scispace - formally typeset
Search or ask a question
Institution

Saint Louis University

EducationSt Louis, Missouri, United States
About: Saint Louis University is a education organization based out in St Louis, Missouri, United States. It is known for research contribution in the topics: Population & Health care. The organization has 18927 authors who have published 34895 publications receiving 1267475 citations. The organization is also known as: SLU & St. Louis University.


Papers
More filters
Journal ArticleDOI
24 Jul 1981-Science
TL;DR: Cloning and sequencing of viral DNA have made possible studies on the structure of the genome and on certain aspects of the biology of the virus, hitherto constrained for a lack of tissue culture systems and laboratory animal models useful in its propagation.
Abstract: Immunochemical investigations of the viral antigens and molecular characterization of the viral DNA have elucidated the nature of the hepatitis B virus infection underlying acute, chronic, and oncogenic disorders of the liver in man. Cloning and sequencing of viral DNA have made possible studies on the structure of the genome and on certain aspects of the biology of the virus, hitherto constrained for a lack of tissue culture systems and laboratory animal models useful in its propagation.

367 citations

Journal ArticleDOI
23 Dec 2010-Nature
TL;DR: It is demonstrated that mH2A is a critical component of chromatin that suppresses the development of malignant melanoma, a highly intractable cutaneous neoplasm.
Abstract: The histone variant mH2A is shown to be expressed at reduced levels in many melanomas. Loss of mH2A promotes tumour growth and metastasis, by transcriptional upregulation of CDK8, a known oncogene. This study therefore reveals a new tumour-suppression mechanism exerted by chromatin modification. The histone variant mH2A is shown to be expressed at reduced levels in many melanomas. Loss of mH2A promotes tumour growth and metastasis via transcriptional upregulation of CDK8, a known oncogene. This study therefore reveals a new tumour suppression mechanism exerted by epigenetic modifications. Cancer is a disease consisting of both genetic and epigenetic changes. Although increasing evidence demonstrates that tumour progression entails chromatin-mediated changes such as DNA methylation, the role of histone variants in cancer initiation and progression currently remains unclear. Histone variants replace conventional histones within the nucleosome and confer unique biological functions to chromatin1,2,3. Here we report that the histone variant macroH2A (mH2A) suppresses tumour progression of malignant melanoma. Loss of mH2A isoforms, histone variants generally associated with condensed chromatin and fine-tuning of developmental gene expression programs1,4,5,6, is positively correlated with increasing malignant phenotype of melanoma cells in culture and human tissue samples. Knockdown of mH2A isoforms in melanoma cells of low malignancy results in significantly increased proliferation and migration in vitro and growth and metastasis in vivo. Restored expression of mH2A isoforms rescues these malignant phenotypes in vitro and in vivo. We demonstrate that the tumour-promoting function of mH2A loss is mediated, at least in part, through direct transcriptional upregulation of CDK8. Suppression of CDK8, a colorectal cancer oncogene7,8, inhibits proliferation of melanoma cells, and knockdown of CDK8 in cells depleted of mH2A suppresses the proliferative advantage induced by mH2A loss. Moreover, a significant inverse correlation between mH2A and CDK8 expression levels exists in melanoma patient samples. Taken together, our results demonstrate that mH2A is a critical component of chromatin that suppresses the development of malignant melanoma, a highly intractable cutaneous neoplasm.

366 citations

Journal Article
TL;DR: Mixed-race or white high-poverty areas and all African American areas were less likely than predominantly white higher-income communities to have access to foods that enable individuals to make healthy choices, according to racial distribution and poverty rates.
Abstract: INTRODUCTION The increase in obesity and disparities in obesity and related chronic diseases across racial and ethnic and income groups have led researchers to focus on the social and environmental factors that influence dietary intake. The question guiding the current study was whether all communities have equal access to foods that enable individuals to make healthy dietary choices. METHODS We conducted audits of community supermarkets and fast food restaurants to assess location and availability of food choices that enable individuals to meet the dietary guidelines established by the U.S. Department of Agriculture (e.g., fruit and vegetable consumption, low-fat options). We used 2000 census data to assess the racial distribution and the percentage of individuals living below the federal poverty level in a defined area of St Louis, Mo. Spatial clustering of supermarkets and fast food restaurants was determined using a spatial scan statistic. RESULTS The spatial distribution of fast food restaurants and supermarkets that provide options for meeting recommended dietary intake differed according to racial distribution and poverty rates. Mixed-race or white high-poverty areas and all African American areas (regardless of income) were less likely than predominantly white higher-income communities to have access to foods that enable individuals to make healthy choices. CONCLUSION Without access to healthy food choices, individuals cannot make positive changes to their diets. If certain eating behaviors are required to reduce chronic disease and promote health, then some communities will continue to have disparities in critical health outcomes unless we increase access to healthy food.

