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Institution

University of New Mexico

EducationAlbuquerque, New Mexico, United States
About: University of New Mexico is a education organization based out in Albuquerque, New Mexico, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 28870 authors who have published 64767 publications receiving 2578371 citations. The organization is also known as: UNM & Universitatis Novus Mexico.


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Journal ArticleDOI
TL;DR: Theoretical investigations of entertainment education should pay greater attention to the tremendous variability among entertainment education interventions and to the various resistances to entertainment-education interventions as mentioned in this paper, and also benefit from close investigations of the rhetorical, play, and affective aspects of E-E.
Abstract: With the growing number of entertainment—education (E—E) interventions worldwide, and the extensive evaluation research on their impacts, the time is ripe to explore in—depth the theoretical underpinnings of entertainment—education. This introductory article provides a historical background to this special issue of Communication Theory on entertainment—education, and charts a 5—pronged theoretical agenda for future research on entertainment—education. Theoretical investigations of entertainment—education should pay greater attention to the tremendous variability among entertainment—education interventions and to the various resistances to entertainment—education interventions. E—E theorizing will also benefit from close investigations of the rhetorical, play, and affective aspects of E—E. Further, E—E “effects” research should consider employing a broader understanding of individual, group, and social—level changes and be more receptive to methodological pluralism and measurement ingenuity.

365 citations

Journal ArticleDOI
TL;DR: Although virtually all HPV infections clear within 2 years, the remaining infections have a high potential for persistence and, by implication, progression to precancer and cancer.
Abstract: Background Cervical cancer is caused by persistent infection with human papillomavirus (HPV). Most infections and associated lesions clear spontaneously. It is important to define the determinants and timing of clearance, so that viral persistence can be recognized and managed. Methods We investigated HPV natural history among 4504 subjects from ALTS (Atypical Squamous Cells of Undetermined Significance/Low-Grade Squamous Intraepithelial Lesions Triage Study). A discrete-time Markov model was used to simultaneously describe the prevalence, incidence, and persistence of type-specific HPV infection over 24 months in women with equivocal or mildly abnormal cytological results. Interactions between multiple HPV types infecting the same woman were examined for incidence of new infection (after an HPV-16 infection) and persistence of a current infection within groups defined by phylogenetic relatedness or by carcinogenicity. Results Ninety-one percent (95% credible interval [CI], 90%-92%) of prevalent HPV infections at enrollment cleared within 24 months. The probability that an infection would persist for a further 6 months increased with the duration of infection, from 37% (95% CI, 35%-39%) for a newly observed infection to 65% (95% CI, 61%-70%) for an infection that had already persisted for > or =18 months. No consistent evidence of interactions was found between multiple HPV types regarding the incidence of new infection after an HPV-16 infection or regarding persistence of current HPV infection. Conclusion Although virtually all HPV infections clear within 2 years, the remaining infections have a high potential for persistence and, by implication, progression to precancer and cancer. Once biological and behavioral determinants are controlled for, HPV infections with different types seem to be independent of each other.

365 citations

Journal ArticleDOI
TL;DR: In this article, the aqueous phase oxidation of 5-hydroxymethylfurfural (HMF) to 2,5-furandicarboxylic acid (FDCA) at 295 K and high pH in a semibatch reactor was evaluated.

