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Book: Disease gene identification

DiStefano, Johanna K.

methods and protocols

(Methods in molecular biology ; 1706 ; Springer protocols)

2018

Author's details	edited by Johanna DiStefano
Series title	Methods in molecular biology ; 1706 Springer protocols
Collection
Keywords	biomarker discovery ; exome sequencing ; ChIP assay ; CRISPR ; Parkinson’s
Subject code	610
Language	English
Size	X, 400 Seiten, Illustrationen, 25.4 cm x 17.8 cm
Edition	Second edition
Publisher	Humana Press
Publishing place	New York, NY
Publishing country	United States
Document type	Book
HBZ-ID	HT019553357
ISBN	978-1-4939-7470-2 ; 1-4939-7470-X ; 9781493974719 ; 1493974718
Database	Catalogue ZB MED Medicine, Health

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Zs A 7042 -1706-	verfügbar in Königswinter	Königswinter

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Article ; Online: The Role of Choline, Soy Isoflavones, and Probiotics as Adjuvant Treatments in the Prevention and Management of NAFLD in Postmenopausal Women.

DiStefano, Johanna K

Nutrients

2023 Volume 15, Issue 12

Abstract: Nonalcoholic fatty liver disease (NAFLD) is a prevalent condition among postmenopausal women that can lead to severe liver dysfunction and increased mortality. In recent years, research has focused on identifying potential lifestyle dietary interventions ...

Abstract	Nonalcoholic fatty liver disease (NAFLD) is a prevalent condition among postmenopausal women that can lead to severe liver dysfunction and increased mortality. In recent years, research has focused on identifying potential lifestyle dietary interventions that may prevent or treat NAFLD in this population. Due to the complex and multifactorial nature of NAFLD in postmenopausal women, the disease can present as different subtypes, with varying levels of clinical presentation and variable treatment responses. By recognizing the significant heterogeneity of NAFLD in postmenopausal women, it may be possible to identify specific subsets of individuals who may benefit from targeted nutritional interventions. The purpose of this review was to examine the current evidence supporting the role of three specific nutritional factors-choline, soy isoflavones, and probiotics-as potential nutritional adjuvants in the prevention and treatment of NAFLD in postmenopausal women. There is promising evidence supporting the potential benefits of these nutritional factors for NAFLD prevention and treatment, particularly in postmenopausal women, and further research is warranted to confirm their effectiveness in alleviating hepatic steatosis in this population.
MeSH term(s)	Humans ; Female ; Non-alcoholic Fatty Liver Disease/prevention & control ; Non-alcoholic Fatty Liver Disease/epidemiology ; Postmenopause ; Choline/therapeutic use ; Probiotics/therapeutic use ; Isoflavones/therapeutic use
Chemical Substances	Choline (N91BDP6H0X) ; Isoflavones
Language	English
Publishing date	2023-06-08
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2518386-2
ISSN	2072-6643 ; 2072-6643
ISSN (online)	2072-6643
ISSN	2072-6643
DOI	10.3390/nu15122670
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Book: Disease gene identification

DiStefano, Johanna K.

methods and protocols

(Methods in molecular biology ; 700 ; Springer protocols)

2011

Author's details	ed. by Johanna K. DiStefano
Series title	Methods in molecular biology ; 700 Springer protocols
Collection
Language	English
Size	XII, 312 S. : zahlr. Ill., graph. Darst.
Publisher	Humana Press
Publishing place	New York u.a.
Publishing country	United States
Document type	Book
HBZ-ID	HT016580818
ISBN	978-1-61737-953-6 ; 9781617379543 ; 1-61737-953-0 ; 1617379549
Database	Catalogue ZB MED Medicine, Health

In stock of ZB MED Cologne/Königswinter

Shelf mark	Loan status	Location
2011 A 466	order for loan	Magazin

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Article ; Online: Effects of dietary sugar restriction on hepatic fat in youth with obesity.

