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Article: Mammalian Non-CpG Methylation: Stem Cells and Beyond.

Pinney, Sara E

2014 Volume 3, Issue 4, Page(s) 739–751

Abstract: Although CpG dinucleotides remain the primary site for DNA methylation in mammals, there is emerging evidence that DNA methylation at non-CpG sites (CpA, CpT and CpC) is not only present in mammalian cells, but may play a unique role in the regulation of ...

Abstract	Although CpG dinucleotides remain the primary site for DNA methylation in mammals, there is emerging evidence that DNA methylation at non-CpG sites (CpA, CpT and CpC) is not only present in mammalian cells, but may play a unique role in the regulation of gene expression. For some time it has been known that non-CpG methylation is abundant in plants and present in mammalian embryonic stem cells, but non-CpG methylation was thought to be lost upon cell differentiation. However, recent publications have described a role for non-CpG methylation in adult mammalian somatic cells including the adult mammalian brain, skeletal muscle, and hematopoietic cells and new interest in this field has been stimulated by the availability of high throughput sequencing techniques that can accurately measure this epigenetic modification. Genome wide assays indicate that non-CpG methylation is negligible in human fetal brain, but abundant in human adult brain tissue. Genome wide measurement of non-CpG methylation coupled with RNA-Sequencing indicates that in the human adult brain non-CpG methylation levels are inversely proportional to the abundance of mRNA transcript at the associated gene. Additionally specific examples where alterations in non-CpG methylation lead to changes in gene expression have been described; in PGC1α in human skeletal muscle, IFN-γ in human T-cells and SYT11 in human brain, all of which contribute to the development of human disease.
Language	English
Publishing date	2014-11-11
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2661517-4
ISSN	2079-7737
ISSN	2079-7737
DOI	10.3390/biology3040739
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Article: Intrauterine Growth Retardation - A Developmental Model of Type 2 Diabetes.

Pinney, Sara E

Drug discovery today. Disease models

2014 Volume 10, Issue 2, Page(s) e71–e77

Abstract: Intrauterine growth retardation has been linked to the development of type 2 diabetes later in life and the mechanisms underlying this phenomena are unknown. Epidemiological studies in humans show a distinct link with the exposure to an intrauterine ... ...

Abstract	Intrauterine growth retardation has been linked to the development of type 2 diabetes later in life and the mechanisms underlying this phenomena are unknown. Epidemiological studies in humans show a distinct link with the exposure to an intrauterine insult that results in low birth weight and the development of type 2 diabetes in adulthood. Intrauterine growth retardation can be induced in rodent models by exposing the pregnant rat to a low protein diet, total calorie restriction, high dose glucocorticoids or inducing uteroplacental insufficiency, all which result in abnormalities in glucose homeostasis in the offspring later in life. Animal models of intrauterine growth retardation allow for a better characterization of changes in glucose homeostasis and corresponding changes in gene expression that can provide insight in the mechanisms by which intrauterine growth retardation leads to type 2 diabetes.
Language	English
Publishing date	2014-05-27
Publishing country	Netherlands
Document type	Journal Article
ISSN	1740-6757
ISSN	1740-6757
DOI	10.1016/j.ddmod.2013.01.003
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Article ; Online: Identification of Novel Regulatory Regions Induced by Intrauterine Growth Restriction in Rat Islets.

Lien, Yu-Chin / Pinney, Sara E / Lu, Xueqing Maggie / Simmons, Rebecca A

Endocrinology

2021 Volume 163, Issue 2

Abstract: Intrauterine growth restriction (IUGR) leads to the development of type 2 diabetes in adulthood, and the permanent alterations in gene expression implicate an epigenetic mechanism. Using a rat model of IUGR, we performed TrueSeq-HELP Tagging to assess ... ...