366 citations

Journal ArticleDOI
01 Sep 2011-Surgery
TL;DR: In a group of patients undergoing scheduled colorectal surgery, meaningful changes in functional capacity can be achieved over several weeks of prehabilitation, and patients and those who care for them, especially those with poor physical capacity, should consider aPrehabilitation regimen to enhance functional exercise capacity before colectomy.

366 citations

Journal ArticleDOI
TL;DR: A reduction or increase in preload may induce a diastsolic filling pattern that mimics or masks diastolic dysfunction, respectively, and Relaxation and chamber stiffness were unchanged.
Abstract: We examined the influence of alterations in preload on pulsed Doppler indexes of left ventricular diastolic function in 50 patients including 12 without cardiovascular disease, 29 with coronary artery disease, and nine with critical aortic stenosis. Micromanometer left ventricular pressure was recorded simultaneously with pulsed Doppler echocardiography of left ventricular inflow and M-mode echocardiography of left ventricular diameter. Chamber stiffness constants, kd and kv, were obtained from the diastolic pressure-diameter and pressure-volume relations, respectively. Relaxation was measured by the isovolumic relaxation time constants, TL and TD, derived from the exponential left ventricular pressure decay and maximum negative dP/dt. In 41 patients after nitroglycerin treatment, left ventricular end-diastolic pressure decreased from 18 +/- 5 to 13 +/- 4 mm Hg (p less than 0.001). The ratio of peak early to peak atrial filling velocities and time-velocity integral ratios decreased from 1.08 +/- 0.57 to 0.90 +/- 0.42 (p less than 0.001) and from 1.77 +/- 0.95 to 1.41 +/- 0.71 (p less than 0.001), respectively. The peak early filling velocity and time-velocity integral decreased from 56.1 +/- 15.7 to 49.9 +/- 14.5 cm/sec (p less than 0.001) and from 7.9 +/- 2.7 to 6.8 +/- 2.8 cm (p less than 0.001), respectively. Relaxation (TL, TD, and maximum negative dP/dt) and chamber stiffness (kd and kv) were not impaired after nitroglycerin administration. In 48 patients after ventriculography, left ventricular end-diastolic pressure increased from 18 +/- 6 to 22 +/- 8 mm Hg (p less than 0.001). The peak early and peak atrial filling velocities increased from 57.4 +/- 15.2 to 68.3 +/- 19.7 cm/sec (p less than 0.001) and from 61.0 +/- 22.7 to 69.4 +/- 23.2 cm/sec (p less than 0.01), respectively. As a result, the ratio of peak early to peak atrial filling velocity was unchanged. However, in the aortic stenosis group, the ratio of peak early to peak atrial filling velocity increased from 0.95 +/- 0.64 to 1.10 +/- 0.72 (p less than 0.02). Relaxation and chamber stiffness were unchanged. Thus, a reduction or increase in preload may induce a diastolic filling pattern that mimics or masks diastolic dysfunction, respectively. Preload conditions need to be accounted for when the status of diastolic function is extrapolated from the pulsed Doppler mitral inflow velocity profile.

364 citations


Authors

Showing all 19076 results

NameH-indexPapersCitations
Douglas G. Altman2531001680344
John E. Morley154137797021
Roberto Romero1511516108321
Daniel S. Berman141136386136
Gregory J. Gores14168666269
Thomas J. Smith1401775113919
Richard T. Lee13181062164
George K. Aghajanian12127748203
Reza Malekzadeh118900139272
Robert N. Weinreb117112459101
Leslee J. Shaw11680861598
Thomas J. Ryan11667567462
Josep M. Llovet11639983871
Robert V. Farese11547348754
Michael Horowitz11298246952
Network Information
Related Institutions (5)
University of Pittsburgh
201K papers, 9.6M citations

95% related

University of North Carolina at Chapel Hill
185.3K papers, 9.9M citations

95% related

Yale University
220.6K papers, 12.8M citations

94% related

Duke University
200.3K papers, 10.7M citations

94% related

University of California, San Francisco
186.2K papers, 12M citations

94% related

Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202344
2022233
20211,619
20201,600
20191,457
20181,375