Distefano, Johanna K / Gerhard, Glenn S

Minerva pediatrics

2023

Abstract: Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease in children. Like adults, children can develop the progressive form of NAFLD, nonalcoholic steatohepatitis (NASH), which is characterized by hepatic inflammation, often in the ... ...

Abstract	Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease in children. Like adults, children can develop the progressive form of NAFLD, nonalcoholic steatohepatitis (NASH), which is characterized by hepatic inflammation, often in the presence of fibrosis. Children with NAFLD are at higher risk of liver-related complications, metabolic dysfunction, and cardiovascular disease in adulthood. Many factors contribute to the escalating prevalence of NAFLD in the pediatric population, among which are an array of dietary patterns such as overnutrition, poor diet quality, and heavy consumption of fat and sugar, including fructose. Findings from an increasing number of epidemiological studies support a connection between high habitual sugar consumption and NAFLD, especially within the context of obesity, but these studies are not able to demonstrate whether sugar is a contributing factor or instead an indicator of an overall poor diet (or lifestyle) quality. To date, only four randomized controlled dietary interventions assessing the effects of sucrose/fructose restriction on hepatic fat fraction in youth with obesity have been published. The objectives of this review are to summarize the key findings from these dietary interventions to achieve a better understanding of the strength of the relationship between dietary sugar restriction and liver fat reduction, despite their inherent limitations, and to discuss the potential impact of weight loss and fat mass reduction on improvement in hepatic steatosis.
Language	English
Publishing date	2023-06-07
Publishing country	Italy
Document type	Journal Article
ZDB-ID	3062664-X
ISSN	2724-5780
ISSN (online)	2724-5780
DOI	10.23736/S2724-5276.23.07209-9
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Article ; Online: Comprehensive meta-analysis reveals distinct gene expression signatures of MASLD progression.

Piras, Ignazio S / DiStefano, Johanna K

Life science alliance

2024 Volume 7, Issue 6

Abstract: Metabolic dysfunction-associated steatotic liver disease (MASLD) and its progressive form, metabolic dysfunction-associated steatohepatitis (MASH), pose significant risks of severe fibrosis, cirrhosis, and hepatocellular carcinoma. Despite their ... ...

Abstract	Metabolic dysfunction-associated steatotic liver disease (MASLD) and its progressive form, metabolic dysfunction-associated steatohepatitis (MASH), pose significant risks of severe fibrosis, cirrhosis, and hepatocellular carcinoma. Despite their widespread prevalence, the molecular mechanisms underlying the development and progression of these common chronic hepatic conditions are not fully understood. Here, we conducted the most extensive meta-analysis of hepatic gene expression datasets from liver biopsy samples to date, integrating 10 RNA-sequencing and microarray datasets (1,058 samples). Using a random-effects meta-analysis model, we compared over 12,000 shared genes across datasets. We identified 685 genes differentially expressed in MASLD versus normal liver, 1,870 in MASH versus normal liver, and 3,284 in MASLD versus MASH. Integrating these results with genome-wide association studies and coexpression networks, we identified two functionally relevant, validated coexpression modules mainly driven by SMOC2, ITGBL1, LOXL1, MGP, SOD3, and TAT, HGD, SLC25A15, respectively, the latter not previously associated with MASLD and MASH. Our findings provide a comprehensive and robust analysis of hepatic gene expression alterations associated with MASLD and MASH and identify novel key drivers of MASLD progression.
MeSH term(s)	Humans ; Genome-Wide Association Study ; Transcriptome/genetics ; Fatty Liver ; Carcinoma, Hepatocellular/genetics ; Liver Neoplasms/genetics ; Integrin beta1
Chemical Substances	ITGBL1 protein, human ; Integrin beta1
Language	English
Publishing date	2024-04-02
Publishing country	United States
Document type	Meta-Analysis ; Journal Article
ISSN	2575-1077
ISSN (online)	2575-1077
DOI	10.26508/lsa.202302517
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Metabolic dysfunction and nonalcoholic fatty liver disease risk in individuals with a normal body mass index.

