scispace - formally typeset
Search or ask a question
Institution

University of Arizona

EducationTucson, Arizona, United States
About: University of Arizona is a education organization based out in Tucson, Arizona, United States. It is known for research contribution in the topics: Population & Galaxy. The organization has 63805 authors who have published 155998 publications receiving 6854915 citations. The organization is also known as: UA & U of A.
Topics: Population, Galaxy, Stars, Redshift, Star formation


Papers
More filters
Journal ArticleDOI
TL;DR: In this article, a flow model is presented by which to view the "life history" or processes of systemic context of any material element, and different refuse disposal patterns are examined as they affect artifact location and association.
Abstract: The cultural aspect of the processes responsible for forming the archaeological record is argued to be an underdeveloped branch of archaeological theory. A flow model is presented by which to view the "life history" or processes of systemic context of any material element. This model accounts for the production of a substantial portion of the archaeological record. The basic processes of this model are: procurement, manufacture, use, maintenance, and discard. Refuse labels the state of an element in archaeological context. The spatial implications of the model suggest a largely untapped source of behavioral information. Differential refuse disposal patterns are examined as they affect artifact location and association. The meaning of element relative frequencies in refuse is discussed.

942 citations

Journal ArticleDOI
TL;DR: Evidence is provided to support the notion that decreasedvagal function precedes the development of a number of risk factors and that modification of risk profiles in the direction of lower risk is associated with increased vagal function.

940 citations

Journal ArticleDOI
TL;DR: A facile method to prepare chemically stable and processable polymeric materials through the direct copolymerization of elemental sulfur with vinylic monomers is reported, which leads to well-defined sulfur-rich micropatterned films created by imprint lithography.
Abstract: An excess of elemental sulfur is generated annually from hydrodesulfurization in petroleum refining processes; however, it has a limited number of uses, of which one example is the production of sulfuric acid. Despite this excess, the development of synthetic and processing methods to convert elemental sulfur into useful chemical substances has not been investigated widely. Here we report a facile method (termed ‘inverse vulcanization’) to prepare chemically stable and processable polymeric materials through the direct copolymerization of elemental sulfur with vinylic monomers. This methodology enabled the modification of sulfur into processable copolymer forms with tunable thermomechanical properties, which leads to well-defined sulfur-rich micropatterned films created by imprint lithography. We also demonstrate that these copolymers exhibit comparable electrochemical properties to elemental sulfur and could serve as the active material in Li–S batteries, exhibiting high specific capacity (823 mA h g−1 at 100 cycles) and enhanced capacity retention. A polymerization method for converting elemental sulfur into a chemically stable, processable and electrochemically active copolymer has been described. This methodology — termed inverse vulcanization — is conducted by a one-step process using liquid sulfur, as both reaction medium and reactant, and vinylic comonomers to form polymeric materials with a high content of sulfur (50–90 wt%).

938 citations

Journal ArticleDOI
TL;DR: Combination therapy with an ACE inhibitor and an ARB was associated with an increased risk of adverse events among patients with diabetic nephropathy and safety outcomes included mortality, hyperkalemia, and acute kidney injury.
Abstract: Background Combination therapy with angiotensin-converting–enzyme (ACE) inhibitors and angiotensin-receptor blockers (ARBs) decreases proteinuria; however, its safety and effect on the progression of kidney disease are uncertain. Methods We provided losartan (at a dose of 100 mg per day) to patients with type 2 diabetes, a urinary albumin-to-creatinine ratio (with albumin measured in milligrams and creatinine measured in grams) of at least 300, and an estimated glomerular filtration rate (GFR) of 30.0 to 89.9 ml per minute per 1.73 m 2 of body-surface area and then randomly assigned them to receive lisinopril (at a dose of 10 to 40 mg per day) or placebo. The primary end point was the first occurrence of a change in the estimated GFR (a decline of ≥30 ml per minute per 1.73 m 2 if the initial estimated GFR was ≥60 ml per minute per 1.73 m 2 or a decline of ≥50% if the initial estimated GFR was <60 ml per minute per 1.73 m 2 ), end-stage renal disease (ESRD), or death. The secondary renal end point was the first occurrence of a decline in the estimated GFR or ESRD. Safety outcomes included mortality, hyperkalemia, and acute kidney injury. Results The study was stopped early owing to safety concerns. Among 1448 randomly assigned patients with a median follow-up of 2.2 years, there were 152 primary endpoint events in the monotherapy group and 132 in the combination-therapy group (hazard ratio with combination therapy, 0.88; 95% confidence interval [CI], 0.70 to 1.12; P = 0.30). A trend toward a benefit from combination therapy with respect to the secondary end point (hazard ratio, 0.78; 95% CI, 0.58 to 1.05; P = 0.10) decreased with time (P = 0.02 for nonproportionality). There was no benefit with respect to mortality (hazard ratio for death, 1.04; 95% CI, 0.73 to 1.49; P = 0.75) or cardiovascular events. Combination therapy increased the risk of hyperkalemia (6.3 events per 100 person-years, vs. 2.6 events per 100 person-years with monotherapy; P<0.001) and acute kidney injury (12.2 vs. 6.7 events per 100 person-years, P<0.001). Conclusions Combination therapy with an ACE inhibitor and an ARB was associated with an increased risk of adverse events among patients with diabetic nephropathy. (Funded by the Cooperative Studies Program of the Department of Veterans Affairs Office of Research and Development; VA NEPHRON-D ClinicalTrials.gov number, NCT00555217.)