Abstract	Intrauterine growth restriction (IUGR) leads to the development of type 2 diabetes in adulthood, and the permanent alterations in gene expression implicate an epigenetic mechanism. Using a rat model of IUGR, we performed TrueSeq-HELP Tagging to assess the association of DNA methylation changes and gene dysregulation in islets. We identified 511 differentially methylated regions (DMRs) and 4377 significantly altered single CpG sites. Integrating the methylome and our published transcriptome data sets resulted in the identification of pathways critical for islet function. The identified DMRs were enriched with transcription factor binding motifs, such as Elk1, Etv1, Foxa1, Foxa2, Pax7, Stat3, Hnf1, and AR. In silico analysis of 3-dimensional chromosomal interactions using human pancreas and islet Hi-C data sets identified interactions between 14 highly conserved DMRs and 35 genes with significant expression changes at an early age, many of which persisted in adult islets. In adult islets, there were far more interactions between DMRs and genes with significant expression changes identified with Hi-C, and most of them were critical to islet metabolism and insulin secretion. The methylome was integrated with our published genome-wide histone modification data sets from IUGR islets, resulting in further characterization of important regulatory regions of the genome altered by IUGR containing both significant changes in DNA methylation and specific histone marks. We identified novel regulatory regions in islets after exposure to IUGR, suggesting that epigenetic changes at key transcription factor binding motifs and other gene regulatory regions may contribute to gene dysregulation and an abnormal islet phenotype in IUGR rats.
MeSH term(s)	Animals ; Binding Sites ; CpG Islands ; DNA Methylation/genetics ; Diabetes Mellitus, Type 2/genetics ; Epigenesis, Genetic ; Female ; Fetal Growth Retardation/genetics ; Gene Expression Regulation ; Genome-Wide Association Study ; Histones/chemistry ; Humans ; Islets of Langerhans/chemistry ; Islets of Langerhans/embryology ; Islets of Langerhans/metabolism ; Male ; Pregnancy ; Rats ; Rats, Sprague-Dawley ; Transcription Factors/metabolism
Chemical Substances	Histones ; Transcription Factors
Language	English
Publishing date	2021-12-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/endocr/bqab251
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Article ; Online: Diagnostic and management considerations in pseudohypoaldosteronism type 1b.

Kelchtermans, Jelte / Pinney, Sara E / Leonard, Jacqueline M M / Mcgrath-Morrow, Sharon

BMJ case reports

2022 Volume 15, Issue 1

Abstract: Pseudohypoaldosteronism type 1B is a rare autosomal recessive disorder caused by dysfunction of amiloride-sensitive epithelial sodium channels (ENaCs). We present the case of a neonate with cardiogenic shock after cardiac arrest due to profound ... ...

Abstract	Pseudohypoaldosteronism type 1B is a rare autosomal recessive disorder caused by dysfunction of amiloride-sensitive epithelial sodium channels (ENaCs). We present the case of a neonate with cardiogenic shock after cardiac arrest due to profound hyperkalaemia. Genetic testing revealed a novel homozygous variant in
MeSH term(s)	Amiloride ; Epithelial Sodium Channels/genetics ; Homozygote ; Humans ; Hyperkalemia/diagnosis ; Hyperkalemia/etiology ; Infant, Newborn ; Pseudohypoaldosteronism/complications ; Pseudohypoaldosteronism/diagnosis ; Pseudohypoaldosteronism/genetics
Chemical Substances	Epithelial Sodium Channels ; Amiloride (7DZO8EB0Z3)
Language	English
Publishing date	2022-01-03
Publishing country	England
Document type	Case Reports ; Journal Article
ISSN	1757-790X
ISSN (online)	1757-790X
DOI	10.1136/bcr-2021-246538
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Article ; Online: DNA methylation and its role in the pathogenesis of diabetes.

Bansal, Amita / Pinney, Sara E

Pediatric diabetes

2017 Volume 18, Issue 3, Page(s) 167–177

Abstract: Although the factors responsible for the recent increase in the prevalence of diabetes worldwide are not entirely known, the morbidity associated with this disease results in substantial health and economic burden on society. Epigenetic modifications, ... ...

