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Coral Gables, FL, United States

The University of Miami is a private, nonsectarian university located in Coral Gables, Florida, United States. As of 2012, the university currently enrolls 15,613 students in 12 separate colleges, including a medical school located in Miami's Civic Center neighborhood, a law school on the main campus, and a school focused on the study of oceanography and atmospheric science on Virginia Key. These colleges offer approximately 115 undergraduate, 114 master's, 51 doctoral, and two professional areas of study. Over the years, the University's students have represented all 50 states and close to 150 foreign countries. With more than 13,000 full and part-time faculty and staff, UM is the sixth largest employer in Miami-Dade County.Research is a component of each academic division, with UM attracting $346.6 million per year in sponsored research grants. UM offers a large library system with over 3.1 million volumes and exceptional holdings in Cuban heritage and music. UM also offers a wide range of student activities, including fraternities and sororities, a student newspaper and radio station. UM's intercollegiate athletic teams, collectively known as the Miami Hurricanes, compete in Division I of the National Collegiate Athletic Association, and its football team has won five national championships since 1983. Wikipedia.


Kaifer A.E.,University of Miami
Accounts of Chemical Research | Year: 2014

ConspectusThe cucurbit[n]uril (CBn) host family consists of a group of rigid macrocyclic hosts with barrel-like shapes and limited solubility in aqueous media. These hosts are capable of reaching high binding affinities with positively charged hydrophobic guests. In optimum cases, equilibrium association constant (K) values as high as 1017 M-1 have been reported, exceeding the binding affinity of the avidin-biotin host-guest pair. The synthetic CBn receptors have shattered the notion that highly stable noncovalent complexes can form only when one of the partners is a molecule of biological origin.The work described in this Account is concerned with the development of methods geared toward the reversible modulation of the binding affinity of CBn inclusion complexes under mild conditions. A good fraction of the research work has dealt with redox active guests, such as 4,4′-bipyridinium (viologen), ferrocene, and cobaltocenium derivatives. Our experimental results show that the thermodynamics and kinetics of the electron transfer reactions of these compounds can be substantially altered by complexation with CBn hosts, and therefore, electron transfer reactions can be used to exert a measure of control on the overall binding affinity of the CBn complexes. We have also developed systems in which proton transfer reactions have a strong effect on the binding affinity. With more structurally elaborate guests containing more than one adjacent binding sites, proton transfer reactions may affect the average location of the CBn host within the complexes.A series of guest compounds containing paramagnetic 2,2,6,6- tetramethylpiperidine-1-oxyl (TEMPO) residues also exhibit interesting binding properties with CB7 and CB8. The latter host forms a very stable host-guest pair with TEMPO subunits, in which the nitroxide group resides inside the host cavity. Finally, with suitable ditopic guests, we have detected distinct microscopic complexes using experimental techniques with relatively slow time scales, such as NMR spectroscopy. These unusual findings are the result of the considerable thermodynamic and kinetic stability of CBn inclusion complexes. © 2014 American Chemical Society.


Barber G.N.,University of Miami
Immunological Reviews | Year: 2011

The innate immune system is responsible for detecting microbial invasion of the cell and for stimulating host defense countermeasures. These anti-pathogen procedures include the transcriptional activation of powerful antiviral genes such as the type I interferons (IFNs) or the triggering of inflammatory responses through interleukin-1 (IL-1) production. Over the past decade, key cellular sensors responsible for triggering innate immune signaling pathways and host defense have started to be resolved and include the Toll-like receptor (TLR), RIG-I-like helicase, and the cytoplasmic nucleotide-binding oligermerization domain-like receptor families. These sensors recognize non-self pathogen-associated molecular patterns such as microbial lipopolysaccharides and nucleic acids. For example, TLR9 has evolved to detect CpG DNA commonly found in bacteria and viruses and to initiate the production of IFN and other cytokines. In contrast, AIM2 (absent in melanoma 2) has been shown to be essential for mediating inflammatory responses involving IL-1β following the sensing of microbial DNA. Recently, a molecule referred to as STING (stimulator of IFN genes) was demonstrated as being vital for recognizing cytoplasmic DNA and for activating the production of innate immune genes in response to a variety of DNA pathogens and even certain RNA viruses. Comprehending the mechanisms of intracellular DNA-mediated innate immune signaling may lead to the design of new adjuvant concepts that will facilitate vaccine development and may provide important information into the origins of autoimmune disease. © 2011 John Wiley & Sons A/S.


