North Chicago, IL, United States
North Chicago, IL, United States

Rosalind Franklin University of Medicine and Science is a non-profit, private, interprofessional graduate school located in North Chicago, Illinois. It has more than 2,000 students in five schools: the Chicago Medical School, the College of Health Professions, the College of Pharmacy, the School of Graduate and Postdoctoral Studies, and the Dr. William M. Scholl College of Podiatric Medicine.The university is named for Rosalind Franklin, the DNA crystallographer. Photo 51, Dr. Franklin's X-ray diffraction pattern for B-DNA, was pivotal in the history of biology in the twentieth century, and this photograph is the basis for the university's seal and logo.The university offers over 29 study programs in graduate health-related subjects, including PhD programs for medical and basic research.Facilities include a multi-media laboratory, a virtual microscopy lab, a simulation lab, and the Education and Evaluation Center, with high-tech opportunities for education and research.The University is located to the west of the Naval Station Great Lakes and to the south of the Captain James A. Lovell Federal Health Care Center. Wikipedia.


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Patent
Rosalind Franklin University of Medicine, Science and Chinese University of Hong Kong | Date: 2016-08-11

Disclosed herein are methods and compositions for the delivery of polypeptides, including vaccine candidate polypeptides, into mammalian cells comprising the use of photosensitized trypanosomatid organisms. Also disclosed are methods of treatment of trypanosomatid infections comprising administering phthalocyanine compounds or phthalocyanine-treated trypanosomatid microorganisms as vaccines, as well as and polypeptide delivery vectors comprising phthalocyanine-treated trypanosomatid microorganisms.


Patent
Rosalind Franklin University of Medicine, Science and The McLean Hospital Corporation | Date: 2016-11-11

The present disclosure relates generally to compounds comprising oligonucleotides complementary to a Leucine-Rich-Repeat-Kinase (LRRK2) RNA transcript. Certain such compounds are useful for hybridizing to a LRRK2 RNA transcript, including but not limited to a LRRK2 RNA transcript in a cell. In certain embodiments, such hybridization results in modulation of splicing of the LRRK2 transcript. In certain embodiments, such compounds are used to treat one or more symptoms associated with Parkinsons disease.


Santiago J.A.,Rosalind Franklin University of Medicine and Science | Potashkin J.A.,Rosalind Franklin University of Medicine and Science
Trends in Molecular Medicine | Year: 2013

Recent evidence indicates that Parkinson's disease and diabetes, both age-related chronic diseases, share remarkably similar dysregulated pathways. Exposure to environmental factors and genetic susceptibility play a role in the etiology and progression of both diseases. In light of recent findings, an intriguing hypothesis has emerged that suggests that mitochondrial dysfunction, endoplasmic reticulum stress, inflammation, and alterations in metabolism may lead to insulin resistance and, ultimately, to diabetes and/or neurodegeneration. In this article, we summarize the studies that have addressed the relationship between Parkinson's disease and diabetes and propose that disruptions in these shared molecular networks lead to both chronic diseases. © 2013 Elsevier Ltd.


Katara G.K.,Rosalind Franklin University of Medicine and Science
Oncogene | Year: 2014

Macrophage polarization contributes to distinct human pathologies. In tumors, a polarized M2 phenotype called tumor-associated macrophages (TAMs) are associated with promotion of invasion and angiogenesis. In cancer cells, vacuolar ATPase (V-ATPase), a multi-subunit enzyme, is expressed on the plasma/vesicular membranes and critically influences the metastatic behavior. In addition, the soluble, cleaved N-terminal domain of a2 isoform of V-ATPase (a2NTD) is associated with in vitro induction of pro-tumorigenic properties in monocytes. This activity of a2 isoform of V-ATPase (a2V) caused us to investigate its role in cancer progression through the evaluation of the immunomodulatory properties of a2NTD. Here, we present direct evidence that surface expression of V-ATPase is associated with macrophage polarization in tumor tissue. Macrophages from BALB/c mice (peritoneal/bone marrow derived) were stimulated with recombinant a2NTD in both ex vivo and in vivo systems and evaluated for TAM characteristics. a2V was highly expressed in tumor tissues (breast and skin) as well as on the surface of tumor cell lines. The a2NTD-stimulated macrophages (a2MΦ) acquired TAM phenotype, which was characterized by elevated expression of mannose receptor-1, Arginase-1, interleukin-10 and transforming growth factor-β. a2MΦ also exhibited increased production of other tumorigenic factors including matrix metalloproteinase-9 and vascular endothelial growth factor. Further, a2MΦ were cocultured with mouse B-16F0 melanoma cells for their functional characterization. The coculture of these a2MΦ subsequently increased the invasion and angiogenesis of less invasive B-16F0 cells. When cocultured with naive T cells, a2MΦ significantly inhibited T-cell activation. The present data establish the role of V-ATPase in modulating a macrophage phenotype towards TAMs through the action of a2NTD, suggesting it to be a potential therapeutic target in cancer.