Abstract	Although the factors responsible for the recent increase in the prevalence of diabetes worldwide are not entirely known, the morbidity associated with this disease results in substantial health and economic burden on society. Epigenetic modifications, including DNA methylation have been identified as one mechanism by which the environment interacts with the genome and there is evidence that alterations in DNA methylation may contribute to the increased prevalence of both type 1 and type 2 diabetes. This review provides a summary of DNA methylation and its role in gene regulation, and includes descriptions of various techniques to measure site-specific and genome-wide DNA methylation changes. In addition, we review current literature highlighting the complex relationship between DNA methylation, gene expression, and the development of diabetes and related complications. In studies where both DNA methylation and gene expression changes were reported, DNA methylation status had a strong inverse correlation with gene expression, suggesting that this interaction may be a potential future therapeutic target. We highlight the emerging use of genome-wide DNA methylation profiles as a biomarker to predict patients at risk of developing diabetes or specific complications of diabetes. The development of a predictive model that incorporates both genetic sequencing and DNA methylation data may be an effective diagnostic approach for all types of diabetes and could lead to additional innovative therapies.
MeSH term(s)	Animals ; Biomarkers/metabolism ; Combined Modality Therapy ; DNA Methylation ; Diabetes Complications/epidemiology ; Diabetes Complications/prevention & control ; Diabetes Mellitus, Type 1/complications ; Diabetes Mellitus, Type 1/genetics ; Diabetes Mellitus, Type 1/metabolism ; Diabetes Mellitus, Type 1/therapy ; Diabetes Mellitus, Type 2/complications ; Diabetes Mellitus, Type 2/genetics ; Diabetes Mellitus, Type 2/metabolism ; Diabetes Mellitus, Type 2/therapy ; Epigenesis, Genetic ; Gene Expression Regulation, Developmental ; Health Transition ; Humans ; Insulin Resistance ; Risk Factors
Chemical Substances	Biomarkers
Language	English
Publishing date	2017-04-12
Publishing country	Denmark
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural
ZDB-ID	1502504-4
ISSN	1399-5448 ; 1745-1426 ; 1399-543X
ISSN (online)	1399-5448
ISSN	1745-1426 ; 1399-543X
DOI	10.1111/pedi.12521
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Article ; Online: The highly selective Bruton tyrosine kinase inhibitor acalabrutinib leaves macrophage phagocytosis intact.

Pinney, Jonathan J / Blick-Nitko, Sara K / Baran, Andrea M / Peterson, Derick R / Whitehead, Hannah E / Izumi, Raquel / Munugalavadla, Veerendra / Van DerMeid, Karl R / Barr, Paul M / Zent, Clive S / Elliott, Michael R / Chu, Charles C

Haematologica

2022 Volume 107, Issue 6, Page(s) 1460–1465

MeSH term(s)	Benzamides ; Humans ; Leukemia, Lymphocytic, Chronic, B-Cell ; Macrophages ; Phagocytosis ; Plant Leaves ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Pyrazines
Chemical Substances	Benzamides ; Protein Kinase Inhibitors ; Pyrazines ; acalabrutinib (I42748ELQW)
Language	English
Publishing date	2022-06-01
Publishing country	Italy
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2333-4
ISSN	1592-8721 ; 0017-6567 ; 0390-6078
ISSN (online)	1592-8721
ISSN	0017-6567 ; 0390-6078
DOI	10.3324/haematol.2021.279560
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Article ; Online: Complex relationships between perfluorooctanoate, body mass index, insulin resistance and serum lipids in young girls.

Fassler, Cecily S / Pinney, Sara E / Xie, Changchun / Biro, Frank M / Pinney, Susan M

Environmental research

2019 Volume 176, Page(s) 108558

Abstract: Background: Perfluorooctanoate (PFOA) has been used extensively in the manufacture of both commercial and household products. PFOA serum concentrations have been associated with adverse health effects, including lower body mass in children and infants.!# ...