DiStefano, Johanna K / Gerhard, Glenn S

Current opinion in gastroenterology

2023 Volume 39, Issue 3, Page(s) 156–162

Abstract: Purpose of review: Nonalcoholic fatty liver disease (NAFLD) is strongly associated with obesity, but is also common in individuals with a normal body mass index (BMI), who also experience the hepatic inflammation, fibrosis, and decompensated cirrhosis ... ...

Abstract	Purpose of review: Nonalcoholic fatty liver disease (NAFLD) is strongly associated with obesity, but is also common in individuals with a normal body mass index (BMI), who also experience the hepatic inflammation, fibrosis, and decompensated cirrhosis associated with NAFLD progression. The clinical evaluation and treatment of NAFLD in this patient population are challenging for the gastroenterologist. A better understanding of the epidemiology, natural history, and outcomes of NAFLD in individuals with normal BMI is emerging. This review examines the relationship between metabolic dysfunction and clinical characteristics associated with NAFLD in normal-weight individuals. Recent findings: Despite a more favorable metabolic profile, normal-weight NAFLD patients exhibit metabolic dysfunction. Visceral adiposity may be a critical risk factor for NAFLD in normal-weight individuals, and waist circumference may be better than BMI for assessing metabolic risk in these patients. Although screening for NAFLD is not presently recommended, recent guidelines may assist clinicians in the diagnosis, staging, and management of NAFLD in individuals with a normal BMI. Summary: Individuals with a normal BMI likely develop NAFLD as a result of different etiologies. Subclinical metabolic dysfunction may be a key component of NAFLD in these patients, and efforts to better understand this relationship in this patient population are needed.
MeSH term(s)	Humans ; Non-alcoholic Fatty Liver Disease/complications ; Non-alcoholic Fatty Liver Disease/epidemiology ; Non-alcoholic Fatty Liver Disease/diagnosis ; Body Mass Index ; Risk Factors ; Obesity/complications ; Obesity/epidemiology ; Liver Cirrhosis/etiology ; Liver Cirrhosis/complications
Language	English
Publishing date	2023-03-01
Publishing country	United States
Document type	Review ; Journal Article
ZDB-ID	632571-3
ISSN	1531-7056 ; 0267-1379
ISSN (online)	1531-7056
ISSN	0267-1379
DOI	10.1097/MOG.0000000000000920
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 2072: Show issues

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Jg. 1995 - 2021: Lesesall (1.OG)
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Article ; Online: NAFLD and NASH in Postmenopausal Women: Implications for Diagnosis and Treatment.

DiStefano, Johanna K

Endocrinology

2020 Volume 161, Issue 10

Abstract: Nonalcoholic fatty liver disease (NAFLD) prevalence in women is increasing worldwide. Women of reproductive age have lower rates of NAFLD compared with men; however, this protection is lost following the menopausal transition when NAFLD prevalence in ... ...

