substance use disorders. This chapter will focus on epigenetic modifications to DNA, which include DNA methylation and several recently defined additional DNA epigenetic changes. We will discuss the functions of DNA modifications and methods for detecting them, followed by a description of the research investigating the function and consequences of drug-induced changes in DNA methylation patterns. Understanding these epigenetic changes may provide us translational tools for the diagnosis and treatment of addiction in the future.
[Mh] MeSH terms primary: Epigenesis, Genetic/genetics
Substance-Related Disorders/genetics
[Mh] MeSH terms secundary: Animals
DNA/metabolism
DNA Adducts/analysis
DNA Adducts/metabolism
DNA Methylation/drug effects
DNA Methylation/physiology
Disease Models, Animal
Female
Gene-Environment Interaction
Genetic Predisposition to Disease
Genome-Wide Association Study
Humans
Inheritance Patterns
Preconception Injuries/genetics
Pregnancy
Pregnancy Complications/chemically induced
Pregnancy Complications/physiopathology
Prenatal Exposure Delayed Effects
Rodentia
Street Drugs/pharmacology
Street Drugs/toxicity
Substance-Related Disorders/metabolism
Transcription, Genetic/drug effects
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Nm] Name of substance:0 (DNA Adducts); 0 (Street Drugs); 9007-49-2 (DNA)
[Em] Entry month:1709
[Cu] Class update date: 170927
[Lr] Last revision date:170927
[Js] Journal subset:IM
[Da] Date of entry for processing:170520
[St] Status:MEDLINE
[do] DOI:10.1007/978-3-319-53889-1_6

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[PMID]: 28523541
[Au] Autor:Siu MT; Weksberg R
[Ad] Address:Program in Genetics and Genome Biology, The Hospital for Sick Children, 555 University Ave, Toronto, ON, M5G 1X8, Canada.
[Ti] Title:Epigenetics of Autism Spectrum Disorder.
[So] Source:Adv Exp Med Biol;978:63-90, 2017.
[Is] ISSN:0065-2598
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Autism spectrum disorder (ASD), one of the most common childhood neurodevelopmental disorders (NDDs), is diagnosed in 1 of every 68 children. ASD is incredibly heterogeneous both clinically and aetiologically. The etiopathogenesis of ASD is known to be complex, including genetic, environmental and epigenetic factors. Normal epigenetic marks modifiable by both genetics and environmental exposures can result in epigenetic alterations that disrupt the regulation of gene expression, negatively impacting biological pathways important for brain development. In this chapter we aim to summarize some of the important literature that supports a role for epigenetics in the underlying molecular mechanism of ASD. We provide evidence from work in genetics, from environmental exposures and finally from more recent studies aimed at directly determining ASD-specific epigenetic patterns, focusing mainly on DNA methylation (DNAm). Finally, we briefly discuss some of the implications of current research on potential epigenetic targets for therapeutics and novel avenues for future work.
[Mh] MeSH terms primary: Autism Spectrum Disorder/genetics
Epigenesis, Genetic/genetics
[Mh] MeSH terms secundary: Autism Spectrum Disorder/etiology
Autism Spectrum Disorder/therapy
DNA Methylation
Diseases in Twins/epidemiology
Diseases in Twins/genetics
Environmental Exposure
Female
Forecasting
Gene-Environment Interaction
Genetic Diseases, Inborn/genetics
Genetic Diseases, Inborn/psychology
Humans
Infant, Newborn
Preconception Injuries
Pregnancy
Prenatal Exposure Delayed Effects
Risk
Twin Studies as Topic
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1709
[Cu] Class update date: 170927
[Lr] Last revision date:170927
[Js] Journal subset:IM
[Da] Date of entry for processing:170520
[St] Status:MEDLINE
[do] DOI:10.1007/978-3-319-53889-1_4

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[PMID]: 27687803
[Au] Autor:Doherty TS; Roth TL
[Ad] Address:University of Delaware,Newark.
[Ti] Title:Insight from animal models of environmentally driven epigenetic changes in the developing and adult brain.
[So] Source:Dev Psychopathol;28(4pt2):1229-1243, 2016 Nov.