Abstract	Background: Perfluorooctanoate (PFOA) has been used extensively in the manufacture of both commercial and household products. PFOA serum concentrations have been associated with adverse health effects, including lower body mass in children and infants. Objective: To determine if there is an association between serum PFOA concentration and body mass, serum insulin and lipid profile in exposed young girls. Methods: We conducted a cross-sectional study of PFAS environmental biomarkers and insulin resistance in 6 to 8 year-old girls from Greater Cincinnati (n=353). In 2004-2006, blood samples were obtained to measure polyfluoroalkyl substances (PFAS), fasting insulin, glucose and lipids. Clinical exams included anthropometric measurements and pubertal maturation staging. Linear regression and mediation analyses, specifically structural equation modeling (SEM), were used to determine the strength and direction of the relationships between PFAS, pubertal maturation status, body mass index (BMI), cholesterol and insulin resistance. Results: The median PFOA (7.7ng/ml) was twice the National Health and Nutrition Examination Survey (2005-2006). Only PFOA, a PFAS sub-species, showed statistically significant relationships with the outcomes. In regression models, PFOA was associated with decreased BMI and waist-to-height ratio (p=0.0008; p=0.0343), HDL-cholesterol (p=0.0046) and had a borderline inverse association with the HOMA Index of insulin resistance (p=0.0864). In SEM, PFOA retained an inverse relationship with BMI (p<0.0001) but the relationships with HOMA and HDL-cholesterol were no longer statistically significant. Pubertal initiation (Tanner breast or pubic stage 2 or greater) and BMI were associated with increased HOMA Index (p<0.0001). Conclusions: These findings suggest PFOA exposure in young girls affects both BMI and ultimately insulin resistance. In mediation analysis with puberty in the model, the direct effects of PFOA on insulin resistance and were reduced.
MeSH term(s)	Body Mass Index ; Caprylates ; Child ; Cross-Sectional Studies ; Environmental Exposure/statistics & numerical data ; Environmental Pollutants/analysis ; Female ; Fluorocarbons ; Humans ; Insulin ; Insulin Resistance ; Lipids/blood ; Nutrition Surveys ; Sexual Maturation
Chemical Substances	Caprylates ; Environmental Pollutants ; Fluorocarbons ; Insulin ; Lipids ; perfluorooctanoic acid (947VD76D3L)
Language	English
Publishing date	2019-06-26
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	205699-9
ISSN	1096-0953 ; 0013-9351
ISSN (online)	1096-0953
ISSN	0013-9351
DOI	10.1016/j.envres.2019.108558
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Article ; Online: Overview of Atypical Diabetes.

Tamaroff, Jaclyn / Kilberg, Marissa / Pinney, Sara E / McCormack, Shana

Endocrinology and metabolism clinics of North America

2020 Volume 49, Issue 4, Page(s) 695–723

Abstract: Although type 1 diabetes mellitus and, to a lesser extent, type 2 diabetes mellitus, are the prevailing forms of diabetes in youth, atypical forms of diabetes are not uncommon and may require etiology-specific therapies. By some estimates, up to 6.5% of ... ...

Abstract	Although type 1 diabetes mellitus and, to a lesser extent, type 2 diabetes mellitus, are the prevailing forms of diabetes in youth, atypical forms of diabetes are not uncommon and may require etiology-specific therapies. By some estimates, up to 6.5% of children with diabetes have monogenic forms. Mitochondrial diabetes and cystic fibrosis related diabetes are less common but often noted in the underlying disease. Atypical diabetes should be considered in patients with a known disorder associated with diabetes, aged less than 25 years with nonautoimmune diabetes and without typical characteristics of type 2 diabetes mellitus, and/or with comorbidities associated with atypical diabetes.
MeSH term(s)	Adolescent ; Adult ; Child ; Child, Preschool ; Cystic Fibrosis/complications ; Diabetes Mellitus/diagnosis ; Diabetes Mellitus/etiology ; Diabetes Mellitus/genetics ; Diabetes Mellitus/therapy ; Humans ; Infant ; Infant, Newborn ; Mitochondrial Diseases/complications ; Young Adult
Language	English
Publishing date	2020-10-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	92116-6
ISSN	1558-4410 ; 0889-8529
ISSN (online)	1558-4410
ISSN	0889-8529
DOI	10.1016/j.ecl.2020.07.004
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Article: Mammalian Non-CpG Methylation: Stem Cells and Beyond