Dundr M.,Rosalind Franklin University of Medicine and Science
Current Opinion in Cell Biology | Year: 2012

It has become increasingly apparent that gene expression is regulated by the functional interplay between spatial genome organization and nuclear architecture. Within the nuclear environment a variety of distinct nuclear bodies exist. They are dynamic, self-organizing structures that do not assemble as pre-formed entities but rather emerge as a direct reflection of specific activities associated with gene expression and genome maintenance. Here I summarize recent findings on functions of some of the most prominent nuclear bodies, including the nucleolus, Cajal body, PML nuclear body, Polycomb group body and the 53BP1 nuclear body. The emerging view is that their organization is orchestrated by similar principles, and they function in fundamental cellular processes involved in homeostasis, differentiation, development and disease. © 2012 Elsevier Ltd.


Shevtsov S.P.,Rosalind Franklin University of Medicine and Science | Dundr M.,Rosalind Franklin University of Medicine and Science
Nature Cell Biology | Year: 2011

The biogenesis of the many functional compartments contained in the mammalian cell nucleus is poorly understood. More specifically, little is known regarding the initial nucleation step required for nuclear body formation. Here we show that RNA can function as a structural element and a nucleator of nuclear bodies. We find that several types of coding and noncoding RNAs are sufficient to de novo assemble, and are physiologically enriched in, histone locus bodies (with associated Cajal bodies), nuclear speckles, paraspeckles and nuclear stress bodies. Formation of nuclear bodies occurs through recruitment and accumulation of proteins resident in the nuclear bodies by nucleating RNA. These results demonstrate that transcription is a driving force in nuclear body formation and RNA transcripts can function as a scaffold in the formation of major nuclear bodies. Together, these data suggest that RNA-primed biogenesis of nuclear bodies is a general principle of nuclear organization. © 2011 Macmillan Publishers Limited. All rights reserved.


Patent
Rosalind Franklin University of Medicine and Science | Date: 2015-08-07

The present invention provides a method for treating a human patient with a pathology by administering to the subject an effective amount of an agent selected from the group of: native full-length CCN3 proteins; analog CCN3 full-length proteins with native cysteine residues substituted by a replacement amino acid; CCNp native peptide fragments having from about 12 to about 20 amino acids; analog CCNp peptide fragments with native cysteine residues substituted with a replacement amino acid; and combinations thereof.


Patent
Rosalind Franklin University of Medicine and Science | Date: 2016-02-17

The present disclosure relates generally to compounds comprising oligonucleotides complementary to a cystic fibrosis transmembrane conductance regulator (CFTR) RNA transcript. Certain such compounds are useful for hybridizing to a CFTR RNA transcript, including but not limited to a CFTR RNA transcript in a cell. In certain embodiments, such hybridization results in modulation of splicing of the CFTR transcript. In certain embodiments, such compounds are used to treat one or more symptoms associated with Cystic Fibrosis.


Patent
Rosalind Franklin University of Medicine and Science | Date: 2015-09-30

Increasing evidence indicates that Parkinsons disease (PD) and type 2 diabetes (T2DM) share dysregulated molecular networks. 84 genes shared between PD and T2DM were identified from curated disease-gene databases. Nitric oxide biosynthesis, lipid and carbohydrate metabolism, insulin secretion and inflammation were identified as common dysregulated pathways. A network prioritization approach was implemented to rank genes according to their distance to seed genes and their involvement in common biological pathways. This disclosure reinforces the idea that shared molecular networks between PD and T2DM provide an additional source of biologically meaningful biomarkers.


Patent
Rosalind Franklin University of Medicine and Science | Date: 2015-09-30

Network-based meta-analysis of four independent microarray studies identified the hepatocyte nuclear factor (HNF4A), a transcription factor associated with gluconeogenesis and diabetes, as a central regulatory hub gene upregulated in blood of PD patients. In parallel, the polypyrimidine tract binding protein 1 (PTBP1), involved in the stabilization and mRNA translation of insulin, was identified as the most downregulated gene. Using both markers, PD patients were classified with 90% sensitivity and 80% specificity. Longitudinal performance analysis demonstrated that relative abundance of HNF4A and PTBP1 mRNAs significantly decreased and increased, respectively, in PD patients during 3 years follow up period. The inverse regulation of HNF4A and PTBP1 provides a molecular rationale for the altered insulin signaling observed in PD patients. The longitudinally dynamic biomarkers identified in this study may be useful for monitoring disease-modifying therapies for PD.

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