Institution
Ohio State University
Education•Columbus, Ohio, United States•
About: Ohio State University is a education organization based out in Columbus, Ohio, United States. It is known for research contribution in the topics: Population & Cancer. The organization has 102421 authors who have published 222715 publications receiving 8373403 citations. The organization is also known as: Ohio State & The Ohio State University.
Topics: Population, Cancer, Poison control, Galaxy, Context (language use)
Papers published on a yearly basis
Papers
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TL;DR: Although rituximab therapy led to more responders and greater reductions in anti-dsDNA and C3/C4 levels, it did not improve clinical outcomes after 1 year of treatment.
Abstract: Objective
To evaluate the efficacy and safety of rituximab in a randomized, double-blind, placebo-controlled phase III trial in patients with lupus nephritis treated concomitantly with mycophenolate mofetil (MMF) and corticosteroids.
Methods
Patients (n = 144) with class III or class IV lupus nephritis were randomized 1:1 to receive rituximab (1,000 mg) or placebo on days 1, 15, 168, and 182. The primary end point was renal response status at week 52.
Results
Rituximab depleted peripheral CD19+ B cells in 71 of 72 patients. The overall (complete and partial) renal response rates were 45.8% among the 72 patients receiving placebo and 56.9% among the 72 patients receiving rituximab (P = 0.18); partial responses accounted for most of the difference. The primary end point (superior response rate with rituximab) was not achieved. Eight placebo-treated patients and no rituximab-treated patients required cyclophosphamide rescue therapy through week 52. Statistically significant improvements in serum complement C3, C4, and anti–double-stranded DNA (anti-dsDNA) levels were observed among patients treated with rituximab. In both treatment groups, a reduction in anti-dsDNA levels greater than the median reduction was associated with reduced proteinuria. The rates of serious adverse events, including infections, were similar in both groups. Neutropenia, leukopenia, and hypotension occurred more frequently in the rituximab group.
Conclusion
Although rituximab therapy led to more responders and greater reductions in anti-dsDNA and C3/C4 levels, it did not improve clinical outcomes after 1 year of treatment. The combination of rituximab with MMF and corticosteroids did not result in any new or unexpected safety signals.
1,073 citations
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University of Chicago1, University of Arizona2, Fermilab3, Princeton University4, Johns Hopkins University5, University of Pittsburgh6, Carnegie Mellon University7, Yale University8, University of Chile9, University of Tokyo10, New York University11, Space Telescope Science Institute12, California Institute of Technology13, Rochester Institute of Technology14, Pennsylvania State University15, Drexel University16, Ohio State University17
TL;DR: In this paper, the authors describe the target selection and resulting properties of a spectroscopic sample of luminous red galaxies (LRGs) from the imaging data of the Sloan Digital Sky Survey (SDSS).
Abstract: We describe the target selection and resulting properties of a spectroscopic sample of luminous red galaxies (LRGs) from the imaging data of the Sloan Digital Sky Survey (SDSS). These galaxies are selected on the basis of color and magnitude to yield a sample of luminous intrinsically red galaxies that extends fainter and farther than the main flux-limited portion of the SDSS galaxy spectroscopic sample. The sample is designed to impose a passively evolving luminosity and rest-frame color cut to a redshift of 0.38. Additional, yet more luminous red galaxies are included to a redshift of ~0.5. Approximately 12 of these galaxies per square degree are targeted for spectroscopy, so the sample will number over 100,000 with the full survey. SDSS commissioning data indicate that the algorithm efficiently selects luminous (M^+_g ≈ -21.4) red galaxies, that the spectroscopic success rate is very high, and that the resulting set of galaxies is approximately volume limited out to z = 0.38. When the SDSS is complete, the LRG spectroscopic sample will fill over 1 h^(-3) Gpc^3 with an approximately homogeneous population of galaxies and will therefore be well suited to studies of large-scale structure and clusters out to z = 0.5.
1,073 citations
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University of California, San Diego1, Hong Kong University of Science and Technology2, Rockefeller University3, National Institutes of Health4, Keio University5, University of Vienna6, Tufts University7, University of Michigan8, Boston Children's Hospital9, Ohio State University10, University of Texas Southwestern Medical Center11, La Jolla Institute for Allergy and Immunology12
TL;DR: It is proposed that barrier deterioration induced by colorectal-cancer-initiating genetic lesions results in adenoma invasion by microbial products that trigger tumour-elicited inflammation, which in turn drives tumour growth.