[Is] ISSN:1469-2198
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The efforts of many neuroscientists are directed toward understanding the appreciable plasticity of the brain and behavior. In recent years, epigenetics has become a core of this focus as a prime mechanistic candidate for behavioral modifications. Animal models have been instrumental in advancing our understanding of environmentally driven changes to the epigenome in the developing and adult brain. This review focuses mainly on such discoveries driven by adverse environments along with their associated behavioral outcomes. While much of the evidence discussed focuses on epigenetics within the central nervous system, several peripheral studies in humans who have experienced significant adversity are also highlighted. As we continue to unravel the link between epigenetics and phenotype, discerning the complexity and specificity of epigenetic changes induced by environments is an important step toward understanding optimal development and how to prevent or ameliorate behavioral deficits bred by disruptive environments.
[Mh] MeSH terms primary: Disease Models, Animal
Epigenesis, Genetic/genetics
Models, Genetic
Social Environment
[Mh] MeSH terms secundary: Adult
Animals
Brain/physiology
DNA Methylation/genetics
Female
Genomic Imprinting/genetics
Humans
Infant, Newborn
Male
Phenotype
Preconception Injuries/genetics
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1707
[Cu] Class update date: 171101
[Lr] Last revision date:171101
[Js] Journal subset:IM
[Da] Date of entry for processing:161001
[St] Status:MEDLINE

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[PMID]: 27143854
[Au] Autor:Al-Saleem AI; Al-Jobair AM
[Ad] Address:Dental Department, Prince Sultan Military Medical City, Riyadh, Saudi Arabia.
[Ti] Title:Possible association between acetazolamide administration during pregnancy and multiple congenital malformations.
[So] Source:Drug Des Devel Ther;10:1471-6, 2016.
[Is] ISSN:1177-8881
[Cp] Country of publication:New Zealand
[La] Language:eng
[Ab] Abstract:Congenital malformations might occur because of environmental or genetic factors, and sometimes occur because of unknown causes. Acetazolamide is a carbonic anhydrase inhibitor that is used to treat idiopathic intracranial hypertension, glaucoma, and epilepsy. The use of acetazolamide has not been recommended for pregnant women because of reported teratogenic risks. Congenital malformations, such as ectrodactyly, syndactyly, cleft lip/palate, and retarded incisor teeth development, have been reported in experimental animals. However, tooth agenesis due to the use of acetazolamide has not been reported yet. Oligodontia is a severe type of tooth agenesis involving six or more congenitally missing teeth. The causes of oligodontia are attributed to environmental factors, such as irradiation, drugs, trauma, tumors, infection, genetic factors, or a combination. There is no credible evidence of undesirable effects of acetazolamide use in human pregnancy. However, we report a case of a 12-year-old Saudi boy who was exposed to maternal acetazolamide (1,000 mg/day) for treatment of idiopathic intracranial hypertension before pregnancy, during the first trimester, and throughout the pregnancy. This treatment might have resulted in some congenital malformations, such as ectrodactyly, syndactyly, and oligodontia.
[Mh] MeSH terms primary: Abnormalities, Multiple/chemically induced
Acetazolamide/adverse effects
Acetazolamide/therapeutic use
Preconception Injuries/chemically induced
Pregnancy Complications/drug therapy
Pseudotumor Cerebri/drug therapy
[Mh] MeSH terms secundary: Acetazolamide/administration & dosage
Child
Female
Humans
Limb Deformities, Congenital/chemically induced
Male
Pregnancy
Syndactyly/chemically induced
[Pt] Publication type:CASE REPORTS; JOURNAL ARTICLE
[Nm] Name of substance:O3FX965V0I (Acetazolamide)
[Em] Entry month:1612
[Cu] Class update date: 161231
[Lr] Last revision date:161231
[Js] Journal subset:IM
[Da] Date of entry for processing:160505
[St] Status:MEDLINE
[do] DOI:10.2147/DDDT.S99561

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[PMID]: 27080860
[Au] Autor:Agricola E; Gesualdo F; Carloni E; D'Ambrosio A; Russo L; Campagna I; Pandolfi E; Tozzi AE
[Ad] Address:Multifactorial Disease and Complex Phenotype Research Area, Bambino Gesù Children Hospital IRCCS, Piazza S. Onofrio 4, 00165, Rome, Italy. eleonora.agricola@gmail.com.