Abstract	Nonalcoholic fatty liver disease (NAFLD) prevalence in women is increasing worldwide. Women of reproductive age have lower rates of NAFLD compared with men; however, this protection is lost following the menopausal transition when NAFLD prevalence in postmenopausal women becomes similar to or surpasses that in age-matched male counterparts. Ongoing epidemiological, clinical, and experimental studies indicate greater NAFLD risk and higher rates of severe hepatic fibrosis in postmenopausal women relative to premenopausal women, and that older women with NAFLD experience greater mortality than men. Investigations involving ovariectomized animal models demonstrate a causal relationship between estrogen deficiency and heightened susceptibility to the development of fatty liver and steatohepatitis, although dietary factors may exacerbate this complex relationship. The accumulated findings suggest that a better understanding of the interplay among menopausal status, metabolic comorbidities, and sex steroids in NAFLD pathogenesis is needed. Further, the mechanisms underlying the difference in NAFLD risk between postmenopausal and premenopausal women remain incompletely understood. The goals of this review are to summarize studies of NAFLD risk in postmenopausal women, discuss results from animal models of estrogen deficiency, and explore the development of NAFD within the context of altered sex hormone profiles resulting from the menopausal transition. Potential implications for the prevention, diagnosis, and treatment of NAFLD in this relatively understudied cohort are also addressed.
MeSH term(s)	Adult ; Age of Onset ; Animals ; Diagnostic Techniques, Endocrine ; Estrogens/blood ; Estrogens/deficiency ; Female ; Humans ; Middle Aged ; Non-alcoholic Fatty Liver Disease/blood ; Non-alcoholic Fatty Liver Disease/diagnosis ; Non-alcoholic Fatty Liver Disease/epidemiology ; Non-alcoholic Fatty Liver Disease/therapy ; Postmenopause/physiology ; Prevalence ; Risk Factors
Chemical Substances	Estrogens
Language	English
Publishing date	2020-07-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/endocr/bqaa134
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Article ; Online: Fructose-mediated effects on gene expression and epigenetic mechanisms associated with NAFLD pathogenesis.

DiStefano, Johanna K

Cellular and molecular life sciences : CMLS

2019 Volume 77, Issue 11, Page(s) 2079–2090

Abstract: Nonalcoholic fatty liver disease (NAFLD) is a chronic, frequently progressive condition that develops in response to excessive hepatocyte fat accumulation (i.e., steatosis) in the absence of significant alcohol consumption. Liver steatosis develops as a ... ...

Abstract	Nonalcoholic fatty liver disease (NAFLD) is a chronic, frequently progressive condition that develops in response to excessive hepatocyte fat accumulation (i.e., steatosis) in the absence of significant alcohol consumption. Liver steatosis develops as a result of imbalanced lipid metabolism, driven largely by increased rates of de novo lipogenesis and hepatic fatty acid uptake and reduced fatty acid oxidation and/or disposal to the circulation. Fructose is a naturally occurring simple sugar, which is most commonly consumed in modern diets in the form of sucrose, a disaccharide comprised of one molecule of fructose covalently bonded with one molecule of glucose. A number of observational and experimental studies have demonstrated detrimental effects of dietary fructose consumption not only on diverse metabolic outcomes such as insulin resistance and obesity, but also on hepatic steatosis and NAFLD-related fibrosis. Despite the compelling evidence that excessive fructose consumption is associated with the presence of NAFLD and may even promote the development and progression of NAFLD to more clinically severe phenotypes, the molecular mechanisms by which fructose elicits effects on dysregulated liver metabolism remain unclear. Emerging data suggest that dietary fructose may directly alter the expression of genes involved in lipid metabolism, including those that increase hepatic fat accumulation or reduce hepatic fat removal. The aim of this review is to summarize the current research supporting a role for dietary fructose intake in the modulation of transcriptomic and epigenetic mechanisms underlying the pathogenesis of NAFLD.
MeSH term(s)	Animals ; DNA Methylation ; Dietary Sugars/adverse effects ; Dietary Sugars/metabolism ; Disease Models, Animal ; Epigenesis, Genetic ; Fructose/adverse effects ; Fructose/metabolism ; Humans ; Lipid Metabolism ; Non-alcoholic Fatty Liver Disease/etiology ; Non-alcoholic Fatty Liver Disease/genetics ; Non-alcoholic Fatty Liver Disease/metabolism ; Non-alcoholic Fatty Liver Disease/pathology ; Transcriptome
Chemical Substances	Dietary Sugars ; Fructose (30237-26-4)
Language	English
Publishing date	2019-10-25
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-019-03390-0
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: NAFLD in normal weight individuals.

DiStefano, Johanna K / Gerhard, Glenn S

Diabetology & metabolic syndrome

2022 Volume 14, Issue 1, Page(s) 45

Abstract: Nonalcoholic fatty liver disease (NAFLD) can develop in lean individuals. Despite a better metabolic profile, the risk of disease progression to hepatic inflammation, fibrosis, and decompensated cirrhosis in the lean is similar to that in obesity-related ...