937 citations

Journal ArticleDOI
TL;DR: High-resolution, genome-wide copy number analysis coupled with gene-expression profiling provides genetic evidence that the DLBCL subtypes are distinct diseases that use different oncogenic pathways.
Abstract: Gene-expression profiling has been used to define 3 molecular subtypes of diffuse large B-cell lymphoma (DLBCL), termed germinal center B-cell-like (GCB) DLBCL, activated B-cell-like (ABC) DLBCL, and primary mediastinal B-cell lymphoma (PMBL). To investigate whether these DLBCL subtypes arise by distinct pathogenetic mechanisms, we analyzed 203 DLBCL biopsy samples by high-resolution, genome-wide copy number analysis coupled with gene-expression profiling. Of 272 recurrent chromosomal aberrations that were associated with gene-expression alterations, 30 were used differentially by the DLBCL subtypes (P < 0.006). An amplicon on chromosome 19 was detected in 26% of ABC DLBCLs but in only 3% of GCB DLBCLs and PMBLs. A highly up-regulated gene in this amplicon was SPIB, which encodes an ETS family transcription factor. Knockdown of SPIB by RNA interference was toxic to ABC DLBCL cell lines but not to GCB DLBCL, PMBL, or myeloma cell lines, strongly implicating SPIB as an oncogene involved in the pathogenesis of ABC DLBCL. Deletion of the INK4a/ARF tumor suppressor locus and trisomy 3 also occurred almost exclusively in ABC DLBCLs and was associated with inferior outcome within this subtype. FOXP1 emerged as a potential oncogene in ABC DLBCL that was up-regulated by trisomy 3 and by more focal high-level amplifications. In GCB DLBCL, amplification of the oncogenic mir-17-92 microRNA cluster and deletion of the tumor suppressor PTEN were recurrent, but these events did not occur in ABC DLBCL. Together, these data provide genetic evidence that the DLBCL subtypes are distinct diseases that use different oncogenic pathways.

937 citations


Authors

Showing all 64388 results

NameH-indexPapersCitations
Simon D. M. White189795231645
Julie E. Buring186950132967
David H. Weinberg183700171424
Richard Peto183683231434
Xiaohui Fan183878168522
Dennis S. Charney179802122408
Daniel J. Eisenstein179672151720
David Haussler172488224960
Carlos S. Frenk165799140345
Jian-Kang Zhu161550105551
Tobin J. Marks1591621111604
Todd Adams1541866143110
Jane A. Cauley15191499933
Wei Zheng1511929120209
Daniel L. Schacter14959290148
Network Information
Related Institutions (5)
University of California, San Diego
204.5K papers, 12.3M citations

91% related

Cornell University
235.5K papers, 12.2M citations

90% related

University of Washington
305.5K papers, 17.7M citations

90% related

University of Michigan
342.3K papers, 17.6M citations

90% related

Harvard University
530.3K papers, 38.1M citations

90% related

Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023205
2022994
20217,006
20207,325
20196,716
20186,375