[Ti] Title:Investigating paternal preconception risk factors for adverse pregnancy outcomes in a population of internet users.
[So] Source:Reprod Health;13:37, 2016 Apr 14.
[Is] ISSN:1742-4755
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Paternal preconception risk factors such as smoking, exposure to environmental substances, medication use, overweight and advanced age correlate with the occurrence of malformations and birth defects in the offspring. Nonetheless, the prevalence of risk factors for adverse pregnancy outcomes in the male population has been scarcely investigated and no report on preconception interventions targeting prospective fathers is available. We conducted a web-based survey to measure the prevalence of paternal preconception risk factors for adverse pregnancy outcomes in an Italian population of Internet users. METHODS: Prospective or expectant fathers were enrolled during a four-week period through two of the main Italian web-sites dedicated to preconception, pregnancy, childhood and family care. Participants filled in a web questionnaire regarding preconception risk factors for adverse pregnancy outcomes. Logistic regression analysis was used to explore the predictors of paternal preconception risk factors. RESULTS: We enrolled 131 prospective and 205 expectant fathers. More than half of the total participants used medications during the preconception period, 35% were smokers and 8% were obese. Exposure to environmental substances was declared by almost 20% of the participants, with the group including pesticides/herbicides/professional paints being the most prevalent. More than a half of the study sample included men aged over 35 years. According to the multivariate analysis, smoking and exposure to environmental toxics were less frequent among individuals with a university degree (respectively: OR = 0.52; 95% CI 0.32-0.84; OR = 0.52; 95% CI 0.29-0.93). Paternal obesity and medication use in the preconception period were not associated with any of the independent variables. CONCLUSIONS: The prevalence of preconception risk factors among male population should not be neglected when planning preconception interventions, confirming that preconception health must be focused on the couple, rather than on women only.
[Mh] MeSH terms primary: Paint/toxicity
Paternal Behavior
Paternal Exposure/adverse effects
Pesticides/toxicity
Preconception Injuries/etiology
Pregnancy Complications/etiology
Smoking/adverse effects
[Mh] MeSH terms secundary: Adult
Cross-Sectional Studies
Educational Status
Environmental Exposure/adverse effects
Female
Humans
Internet
Italy/epidemiology
Male
Occupational Exposure/adverse effects
Paternal Age
Preconception Injuries/chemically induced
Preconception Injuries/epidemiology
Pregnancy
Pregnancy Complications/chemically induced
Pregnancy Complications/epidemiology
Pregnancy Outcome
Prevalence
Risk Factors
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Pesticides)
[Em] Entry month:1610
[Cu] Class update date: 170220
[Lr] Last revision date:170220
[Js] Journal subset:IM
[Da] Date of entry for processing:160416
[St] Status:MEDLINE
[do] DOI:10.1186/s12978-016-0156-6

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[PMID]: 27058489
[Au] Autor:Yao C; Chen Y; Zhu X; Liu Y; Zhang J; Hou L; Xu Y; Zhang C; Cao J
[Ad] Address:Department of Occupational and Environmental (Yao, Chen, Zhu, Liu, JZhang, Hou, Xu, CZhang, Cao), and The Teaching Center for Preventive Medicine, School of Public Health, Anhui Medical University, China (Cao).
[Ti] Title:Air Pollution and the Risk of Birth Defects in Anqing City, China.
[So] Source:J Occup Environ Med;58(4):e124-7, 2016 Apr.
[Is] ISSN:1536-5948
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVE: This study aimed to explore evidence for the influence of air pollution on the risk of birth defects in China and contribute to establish prevention strategies. METHODS: We conducted a retrospective cohort study in Anqing city, Eastern China, from 2010 to 2012. Binary logistic regression models were used to estimate odds ratios (ORs) per 10 µg/m3 change for SO2, NO2, and PM10. RESULTS: For continuous exposure to SO2 (10 µg/m increase), the adjusted OR for birth defects is 1.20 [95% confidence interval (95% CI) 1.09 to 1.29] in the preconception. A 10 µg/m increase in SO2 (adjusted OR 1.26, 95% CI 1.15 to 1.36) during the second trimester is strongly associated with birth defects. No associations have been observed for NO2 and PM10. CONCLUSION: The results suggested that exposure to ambient SO2 during pregnancy may increase the risk of birth defects.
