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DuPage County, IL, United States

The New Brunswick Laboratory , is a Government-owned, Government-operated, center of excellence in the measurement science of nuclear materials. It was established in 1949 by the Atomic Energy Commission and was located in New Brunswick, New Jersey. It was relocated between 1975 and 1977 and is now located, as a Federal enclave, on the site of Argonne National Laboratory , about 40 kilometers southwest of Chicago, Illinois. NBL is part the Department of Energy's Office of Science Chicago Office.NBL is the U.S. Government's Nuclear Materials Measurements and Reference Materials Laboratory and the National Certifying Authority for nuclear reference materials and measurement calibration standards. As an internationally recognized Federal laboratory, NBL provides reference materials, measurement and interlaboratory measurement evaluation services, and technical expertise for evaluating measurement methods and safeguards measures in use at other facilities for a variety of Federal program sponsors and customers. NBL functions as a Network Laboratory for the International Atomic Energy Agency . Wikipedia.

Lee J.H.,The New School | Chen Y.,The New School | Chan J.L.,The New School | Qian Y.-W.,New Brunswick Laboratory | Goydos J.S.,The New School
Cancer Immunology, Immunotherapy | Year: 2011

Introduction: Sentinel lymph nodes (SLNs) of melanoma patients show evidence of tumor-induced immune dysfunction. Our previous works have shown that IL-10 and IFNγ co-regulate indoleamine-2,3-dioxygenase (IDO)-expressing immunosuppressive dendritic cells (DCs) in melanoma SLNs. The goal of this study is to examine the relationship between melanoma SLN tumor burden and the degree of SLN immune dysfunction as a model to study tumor-induced immune dysfunction. We hypothesize that SLN tumor burden correlates with the degree of SLN immune dysfunction. Methods: Patients undergoing SLN biopsy for clinical stages I and II melanomas were enrolled in the study under an IRB-approved protocol. During the SLN biopsy, non-hot and non-blue portion of the SLN was harvested, flash-frozen in liquid nitrogen, and mRNA was extracted. By using quantitative real-time PCR, gene expressions of cytokines (IL-4, IL-10, IFNγ, TGFβ, GM-CSF) and the surrogates of immunosuppressive regulatory and effector cells (IDO-expressing DCs and Foxp3-expressing T-regs, respectively) were measured and correlated against the SLN tumor burden (MART1) and against each other. The data were log transformed for normalization. Statistical test used Student's t-test and stepwise multivariate regression analysis. Statistical significance was determined at P < 0.05. Results: SLNs of 74 patients were analyzed in this analysis. Ten of seventy-four patients (13.5%) had tumor-positive SLNs. MART1 gene expression showed a significant difference between the SLN (+) and SLN (-) groups (P = 0.04). Among the various cytokines, multivariate analysis showed that only IFNγ gene expression correlated independently with MART1 gene expression (P < 0.0001, r = 0.91). Similar multivariate analyses show that IFNγ (P < 0.0001, r = 0.78), IL-10 (P = 0.0037, r = 0.60), and TGFβ (P < 0.0001, r = 0.95) gene expressions correlated independently with IDO gene expression. IFNγ (P < 0.0001, r = 0.87) and GM-CSF (P = 0.042, r = 0.76) gene expressions correlated independently with Foxp3 gene expression. MART1 gene expression showed independent correlation with IDO (P = 0.0002, r = 0.75) and Foxp3 (P = 0.0002, r = 0.75) gene expressions. Conclusion: SLN tumor burden correlates with immunosuppressive IDO and Foxp3 expressions within the SLNs of melanoma patients. Our data are consistent with our theory that melanoma induces expressions of specific cytokines, which in turn, stimulate immune suppressors within the SLN. This study also supports our previous finding that IL-10 and IFNγ co-regulate IDO within the SLN. In our data, IFNγ is the sole cytokine that correlates with the SLN tumor burden and seems to play a central role in tumor-induced immunological changes in the SLN immune microenvironment. © 2011 Springer-Verlag. Source

Hill D.A.,University of Pennsylvania | Hoffmann C.,University of Pennsylvania | Abt M.C.,University of Pennsylvania | Du Y.,University of Pennsylvania | And 5 more authors.
Mucosal Immunology | Year: 2010

