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Institution

University of Arkansas for Medical Sciences

EducationLittle Rock, Arkansas, United States
About: University of Arkansas for Medical Sciences is a education organization based out in Little Rock, Arkansas, United States. It is known for research contribution in the topics: Population & Health care. The organization has 14077 authors who have published 26012 publications receiving 973592 citations. The organization is also known as: UAMS.


Papers
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Journal ArticleDOI
15 Jul 2002-Blood
TL;DR: High levels of soluble syndecan-1 present in patients with myeloma may contribute directly to the growth and dissemination of the malignant cells and thus to poor prognosis.

191 citations

Journal ArticleDOI
TL;DR: It is shown that knock-in mice expressing a mutated nonsheddable p55TNFR develop Toll-like receptor–dependent innate immune hyperreactivity, which renders their immune system more efficient at controlling intracellular bacterial infections.
Abstract: Tumor necrosis factor (TNF) is a potent cytokine exerting critical functions in the activation and regulation of immune and inflammatory responses. Due to its pleiotropic activities, the amplitude and duration of TNF function must be tightly regulated. One of the mechanisms that may have evolved to modulate TNF function is the proteolytic cleavage of its cell surface receptors. In humans, mutations affecting shedding of the p55TNF receptor (R) have been linked with the development of the TNFR-associated periodic syndromes, disorders characterized by recurrent fever attacks and localized inflammation. Here we show that knock-in mice expressing a mutated nonsheddable p55TNFR develop Toll-like receptor–dependent innate immune hyperreactivity, which renders their immune system more efficient at controlling intracellular bacterial infections. Notably, gain of function for antibacterial host defenses ensues at the cost of disbalanced inflammatory reactions that lead to pathology. Mutant mice exhibit spontaneous hepatitis, enhanced susceptibility to endotoxic shock, exacerbated TNF-dependent arthritis, and experimental autoimmune encephalomyelitis. These results introduce a new concept for receptor shedding as a mechanism setting up thresholds of cytokine function to balance resistance and susceptibility to disease. Assessment of p55TNFR shedding may thus be of prognostic value in infectious, inflammatory, and autoimmune diseases.

191 citations

Journal ArticleDOI
TL;DR: Findings suggest that a κB-binding transcription factor can act as a coordinator of neuroprotective gene expression in response to cytokines, as well as protect neuronal cells against calcium-mediated damage.

191 citations

Journal ArticleDOI
TL;DR: Tumors that present with complex genetic alterations, even those with a benign histological grade, are potentially aggressive and require closer follow up and the FISH method appears to be more accurate than the standard cytogenetic one in detecting these alterations.
Abstract: Object. The malignant progression of benign tumors is well documented in gliomas and other systemic lesions. It is also well known that some meningiomas become progressively aggressive despite their original benign status. The theory of clonal evolution is widely believed to explain malignant progression in meningioma; however, the data used to explain stepwise progression have typically been derived from the cytogenetic analysis of different types of tumors of different grades and in different patients. In this study, the authors examined the data obtained in a group of patients with meningiomas that showed clear histopathological progression toward a higher grade of malignancy and then analyzed the underlying cytogenetic findings. Methods. Among 175 patients with recurrent meningiomas, 11 tumors showed a histopathological progression toward a higher grade that was associated with an aggressive clinical course. Six tumors progressed to malignancy and five to the atypical category over a period averaging ...

191 citations

Journal ArticleDOI
TL;DR: Since 2005, the number of invasive pneumococcal infections in children has increased at 8 children's hospitals, primarily as a result of serotype 19A isolates, one third of which were resistant to multiple antibiotics in 2007 and 2008.
Abstract: OBJECTIVE: The purpose of this study was to monitor the clinical and microbiologic features of invasive infections caused by Streptococcus pneumoniae among children before and after the introduction of the 7-valent pneumococcal conjugate vaccine (PCV7). DESIGN: We conducted a 15-year prospective surveillance study of all invasive pneumococcal infections in children. The sample included infants and children at 8 children9s hospitals in the United States with culture-proven invasive S pneumoniae infections. RESULTS: Since the implementation of routine PCV7 immunization in 2000, invasive infections have decreased yearly from 2001 through 2004, to a nadir of 151 infections; the rate then increased from 2005 through 2008. Compared with the pre-PCV7 era, a greater proportion of children with invasive pneumococcal infection had an underlying condition in the post-PCV7 period. Compared with the total number of annual admissions, the number of 19A isolates increased significantly from 2001 to 2008 ( P CONCLUSIONS: Since 2005, the number of invasive pneumococcal infections in children has increased at 8 children9s hospitals, primarily as a result of serotype 19A isolates, one third of which were resistant to multiple antibiotics in 2007 and 2008. Continued surveillance is necessary to detect emerging serotypes after the planned introduction of 13-valent or other pneumococcal vaccines.

191 citations


Authors

Showing all 14187 results

NameH-indexPapersCitations
Hagop M. Kantarjian2043708210208
Yusuke Nakamura1792076160313
Kenneth C. Anderson1781138126072
David R. Williams1782034138789
Yang Yang1712644153049
John E. Morley154137797021
Jeffrey L. Cummings148833116067
Hugh A. Sampson14781676492
Michael J. Keating140116976353
Kristine Yaffe13679472250
Nancy J. Cox135778109195
Stephen W. Scherer13568585752
Nikhil C. Munshi13490667349
Siamon Gordon13142077948
Jian-Guo Bian128121980964
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202332
2022156
20211,609
20201,410
20191,214
20181,251