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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
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Journal ArticleDOI
TL;DR: Data demonstrate that MMA(III), an intermediate in in organic arsenic methylation, is highly toxic and again raises the question as to whether methylation of inorganic arsenic is a detoxication process.

674 citations

Journal ArticleDOI
TL;DR: A communication-theory model for the process of image formation is used and it is found that the most likely object has a maximum entropy and is represented by a restoring formula that is positive and not band limited.
Abstract: Given M sampled image values of an incoherent object, what can be deduced as the most likely object? Using a communication-theory model for the process of image formation, we find that the most likely object has a maximum entropy and is represented by a restoring formula that is positive and not band limited. The derivation is an adaptation to optics of a formulation by Jaynes for unbiased estimates of positive probability functions. The restoring formula is tested, via computer simulation, upon noisy images of objects consisting of random impulses. These are found to be well restored, with resolution often exceeding the Rayleigh limit and with a complete absence of spurious detail. The proviso is that the noise in each image input must not exceed about 40% of the signal image. The restoring method is applied to experimental data consisting of line spectra. Results are consistent with those of the computer simulations.

673 citations

Journal ArticleDOI
TL;DR: Findings provide the first demonstration that OT can facilitate amygdala-dependent, socially reinforced learning and emotional empathy in men, as well as two patients with selective bilateral damage to the amygdala.
Abstract: Oxytocin (OT) is becoming increasingly established as a prosocial neuropeptide in humans with therapeutic potential in treatment of social, cognitive, and mood disorders. However, the potential of OT as a general facilitator of human learning and empathy is unclear. The current double-blind experiments on healthy adult male volunteers investigated first whether treatment with intranasal OT enhanced learning performance on a feedback-guided item-category association task where either social (smiling and angry faces) or nonsocial (green and red lights) reinforcers were used, and second whether it increased either cognitive or emotional empathy measured by the Multifaceted Empathy Test. Further experiments investigated whether OT-sensitive behavioral components required a normal functional amygdala. Results in control groups showed that learning performance was improved when social rather than nonsocial reinforcement was used. Intranasal OT potentiated this social reinforcement advantage and greatly increased emotional, but not cognitive, empathy in response to both positive and negative valence stimuli. Interestingly, after OT treatment, emotional empathy responses in men were raised to levels similar to those found in untreated women. Two patients with selective bilateral damage to the amygdala (monozygotic twins with congenital Urbach-Wiethe disease) were impaired on both OT-sensitive aspects of these learning and empathy tasks, but performed normally on nonsocially reinforced learning and cognitive empathy. Overall these findings provide the first demonstration that OT can facilitate amygdala-dependent, socially reinforced learning and emotional empathy in men.

672 citations

Journal ArticleDOI
TL;DR: The authors empirically tested five structural models of corporate bond pricing: those of Merton (1974), Geske (1977), Longstaff and Schwartz (1995), Leland and Toft (1996), and Collin-Dufresne and Goldstein (2001).
Abstract: This article empirically tests five structural models of corporate bond pricing: those of Merton (1974), Geske (1977), Longstaff and Schwartz (1995), Leland and Toft (1996), and Collin-Dufresne and Goldstein (2001). We implement the models using a sample of 182 bond prices from firms with simple capital structures during the period 1986–1997. The conventional wisdom is that structural models do not generate spreads as high as those seen in the bond market, and true to expectations, we find that the predicted spreads in our implementation of the Merton model are too low. However, most of the other structural models predict spreads that are too high on average. Nevertheless, accuracy is a problem, as the newer models tend to severely overstate the credit risk of firms with high leverage or volatility and yet suffer from a spread underprediction problem with safer bonds. The Leland and Toft model is an exception in that it overpredicts spreads on most bonds, particularly those with high coupons. More accurate structural models must avoid features that increase the credit risk on the riskier bonds while scarcely affecting the spreads of the safest bonds. The seminal work of Black and Scholes (1973) and Merton (1974) in the area of corporate bond pricing has spawned an enormous theoretical literature on risky debt pricing. One motivating factor for this burgeoning literature is the perception that the Merton model cannot generate sufficiently high-yield spreads to match those observed in the market. Thus the recent theoretical literature includes a variety of extensions and

672 citations

Journal ArticleDOI
TL;DR: An mRNA decay pathway in which deadenylation leads to either internal cleavage or decapping followed by 5'-->3' exonucleolytic degradation of the mRNA is defined.
Abstract: To determine pathways of mRNA turnover in yeast, we have followed the poly(A) tail removal and degradation of a pulse of newly synthesized transcripts from four different genes. Before decay of both stable and unstable mRNAs initiated, there was a temporal lag during which the poly(A) tail was deadenylated to an oligo(A) length. Altering the deadenylation rate of an mRNA led to a corresponding change in the length of this lag. The rate of deadenylation and the stability of the oligo(A) species varied between mRNAs, explaining the differences in mRNA half-lives. To examine how the transcript body was degraded following deadenylation, we used the strategy of inserting strong RNA secondary structures, which can slow exonucleolytic digestion and thereby trap decay intermediates, into the 3' UTR of mRNAs. Fragments lacking the 5' portion of two different mRNAs accumulated after deadenylation as full-length mRNA levels decreased. Therefore, these results define an mRNA decay pathway in which deadenylation leads to either internal cleavage or decapping followed by 5'-->3' exonucleolytic degradation of the mRNA.

671 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
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023205
2022994
20217,006
20207,325
20196,716
20186,375