Despite widespread use of antibiotics, few studies have measured their effects on the burden or diversity of bacteria in the mammalian intestine. We developed an oral antibiotic treatment protocol and characterized its effects on murine intestinal bacterial communities and immune cell homeostasis. Antibiotic administration resulted in a 10-fold reduction in the amount of intestinal bacteria present and sequencing of 16S rDNA segments revealed significant temporal and spatial effects on luminal and mucosal-associated communities including reductions in luminal Firmicutes and mucosal-associated Lactobacillus species, and persistence of bacteria belonging to the Bacteroidetes and Proteobacteria phyla. Concurrently, antibiotic administration resulted in reduced RELMΒ production, and reduced production of interferon-γ and interleukin-17A by mucosal CD4+ T lymphocytes. This comprehensive temporal and spatial metagenomic analyses will provide a resource and framework to test the influence of bacterial communities in murine models of human disease. © 2010 Society for Mucosal Immunology. Source

Tallia A.F.,University of New Brunswick | Amenta P.S.,New Brunswick Laboratory | Jones S.K.,Johnson University
Academic Medicine | Year: 2010

Academic health centers (AHCs) have opportunities to advance the agenda of U.S. health care reform by tying the needs of populations to the AHCs missions and areas of expertise. Serving as accountable care organizations and advancing the agenda of the patient-centered medical home are two important potential actions AHCs can take. By fostering discovery, learning, and care through rational organizational structures that meet the needs of populations and bend the curve of growing health care expenditures, AHCs can lead health care reform in the 21st century. Copyright © by the Association of American Medical Colleges. Source

Pandya H.J.,University of Maryland University College | Chen W.,Biomedical Imaging Center | Goodell L.A.,New Brunswick Laboratory | Foran D.J.,Biomedical Imaging Center | Desai J.P.,University of Maryland University College
Lab on a Chip - Miniaturisation for Chemistry and Biology | Year: 2014

The mechanical properties of tissue change significantly during the progression from healthy to malignant. Quantifying the mechanical properties of breast tissue within the tumor microenvironment can help to delineate benign from cancerous stages. In this work, we study high-grade invasive ductal carcinoma in comparison with their matched tumor adjacent areas, which exhibit benign morphology. Such paired tissue cores obtained from eight patients were indented using a MEMS-based piezoresistive microcantilever, which was positioned within pre-designated epithelial and stromal areas of the specimen. Field emission scanning electron microscopy studies on breast tissue cores were performed to understand the microstructural changes from benign to malignant. The normal epithelial tissues appeared compact and organized. The appearance of cancer regions, in comparison, not only revealed increased cellularity but also showed disorganization and increased fenestration. Using this technique, reliable discrimination between epithelial and stromal regions throughout both benign and cancerous breast tissue cores was obtained. The mechanical profiling generated using this method has the potential to be an objective, reproducible, and quantitative indicator for detecting and characterizing breast cancer. This journal is © the Partner Organisations 2014. Source

Rothenbacher F.P.,Microbiology and Immunology | Suzuki M.,Kagawa University | Hurley J.M.,Microbiology and Immunology | Montville T.J.,Rutgers University | And 3 more authors.
Journal of Bacteriology | Year: 2012

Clostridium difficile is an important, emerging nosocomial pathogen. The transition from harmless colonization to disease is typically preceded by antimicrobial therapy, which alters the balance of the intestinal flora, enabling C. difficile to proliferate in the colon. One of the most perplexing aspects of the C. difficile infectious cycle is its ability to survive antimicrobial therapy and transition from inert colonization to active infection. Toxin-antitoxin (TA) systems have been implicated in facilitating persistence after antibiotic treatment. We identified only one TA system in C. difficile strain 630 (epidemic type X), designated MazE-cd and MazF-cd, a counterpart of the well-characterized Escherichia coli MazEF TA system. This E. coli MazF toxin cleaves mRNA at ACA sequences, leading to global mRNA degradation, growth arrest, and death. Likewise, MazF-cd expression in E. coli or Clostridium perfringens resulted in growth arrest. Primer extension analysis revealed that MazF-cd cleaved RNA at the five-base consensus sequence UACAU, suggesting that the mRNAs susceptible to cleavage comprise a subset of total mRNAs. In agreement, we observed differential cleavage of several mRNAs by MazF-cd in vivo, revealing a direct correlation between the number of cleavage recognition sites within a given transcript and its susceptibility to degradation by MazF-cd. Interestingly, upon detailed statistical analyses of the C. difficile transcriptome, the major C. difficile virulence factor toxin B (TcdB) and CwpV, a cell wall protein involved in aggregation, were predicted to be significantly resistant to MazF-cd cleavage. © 2012, American Society for Microbiology. Source

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