Hansell D.A.,University of Miami
Annual Review of Marine Science | Year: 2013

Marine dissolved organic carbon (DOC) exhibits a spectrum of reactivity, from very fast turnover of the most bioavailable forms in the surface ocean to long-lived materials circulating within the ocean abyss. These disparate reactivities group DOC by fractions with distinctive functions in the cycling of carbon, ranging from support of the microbial loop to involvement in the biological pump to a hypothesized major source/sink of atmospheric CO2 driving paleoclimate variability. Here, the major fractions constituting the global ocean's recalcitrant DOC pool are quantitatively and qualitatively characterized with reference to their roles in carbon biogeochemistry. A nomenclature for the fractions is proposed based on those roles. © 2013 by Annual Reviews. All rights reserved.


Roper S.D.,University of Miami
Seminars in Cell and Developmental Biology | Year: 2013

Taste buds are peripheral chemosensory organs situated in the oral cavity. Each taste bud consists of a community of 50-100. cells that interact synaptically during gustatory stimulation. At least three distinct cell types are found in mammalian taste buds - Type I cells, Receptor (Type II) cells, and Presynaptic (Type III) cells. Type I cells appear to be glial-like cells. Receptor cells express G protein-coupled taste receptors for sweet, bitter, or umami compounds. Presynaptic cells transduce acid stimuli (sour taste). Cells that sense salt (NaCl) taste have not yet been confidently identified in terms of these cell types. During gustatory stimulation, taste bud cells secrete synaptic, autocrine, and paracrine transmitters. These transmitters include ATP, acetylcholine (ACh), serotonin (5-HT), norepinephrine (NE), and GABA. Glutamate is an efferent transmitter that stimulates Presynaptic cells to release 5-HT. This chapter discusses these transmitters, which cells release them, the postsynaptic targets for the transmitters, and how cell-cell communication shapes taste bud signaling via these transmitters. © 2012 Elsevier Ltd.


Endothelial progenitor cells (EPCs) contribute to the regeneration of endothelium. Aging-associated senescence results in reduced number and function of EPCs, potentially contributing to increased cardiac risk, reduced angiogenic capacity, and impaired cardiac repair effectiveness. The mechanisms underlying EPC senescence are unknown. Increasing evidence supports the role of microRNAs in regulating cellular senescence. We aimed to determine whether microRNAs regulated EPC senescence and, if so, what the underlying mechanisms are. To map the microRNA/gene expression signatures of EPC senescence, we performed microRNA profiling and microarray analysis in lineage-negative bone marrow cells from young and aged wild-type and apolipoprotein E-deficient mice. We identified 2 microRNAs, microRNA-10A* (miR-10A*), and miR-21, and their common target gene Hmga2 as critical regulators for EPC senescence. Overexpression of miR-10A* and miR-21 in young EPCs suppressed Hmga2 expression, caused EPC senescence, as evidenced by senescence-associated β-galactosidase upregulation, decreased self-renewal potential, increased p16(Ink4a)/p19(Arf) expression, and resulted in impaired EPC angiogenesis in vitro and in vivo, resembling EPCs derived from aged mice. In contrast, suppression of miR-10A* and miR-21 in aged EPCs increased Hmga2 expression, rejuvenated EPCs, resulting in decreased senescence-associated β-galactosidase expression, increased self-renewal potential, decreased p16(Ink4a)/p19(Arf) expression, and improved EPC angiogenesis in vitro and in vivo. Importantly, these phenotypic changes were rescued by miRNA-resistant Hmga2 cDNA overexpression. miR-10A* and miR-21 regulate EPC senescence via suppressing Hmga2 expression and modulation of microRNAs may represent a potential therapeutic intervention in improving EPC-mediated angiogenesis and vascular repair.

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