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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.

Barber G.N.,University of Miami
Immunological Reviews

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. Source

Hansell D.A.,University of Miami
Annual Review of Marine Science

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. Source

Wahlestedt C.,University of Miami
Nature Reviews Drug Discovery

The majority of currently available drugs and tool compounds exhibit an inhibitory mechanism of action and there is a relative lack of pharmaceutical agents that are capable of increasing the activity of effectors or pathways for therapeutic benefit. Indeed, the upregulation of many genes, including tumour suppressors, growth factors, transcription factors and genes that are deficient in various genetic diseases, would be desired in specific situations. Recently, key roles for regulatory long non-coding RNAs (lncRNAs) in the regulation of gene expression have begun to emerge. lncRNAs can positively or negatively regulate gene expression and chromatin architecture. Here, we review the current understanding of the mechanisms of action of lncRNAs and their roles in disease, focusing on recent work in the design of inhibitors of the natural antisense transcript (NAT) class of lncRNAs, known as antagoNAT oligonucleotides, and the issues associated with their potential therapeutic application. Source

Berg LLC and University of Miami | Date: 2015-01-13

The invention provides compositions comprising Eno1 for delivery to a muscle. Further, the invention provides a method for normalizing blood glucose in a subject with elevated blood glucose, comprising administering to the subject enolase 1 (Eno1), thereby normalizing blood glucose in the subject. The invention also provides methods of treating one or more conditions including impaired glucose tolerance, insulin resistance, pre-diabetes, and diabetes, especially type 2 diabetes in a subject, comprising administering to the subject enolase 1 (Eno1), thereby treating the condition in the subject. In certain methods of the invention, the Eno1 is delivered to muscle.

University of Miami | Date: 2015-07-29

The invention relates to the fields of medicine, immunology, and oncology. More specifically, the invention relates to methods and compositions for inducing an immune response against a tumor in an animal subject. The invention provides that a lung cancer cell or other tumor cells, genetically modified to express a nucleic acid encoding CD80 (B7.1) and a nucleic acid encoding an HLA antigen, and method for stimulating an immune response to a tumor with the tumor cell so genetically modified. The invention additionally provides a method of inhibiting a tumor, including a cancer such as lung cancer, by administering an allogeneic tumor cell, for example a cancer tumor cell such as a lung cancer tumor cell, genetically modified to express a nucleic acid encoding CD80 (B7.1) and a nucleic acid encoding an HLA antigen.

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