Abstract: Approximately 2% of colorectal cancer is linked to pre-existing inflammation known as colitis-associated cancer, but most develops in patients without underlying inflammatory bowel disease. Colorectal cancer often follows a genetic pathway whereby loss of the adenomatous polyposis coli (APC) tumour suppressor and activation of β-catenin are followed by mutations in K-Ras, PIK3CA and TP53, as the tumour emerges and progresses. Curiously, however, 'inflammatory signature' genes characteristic of colitis-associated cancer are also upregulated in colorectal cancer. Further, like most solid tumours, colorectal cancer exhibits immune/inflammatory infiltrates, referred to as 'tumour-elicited inflammation'. Although infiltrating CD4(+) T(H)1 cells and CD8(+) cytotoxic T cells constitute a positive prognostic sign in colorectal cancer, myeloid cells and T-helper interleukin (IL)-17-producing (T(H)17) cells promote tumorigenesis, and a 'T(H)17 expression signature' in stage I/II colorectal cancer is associated with a drastic decrease in disease-free survival. Despite its pathogenic importance, the mechanisms responsible for the appearance of tumour-elicited inflammation are poorly understood. Many epithelial cancers develop proximally to microbial communities, which are physically separated from immune cells by an epithelial barrier. We investigated mechanisms responsible for tumour-elicited inflammation in a mouse model of colorectal tumorigenesis, which, like human colorectal cancer, exhibits upregulation of IL-23 and IL-17. Here we show that IL-23 signalling promotes tumour growth and progression, and development of a tumoural IL-17 response. IL-23 is mainly produced by tumour-associated myeloid cells that are likely to be activated by microbial products, which penetrate the tumours but not adjacent tissue. Both early and late colorectal neoplasms exhibit defective expression of several barrier proteins. We propose that barrier deterioration induced by colorectal-cancer-initiating genetic lesions results in adenoma invasion by microbial products that trigger tumour-elicited inflammation, which in turn drives tumour growth.
1,069 citations
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TL;DR: In this paper, an alternative formulation of the "perfectly matched layer" mesh truncation scheme is introduced, based on using a layer of diagonally anisotropic material to absorb outgoing waves from the computation domain.
Abstract: An alternative formulation of the "perfectly matched layer" mesh truncation scheme is introduced. The present scheme is based on using a layer of diagonally anisotropic material to absorb outgoing waves from the computation domain. The material properties can be chosen such that the interface between the absorbing material and free space is reflection-less for all frequencies, polarizations, and angles of incidence. This approach does not involve a modification of Maxwell's equations and is easy to implement in codes that allow the use of anisotropic material properties.
1,068 citations
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TL;DR: OPC incidence significantly increased during 1983 to 2002 predominantly in developed countries and at younger ages, underscore a potential role for HPV infection on increasing OPC incidence, particularly among men.
Abstract: Purpose Human papillomavirus (HPV) has been identified as the cause of the increasing oropharyngeal cancer (OPC) incidence in some countries. To investigate whether this represents a global phenomenon, we evaluated incidence trends for OPCs and oral cavity cancers (OCCs) in 23 countries across four continents. Methods We used data from the Cancer Incidence in Five Continents database Volumes VI to IX (years 1983 to 2002). Using age-period-cohort modeling, incidence trends for OPCs were compared with those of OCCs and lung cancers to delineate the potential role of HPV vis-a-vis smoking on incidence trends. Analyses were country specific and sex specific. Results OPC incidence significantly increased during 1983 to 2002 predominantly in economically developed countries. Among men, OPC incidence significantly increased in the United States, Australia, Canada, Japan, and Slovakia, despite nonsignificant or significantly decreasing incidence of OCCs. In contrast, among women, in all countries with increasing ...
1,068 citations
Authors
Showing all 103197 results
Name | H-index | Papers | Citations |
---|---|---|---|
Paul M. Ridker | 233 | 1242 | 245097 |
George Davey Smith | 224 | 2540 | 248373 |
Carlo M. Croce | 198 | 1135 | 189007 |
Eric J. Topol | 193 | 1373 | 151025 |
Bernard Rosner | 190 | 1162 | 147661 |
David H. Weinberg | 183 | 700 | 171424 |
Anil K. Jain | 183 | 1016 | 192151 |
Michael I. Jordan | 176 | 1016 | 216204 |
Kay-Tee Khaw | 174 | 1389 | 138782 |
Richard K. Wilson | 173 | 463 | 260000 |
Yang Yang | 164 | 2704 | 144071 |
Brian L Winer | 162 | 1832 | 128850 |
Jian-Kang Zhu | 161 | 550 | 105551 |
Elaine R. Mardis | 156 | 485 | 226700 |
R. E. Hughes | 154 | 1312 | 110970 |