Pinney, Sara E

Biology. 2014 Nov. 11, v. 3, no. 4

2014

Abstract	Although CpG dinucleotides remain the primary site for DNA methylation in mammals, there is emerging evidence that DNA methylation at non-CpG sites (CpA, CpT and CpC) is not only present in mammalian cells, but may play a unique role in the regulation of gene expression. For some time it has been known that non-CpG methylation is abundant in plants and present in mammalian embryonic stem cells, but non-CpG methylation was thought to be lost upon cell differentiation. However, recent publications have described a role for non-CpG methylation in adult mammalian somatic cells including the adult mammalian brain, skeletal muscle, and hematopoietic cells and new interest in this field has been stimulated by the availability of high throughput sequencing techniques that can accurately measure this epigenetic modification. Genome wide assays indicate that non-CpG methylation is negligible in human fetal brain, but abundant in human adult brain tissue. Genome wide measurement of non-CpG methylation coupled with RNA-Sequencing indicates that in the human adult brain non-CpG methylation levels are inversely proportional to the abundance of mRNA transcript at the associated gene. Additionally specific examples where alterations in non-CpG methylation lead to changes in gene expression have been described; in PGC1α in human skeletal muscle, IFN-γ in human T-cells and SYT11 in human brain, all of which contribute to the development of human disease.
Keywords	DNA methylation ; T-lymphocytes ; adults ; brain ; cell differentiation ; embryonic stem cells ; epigenetics ; gene expression regulation ; genes ; hematopoietic stem cells ; high-throughput nucleotide sequencing ; human diseases ; humans ; interferon-gamma ; messenger RNA ; skeletal muscle ; somatic cells
Language	English
Dates of publication	2014-1111
Size	p. 739-751.
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
Note	Review
ZDB-ID	2661517-4
ISSN	2079-7737
ISSN	2079-7737
DOI	10.3390/biology3040739
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Mammalian Non-CpG Methylation

Sara E. Pinney

Biology, Vol 3, Iss 4, Pp 739-

Stem Cells and Beyond

2014 Volume 751

Abstract	Although CpG dinucleotides remain the primary site for DNA methylation in mammals, there is emerging evidence that DNA methylation at non-CpG sites (CpA, CpT and CpC) is not only present in mammalian cells, but may play a unique role in the regulation of gene expression. For some time it has been known that non-CpG methylation is abundant in plants and present in mammalian embryonic stem cells, but non-CpG methylation was thought to be lost upon cell differentiation. However, recent publications have described a role for non-CpG methylation in adult mammalian somatic cells including the adult mammalian brain, skeletal muscle, and hematopoietic cells and new interest in this field has been stimulated by the availability of high throughput sequencing techniques that can accurately measure this epigenetic modification. Genome wide assays indicate that non-CpG methylation is negligible in human fetal brain, but abundant in human adult brain tissue. Genome wide measurement of non-CpG methylation coupled with RNA-Sequencing indicates that in the human adult brain non-CpG methylation levels are inversely proportional to the abundance of mRNA transcript at the associated gene. Additionally specific examples where alterations in non-CpG methylation lead to changes in gene expression have been described; in PGC1α in human skeletal muscle, IFN-γ in human T-cells and SYT11 in human brain, all of which contribute to the development of human disease.
Keywords	non-CpG methylation ; epigenetics ; bisulfite sequencing ; MeDIP ; RRBS1 ; Biology (General) ; QH301-705.5
Subject code	570
Language	English
Publishing date	2014-11-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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