[Mh] MeSH terms primary: Air Pollution/statistics & numerical data
Congenital Abnormalities/epidemiology
Environmental Exposure/statistics & numerical data
Maternal Exposure/statistics & numerical data
Preconception Injuries/epidemiology
[Mh] MeSH terms secundary: Adult
Air Pollution/adverse effects
China/epidemiology
Cities/epidemiology
Female
Humans
Male
Maternal Age
Nitrogen Dioxide
Odds Ratio
Particulate Matter
Pregnancy
Pregnancy Trimesters
Retrospective Studies
Risk Factors
Sulfur Dioxide
Young Adult
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Particulate Matter); 0UZA3422Q4 (Sulfur Dioxide); S7G510RUBH (Nitrogen Dioxide)
[Em] Entry month:1701
[Cu] Class update date: 170118
[Lr] Last revision date:170118
[Js] Journal subset:IM
[Da] Date of entry for processing:160409
[St] Status:MEDLINE
[do] DOI:10.1097/JOM.0000000000000676

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[PMID]: 26847216
[Au] Autor:Bhat A; Byatt N
[Ad] Address:Department of Psychiatry, University of Washington, Box 35650, Seattle, WA, 98195, USA. amritha@uw.edu.
[Ti] Title:Infertility and Perinatal Loss: When the Bough Breaks.
[So] Source:Curr Psychiatry Rep;18(3):31, 2016 Mar.
[Is] ISSN:1535-1645
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Infertility and perinatal loss are common, and associated with lower quality of life, marital discord, complicated grief, major depressive disorder, anxiety disorders, and post-traumatic stress disorder. Young women, who lack social supports, have experienced recurrent pregnancy loss or a history of trauma and / or preexisting psychiatric illness are at a higher risk of experiencing psychiatric illnesses or symptoms after a perinatal loss or during infertility. It is especially important to detect, assess, and treat depression, anxiety, or other psychiatric symptoms because infertility or perinatal loss may be caused or perpetuated by such symptoms. Screening, psychoeducation, provision of resources and referrals, and an opportunity to discuss their loss and plan for future pregnancies can facilitate addressing mental health concerns that arise. Women at risk of or who are currently experiencing psychiatric symptoms should receive a comprehensive treatment plan that includes the following: (1) proactive clinical monitoring, (2) evidence-based approaches to psychotherapy, and (3) discussion of risks, benefits, and alternatives of medication treatment during preconception and pregnancy.
[Mh] MeSH terms primary: Anxiety Disorders/therapy
Depressive Disorder, Major/therapy
Grief
Infertility/psychology
Quality of Life/psychology
Stillbirth/psychology
Stress Disorders, Post-Traumatic/therapy
[Mh] MeSH terms secundary: Anxiety/psychology
Anxiety/therapy
Anxiety Disorders/psychology
Depression/psychology
Depression/therapy
Depressive Disorder, Major/psychology
Female
Humans
Pregnancy
Stress Disorders, Post-Traumatic/psychology
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Em] Entry month:1609
[Cu] Class update date: 170220
[Lr] Last revision date:170220
[Js] Journal subset:IM
[Da] Date of entry for processing:160206
[St] Status:MEDLINE
[do] DOI:10.1007/s11920-016-0663-8

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[PMID]: 26732620
[Au] Autor:Gharagozloo P; Gutiérrez-Adán A; Champroux A; Noblanc A; Kocer A; Calle A; Pérez-Cerezales S; Pericuesta E; Polhemus A; Moazamian A; Drevet JR; Aitken RJ
[Ad] Address:CellOxess LLC, 15 Roszel Road, Princeton, NJ 08540, USA parviz.gharagozloo@celloxess.com.
