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Albuquerque, NM, United States

The University of New Mexico is a public research university located in Albuquerque, New Mexico, in the United States. It is the state's flagship research institution, the largest post-secondary institution in the state in total enrollment across all campuses, as of 2012, and one of the state's largest employers.Founded in 1889, UNM offers bachelor's, master's, doctoral, and professional degree programs in a wide variety of fields. Its Albuquerque campus currently encompasses over 600 acres , and there are branch campuses in Gallup, Los Alamos, Rio Rancho, Taos, and Los Lunas. UNM is categorized as an RU/VH Research University in the Carnegie Classification of Institutions of Higher Education, with three Nobel laureates affiliated or associated. Wikipedia.

Michener W.K.,University of New Mexico
Trends in ecology & evolution | Year: 2012

Ecology is evolving rapidly and increasingly changing into a more open, accountable, interdisciplinary, collaborative and data-intensive science. Discovering, integrating and analyzing massive amounts of heterogeneous data are central to ecology as researchers address complex questions at scales from the gene to the biosphere. Ecoinformatics offers tools and approaches for managing ecological data and transforming the data into information and knowledge. Here, we review the state-of-the-art and recent advances in ecoinformatics that can benefit ecologists and environmental scientists as they tackle increasingly challenging questions that require voluminous amounts of data across disciplines and scales of space and time. We also highlight the challenges and opportunities that remain. Copyright © 2011 Elsevier Ltd. All rights reserved.

Cavanagh J.F.,University of New Mexico | Frank M.J.,Brown University
Trends in Cognitive Sciences | Year: 2014

Recent advancements in cognitive neuroscience have afforded a description of neural responses in terms of latent algorithmic operations. However, the adoption of this approach to human scalp electroencephalography (EEG) has been more limited, despite the ability of this methodology to quantify canonical neuronal processes. Here, we provide evidence that theta band activities over the midfrontal cortex appear to reflect a common computation used for realizing the need for cognitive control. Moreover, by virtue of inherent properties of field oscillations, these theta band processes may be used to communicate this need and subsequently implement such control across disparate brain regions. Thus, frontal theta is a compelling candidate mechanism by which emergent processes, such as 'cognitive control', may be biophysically realized. © 2014 Elsevier Ltd.

Deretic V.,University of New Mexico
Current Opinion in Immunology | Year: 2012

Autophagy is rapidly developing into a new immunological paradigm. The latest links now include overlaps between autophagy and innate immune signaling via TBK-1 and IKKα/β, and the role of autophagy in inflammation directed by the inflammasome. Autophagy's innate immunity connections include responses to pathogen and damage-associated molecular patterns including alarmins such as HMGB1 and IL-1β, Toll-like receptors, Nod-like receptors including NLRC4, NLRP3 and NLRP4, and RIG-I-like receptors. Autophagic adaptors referred to as SLRs (sequestosome 1/p62-like receptors) are themselves a category of pattern recognition receptors. SLRs empower autophagy to eliminate intracellular microbes by direct capture and by facilitating generation and delivery of antimicrobial peptides, and also serve as inflammatory signaling platforms. SLRs contribute to autophagic control of intracellular microbes, including Mycobacterium tuberculosis, Salmonella, Listeria, Shigella, HIV-1 and Sindbis virus, but act as double-edged sword and contribute to inflammation and cell death. Autophagy roles in innate immunity continue to expand vertically and laterally, and now include antimicrobial function downstream of vitamin D3 action in tuberculosis and AIDS. Recent data expand the connections between immunity-related GTPases and autophagy to include not only IRGM but also several members of the Gbp (guanlyate-binding proteins) family. The efficacy with which autophagy handles microbes, microbial products and sterile endogenous irritants governs whether the outcome will be with suppression of or with excess inflammation, the latter reflected in human diseases that have strong inflammatory components including tuberculosis and Crohn's disease. © 2011 Elsevier Ltd.

Deretic V.,University of New Mexico
Current Opinion in Cell Biology | Year: 2010

Autophagy is a ubiquitous eukaryotic cytoplasmic quality and quantity control pathway. The role of autophagy in cytoplasmic homeostasis seamlessly extends to cell-autonomous defense against intracellular microbes. Recent studies also point to fully integrated, multitiered regulatory and effector connections between autophagy and nearly all facets of innate and adaptive immunity. Autophagy in the immune system as a whole confers measured immune responses; on the flip side, suppression of autophagy can lead to inflammation and tissue damage, as evidenced by Crohn's disease predisposition polymorphisms in autophagy basal apparatus (Atg16L) and regulatory (IRGM) genes. Polymorphisms in the IRGM gene in human populations have also been linked to predisposition to tuberculosis. There are several areas of most recent growth: first, links between autophagy regulators and infectious disease predisposition in human populations; second, demonstration of a role for autophagy in infection control in vivo in animal models; third, the definition of specific antiautophagic defenses in highly evolved pathogens; and fourth, recognition of connections between the ubiquitin system and autophagy of bacteria (and interestingly mitochondria, which are incidentally organelles of bacterial evolutionary origin) via a growing list of modifier and adapter proteins including p62/SQSTM1, NDP52, Atg32, Parkin, and Nix/BNIP3L. © 2010.

Smrt R.D.,University of New Mexico
Stem cells (Dayton, Ohio) | Year: 2010

The maturation of young neurons is regulated by complex mechanisms and dysregulation of this process is frequently found in neurodevepmental disorders. MicroRNAs have been implicated in several steps of neuronal maturation including dendritic and axonal growth, spine development, and synaptogenesis. We demonstrate that one brain-enriched microRNA, miR-137, has a significant role in regulating neuronal maturation. Overexpression of miR-137 inhibits dendritic morphogenesis, phenotypic maturation, and spine development both in brain and cultured primary neurons. On the other hand, a reduction in miR-137 had opposite effects. We further show that miR-137 targets the Mind bomb one (Mib1) protein through the conserved target site located in the 3' untranslated region of Mib1 messenger RNA. Mib1 is an ubiquitin ligase known to be important for neurodevelopment. We show that exogenously expressed Mib1 could partially rescue the phenotypes associated with miR-137 overexpression. These results demonstrate a novel miRNA-mediated mechanism involving miR-137 and Mib1 that function to regulate neuronal maturation and dendritic morphogenesis during development.

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