Aryl hydrocarbon hydroxylase inducibility is not altered in bladder cancer patients or their progeny

Paigen, Beverly; Ward, Elizabeth; Steenland, Kyle; Havens, Mary Bohne; Sartori, Pamela

doi:10.1002/ijc.2910230307

Cited by 17 publications

(2 citation statements)

References 15 publications

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“…The formalin-fixed hearts were embedded in gelatin and sectioned on a cryostat as described (10,13). The number of oil red Q staining lesions was counted in a standardized region of the aorta as described (13).…”

Section: Methodsmentioning

confidence: 99%

Ath-1, a gene determining atherosclerosis susceptibility and high density lipoprotein levels in mice.

Paigen¹,

Mitchell²,

Reue³

et al. 1987

Proc. Natl. Acad. Sci. U.S.A.

250

172

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High density lipoprotein (HDL) is the major plasma lipoprotein found in mice fed normal laboratory chow containing 4% fat. When female mice from some inbred strains, such as C57BL/6, are fed a high fat diet (1.25% cholesterol, 15% fat, and 0.5% cholic acid), the levels of HDL-cholesterol decrease by about 50%, and lipid staining lesions form in the aorta within 14 weeks. In other strains of mice, such as C3H and BALB/c, HDL-lipid levels decrease only slightly, and few or no aortic lesions are observed at 14 weeks.

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Section: Methodsmentioning

confidence: 99%

Ath-1, a gene determining atherosclerosis susceptibility and high density lipoprotein levels in mice.

Paigen¹,

Mitchell²,

Reue³

et al. 1987

Proc. Natl. Acad. Sci. U.S.A.

250

172

View full text Add to dashboard Cite

show abstract

“…However, due to the ease of genetic and physical manipulation of mice, mice are the most popular animal models of atherosclerosis. One of the first models of atherosclerosis in mice was the hypercholesterolemia model developed by Paigen et al [101–104]. It was found that only the C57BL/6J strain could develop atherosclerosis if hypercholesterolemia was induced by genetic mutation and high-fat diet.…”

Section: Atherosclerosis and The Endotheliummentioning

confidence: 99%

The role of endothelial mechanosensitive genes in atherosclerosis and omics approaches

Simmons

Kumar

2016

Archives of Biochemistry and Biophysics

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Atherosclerosis is the leading cause of morbidity and mortality in the U.S., and is a multifactorial disease that preferentially occurs in regions of the arterial tree exposed to disturbed blood flow. The detailed mechanisms by which d-flow induces atherosclerosis involve changes in the expression of genes, epigenetic patterns, and metabolites of multiple vascular cells, especially endothelial cells. This review presents an overview of endothelial mechanobiology and its relation to the pathogenesis of atherosclerosis with special reference to the anatomy of the artery and the underlying fluid mechanics, followed by a discussion of a variety of experimental models to study the role of fluid mechanics and atherosclerosis. Various in vitro and in vivo models to study the role of flow in endothelial biology and pathobiology are discussed in this review. Furthermore, strategies used for the global profiling of the genome, transcriptome, miRNA-nome, DNA methylome, and metabolome, as they are important to define the biological and pathophysiological mechanisms of atherosclerosis. These “omics” approaches, especially those which derive data based on a single animal model, provide unprecedented opportunities to not only better understand the pathophysiology of atherosclerosis development in a holistic and integrative manner, but also to identify novel molecular and diagnostic targets.

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Concepts in causality:Chemically induced human urinary bladder cancer

Lower¹

1982

Cancer

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A significant portion of the incidence of human urinary bladder cancer can be attributed to occupational and cultural (tobacco smoking) situations associated with exposures to various arylamines, many of which represent established human carcinogens. A brief historical overview of research in bladder cancer causality indicates that the identification of causal agents and causal mechanism has been approached and rests upon information gathered at the organismal (geographical/historical), cellular, and molecular levels of biologic organization. This viewpoint speaks of a natural evolution within the biomedical sciences; a natural evolution from descriptive approaches to mechanistic approaches; and a natural evolution from more or less independent discipline-oriented approaches to hierarchically organized multidisciplinary approaches. Available information relevant to bladder cancer causality can be readily integrated into general conceptual frameworks to yield a hierarchial view of the natural history of urinary bladder cancer, a view consistent with contemporary natural systems and information theory and perhaps relevant also to other chemically induced epithelial cancers. Such frameworks are useful in appreciating the spatial and temporal boundaries and interrelationships in causality and the conceptual interrelationships within the biomedical sciences. Recent approaches in molecular epidemiology and the assessment of relative individual susceptibility to bladder cancer indicate that such frameworks are useful in forming hypotheses.

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Aryl hydrocarbon hydroxylase inducibility is not altered in bladder cancer patients or their progeny

Cited by 17 publications

References 15 publications

Ath-1, a gene determining atherosclerosis susceptibility and high density lipoprotein levels in mice.

Ath-1, a gene determining atherosclerosis susceptibility and high density lipoprotein levels in mice.

The role of endothelial mechanosensitive genes in atherosclerosis and omics approaches

Concepts in causality:Chemically induced human urinary bladder cancer

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