[Ti] Title:A novel antioxidant formulation designed to treat male infertility associated with oxidative stress: promising preclinical evidence from animal models.
[So] Source:Hum Reprod;31(2):252-62, 2016 Feb.
[Is] ISSN:1460-2350
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:STUDY QUESTION: Does a novel antioxidant formulation designed to restore redox balance within the male reproductive tract, reduce sperm DNA damage and increase pregnancy rates in mouse models of sperm oxidative stress? SUMMARY ANSWER: Oral administration of a novel antioxidant formulation significantly reduced sperm DNA damage in glutathione peroxidase 5 (GPX5), knockout mice and restored pregnancy rates to near-normal levels in mice subjected to scrotal heat stress. WHAT IS KNOWN ALREADY: Animal and human studies have documented the adverse effect of sperm DNA damage on fertilization rates, embryo quality, miscarriage rates and the transfer of de novo mutations to offspring. Semen samples of infertile men are known to be deficient in several key antioxidants relative to their fertile counterparts. Antioxidants alone or in combination have demonstrated limited efficacy against sperm oxidative stress and DNA damage in numerous human clinical trials, however these studies have not been definitive and an optimum combination has remained elusive. STUDY DESIGN, SIZE, DURATION: The efficacy of the antioxidant formulation was evaluated in two well-established mouse models of oxidative stress, scrotal heating and Gpx5 knockout (KO) mice, (n = 12 per experimental group), by two independent laboratories. Mice were provided the antioxidant product in their drinking water for 2-8 weeks and compared with control groups for sperm DNA damage and pregnancy rates. PARTICIPANTS/MATERIALS, SETTING, METHODS: In the Gpx5 KO model, oxidative DNA damage was monitored in spermatozoa by immunocytochemical detection of 8-hydroxy-2'-deoxyguanosine (8OHdG). In the scrotal heat stress model, male fertility was tested by partnering with three females for 5 days. The percentage of pregnant females, number of vaginal plugs, resorptions per litter, and litter size were recorded. MAIN RESULTS AND ROLE OF CHANCE: Using immunocytochemical detection of 8OHdG as a biomarker of DNA oxidation, analysis of control mice revealed that around 30% of the sperm population was positively stained. This level increased to about 60% in transgenic mice deficient in the antioxidant enzyme, GPX5. Our results indicate that an 8 week pretreatment of Gpx5 KO mice with the antioxidant formulation provided complete protection of sperm DNA against oxidative damage. In mouse models of scrotal heat stress, only 35% (19/54) of female mice became pregnant resulting in 169 fetuses with 18% fetal resorption (30/169). This is in contrast to the antioxidant pretreated group where 74% (42/57) of female mice became pregnant, resulting in 427 fetuses with 9% fetal resorption (38/427). In both animal models the protection provided by the novel antioxidant was statistically significant (P < 0.01 for the reduction of 8OHdG in the spermatozoa of Gpx5 KO mice and P < 0.05 for increase in fertility in the scrotal heat stress model). LIMITATIONS, REASONS FOR CAUTION: It was not possible to determine the exact level of antioxidant consumption for each mouse during the treatment period. WIDER IMPLICATIONS OF THE FINDINGS: Recent clinical studies confirm moderate to severe sperm DNA damage in about 60% of all men visiting IVF centers and in about 80% of men diagnosed with idiopathic male infertility. Our results, if confirmed in humans, will impact clinical fertility practice because they support the concept of using an efficacious antioxidant supplementation as a preconception therapy, in order to optimize fertilization rates, help to maintain a healthy pregnancy and limit the mutational load carried by children. STUDY FUNDING/COMPETING INTERESTS: The study was funded by the Clermont Université and the University of Madrid. P.G. is the Managing Director of CellOxess LLC, which has a commercial interest in the detection and resolution of oxidative stress. A.M. and A.P. are employees of CellOxess, LLC. J.R.D., A.G.-A. and R.J.A. are honorary members of the CellOxess advisory board.