Abstract	Nonalcoholic fatty liver disease (NAFLD) can develop in lean individuals. Despite a better metabolic profile, the risk of disease progression to hepatic inflammation, fibrosis, and decompensated cirrhosis in the lean is similar to that in obesity-related NAFLD and lean individuals may experience more severe hepatic consequences and higher mortality relative to those with a higher body mass index (BMI). In the absence of early symptoms and abnormal laboratory findings, lean individuals are not likely to be screened for NAFLD or related comorbidities; however, given the progressive nature of the disease and the increased risk of morbidity and mortality, a clearer understanding of the natural history of NAFLD in lean individuals, as well as efforts to raise awareness of the potential health risks of NAFLD in lean individuals, are warranted. In this review, we summarize available data on NAFLD prevalence, clinical characteristics, outcomes, and mortality in lean individuals and discuss factors that may contribute to the development of NAFLD in this population, including links between dietary and genetic factors, menopausal status, and ethnicity. We also highlight the need for greater representation of lean individuals in NAFLD-related clinical trials, as well as more studies to better characterize lean NAFLD, develop improved screening algorithms, and determine specific treatment strategies based on underlying etiology.
Language	English
Publishing date	2022-03-24
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2518786-7
ISSN	1758-5996
ISSN	1758-5996
DOI	10.1186/s13098-022-00814-z
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Article ; Online: The Emerging Role of Long Noncoding RNAs in Human Disease.

DiStefano, Johanna K

Methods in molecular biology (Clifton, N.J.)

2018 Volume 1706, Page(s) 91–110

Abstract: Only a small fraction of the human genome corresponds to protein-coding genes. Historically, the vast majority of genomic sequence was dismissed as transcriptionally silent, but recent large-scale investigations have instead revealed a rich array of ... ...

Abstract	Only a small fraction of the human genome corresponds to protein-coding genes. Historically, the vast majority of genomic sequence was dismissed as transcriptionally silent, but recent large-scale investigations have instead revealed a rich array of functionally significant elements, including non-protein-coding transcripts, within the noncoding regions of the human genome. Long noncoding RNAs (lncRNAs), a class of noncoding transcripts with lengths >200 nucleotides, are pervasively transcribed in the genome, and have been shown to bind DNA, RNA, and protein. LncRNAs exert effects through a variety of mechanisms that include guiding chromatin-modifying complexes to specific genomic loci, providing molecular scaffolds, modulating transcriptional programs, and regulating miRNA expression. An increasing number of experimental studies are providing evidence that lncRNAs mediate disease pathogenesis, thereby challenging the concept that protein-coding genes are the sole contributors to the development of human disease. This chapter highlights recent findings linking lncRNAs with human diseases of complex etiology, including hepatocellular carcinoma, Alzheimer's disease, and diabetes.
MeSH term(s)	Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Carcinoma, Hepatocellular/genetics ; Carcinoma, Hepatocellular/metabolism ; Carcinoma, Hepatocellular/pathology ; Chromatin/genetics ; Chromatin/metabolism ; Chromatin Assembly and Disassembly ; Diabetes Mellitus/genetics ; Diabetes Mellitus/metabolism ; Diabetes Mellitus/pathology ; Gene Expression Regulation, Neoplastic ; Genome, Human ; Humans ; Liver Neoplasms/genetics ; Liver Neoplasms/metabolism ; Liver Neoplasms/pathology ; RNA, Long Noncoding/biosynthesis ; RNA, Long Noncoding/genetics ; RNA, Neoplasm/biosynthesis ; RNA, Neoplasm/genetics ; Transcription, Genetic
Chemical Substances	Chromatin ; RNA, Long Noncoding ; RNA, Neoplasm
Language	English
Publishing date	2018-02-08
Publishing country	United States
Document type	Journal Article ; Review
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-7471-9_6
Database	MEDical Literature Analysis and Retrieval System OnLINE

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