365 citations

Journal ArticleDOI
05 Jun 2003-Nature
TL;DR: A general model of ecosystem respiration based on the kinetics of metabolic reactions and the scaling of resource use by individual organisms is derived, predicting that fluxes of CO2 and energy are invariant of ecosystem biomass, but are strongly influenced by temperature, variation in cellular metabolism and rates of supply of limiting resources.
Abstract: Understanding energy and material fluxes through ecosystems is central to many questions in global change biology and ecology1,2,3,4,5,6,7,8,9,10,11. Ecosystem respiration is a critical component of the carbon cycle1,5,6,7 and might be important in regulating biosphere response to global climate change1,2,3. Here we derive a general model of ecosystem respiration based on the kinetics of metabolic reactions11,12,13 and the scaling of resource use by individual organisms14,15. The model predicts that fluxes of CO2 and energy are invariant of ecosystem biomass, but are strongly influenced by temperature, variation in cellular metabolism and rates of supply of limiting resources (water and/or nutrients). Variation in ecosystem respiration within sites, as calculated from a network of CO2 flux towers5,7, provides robust support for the model's predictions. However, data indicate that variation in annual flux between sites is not strongly dependent on average site temperature or latitude. This presents an interesting paradox with regard to the expected temperature dependence. Nevertheless, our model provides a basis for quantitatively understanding energy and material flux between the atmosphere and biosphere.

365 citations

Journal ArticleDOI
University of Michigan1, Cornell University2, University of Pennsylvania3, University of Massachusetts Medical School4, Baylor College of Medicine5, University of Naples Federico II6, Spanish National Research Council7, Complutense University of Madrid8, New York University9, University of Rome Tor Vergata10, Boston Children's Hospital11, NewYork–Presbyterian Hospital12, University of Pittsburgh13, University of Paris14, French Institute of Health and Medical Research15, National University of Cuyo16, Albert Einstein College of Medicine17, University of New Mexico18, Goethe University Frankfurt19, Weizmann Institute of Science20, University of Turku21, Sapienza University of Rome22, Virginia Commonwealth University23, St. Jude Children's Research Hospital24, Discovery Institute25, University of Copenhagen26, University of Tromsø27, Eötvös Loránd University28, Merck & Co.29, University of Freiburg30, Babraham Institute31, University of South Australia32, University of Adelaide33, University of Oviedo34, University of Chicago35, University of Graz36, National Institutes of Health37, Queens College38, City University of New York39, University of Tokyo40, University of Zurich41, Austrian Academy of Sciences42, University of British Columbia43, University of California, San Francisco44, Russian Academy of Sciences45, University Medical Center Groningen46, University of Cambridge47, University of Glasgow48, Rutgers University49, University of Padua50, Kazan Federal University51, University of Bern52, University of Oxford53, University of Oslo54, Oslo University Hospital55, Foundation for Research & Technology – Hellas56, University of Crete57, Francis Crick Institute58, Osaka University59, Chinese Academy of Sciences60, Harvard University61, Icahn School of Medicine at Mount Sinai62, Shanghai Jiao Tong University63, Karolinska Institutet64
TL;DR: In this paper, preclinical data linking autophagy dysfunction to the pathogenesis of major human disorders including cancer as well as cardiovascular, neurodegenerative, metabolic, pulmonary, renal, infectious, musculoskeletal, and ocular disorders.
Abstract: Autophagy is a core molecular pathway for the preservation of cellular and organismal homeostasis. Pharmacological and genetic interventions impairing autophagy responses promote or aggravate disease in a plethora of experimental models. Consistently, mutations in autophagy-related processes cause severe human pathologies. Here, we review and discuss preclinical data linking autophagy dysfunction to the pathogenesis of major human disorders including cancer as well as cardiovascular, neurodegenerative, metabolic, pulmonary, renal, infectious, musculoskeletal, and ocular disorders.

365 citations


Authors

Showing all 29120 results

NameH-indexPapersCitations
Bruce S. McEwen2151163200638
David Miller2032573204840
Jing Wang1844046202769
Paul M. Thompson1832271146736
David A. Weitz1781038114182
David R. Williams1782034138789
John A. Rogers1771341127390
George F. Koob171935112521
John D. Minna169951106363
Carlos Bustamante161770106053
Lewis L. Lanier15955486677
Joseph Wang158128298799
John E. Morley154137797021
Fabian Walter14699983016
Michael F. Holick145767107937
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202390
2022595
20213,060
20203,048
20192,779
20182,729