[Mh] MeSH terms primary: Antioxidants/pharmacology
Oxidative Stress
Spermatozoa/drug effects
[Mh] MeSH terms secundary: Animals
Biomarkers/metabolism
DNA Damage
Deoxyguanosine/analogs & derivatives
Deoxyguanosine/metabolism
Female
Glutathione Peroxidase/genetics
Infertility, Male/drug therapy
Infertility, Male/genetics
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Models, Animal
Pregnancy
Pregnancy Outcome
Pregnancy Rate
Semen Analysis
Spermatozoa/metabolism
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Antioxidants); 0 (Biomarkers); 88847-89-6 (8-oxo-7-hydrodeoxyguanosine); EC 1.11.1.9 (Glutathione Peroxidase); EC 1.11.1.9 (selenium-independent glutathione peroxidase); G9481N71RO (Deoxyguanosine)
[Em] Entry month:1611
[Cu] Class update date: 161230
[Lr] Last revision date:161230
[Js] Journal subset:IM
[Da] Date of entry for processing:160107
[St] Status:MEDLINE
[do] DOI:10.1093/humrep/dev302

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[PMID]: 26410355
[Au] Autor:Yehuda R; Daskalakis NP; Bierer LM; Bader HN; Klengel T; Holsboer F; Binder EB
[Ad] Address:Traumatic Stress Studies Division, Department of Psychiatry, Icahn School of Medicine at Mount Sinai, New York; Mental Health Care Center, PTSD Clinical Research Program & Laboratory of Clinical Neuroendocrinology and Neurochemistry, James J. Peters Veterans Affairs Medical Center, Bronx, New Yo
[Ti] Title:Holocaust Exposure Induced Intergenerational Effects on FKBP5 Methylation.
[So] Source:Biol Psychiatry;80(5):372-80, 2016 Sep 01.
[Is] ISSN:1873-2402
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: The involvement of epigenetic mechanisms in intergenerational transmission of stress effects has been demonstrated in animals but not in humans. METHODS: Cytosine methylation within the gene encoding for FK506 binding protein 5 (FKBP5) was measured in Holocaust survivors (n = 32), their adult offspring (n = 22), and demographically comparable parent (n = 8) and offspring (n = 9) control subjects, respectively. Cytosine-phosphate-guanine sites for analysis were chosen based on their spatial proximity to the intron 7 glucocorticoid response elements. RESULTS: Holocaust exposure had an effect on FKBP5 methylation that was observed in exposed parents as well in their offspring. These effects were observed at bin 3/site 6. Interestingly, in Holocaust survivors, methylation at this site was higher in comparison with control subjects, whereas in Holocaust offspring, methylation was lower. Methylation levels for exposed parents and their offspring were significantly correlated. In contrast to the findings at bin 3/site 6, offspring methylation at bin 2/sites 3 to 5 was associated with childhood physical and sexual abuse in interaction with an FKBP5 risk allele previously associated with vulnerability to psychological consequences of childhood adversity. The findings suggest the possibility of site specificity to environmental influences, as sites in bins 3 and 2 were differentially associated with parental trauma and the offspring's own childhood trauma, respectively. FKBP5 methylation averaged across the three bins examined was associated with wake-up cortisol levels, indicating functional relevance of the methylation measures. CONCLUSIONS: This is the first demonstration of an association of preconception parental trauma with epigenetic alterations that is evident in both exposed parent and offspring, providing potential insight into how severe psychophysiological trauma can have intergenerational effects.
[Mh] MeSH terms primary: Adult Children
Child of Impaired Parents
DNA Methylation/genetics
Holocaust
Stress Disorders, Post-Traumatic/genetics
Tacrolimus Binding Proteins/genetics
[Mh] MeSH terms secundary: Adult Children/psychology
Cohort Studies
Cytosine
Female
Holocaust/psychology
Humans
Male
Parents
Psychiatric Status Rating Scales
Surveys and Questionnaires
Survivors/psychology
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:8J337D1HZY (Cytosine); EC 5.2.1.- (Tacrolimus Binding Proteins); EC 5.2.1.8 (tacrolimus binding protein 5)
[Em] Entry month:1708
[Cu] Class update date: 170830
[Lr] Last revision date:170830
[Js] Journal subset:IM
[Da] Date of entry for processing:150928
[St] Status:MEDLINE


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