Results of the 2001 Becoming an Outdoor-Woman Survey

INHS Human Dimensions Research Program and Illinois Department of Natural Resourcesunpublishednot peer reviewedOpe

1999-00 Illinois Trapper Survey Report

Federal Aid Project Number W-112-R-9, Job Number 101.2, Wildlife Restoration FundReport issued on: January 5, 200

Emerging Roles for Immunomodulatory Functions of Free ISG15

Type I interferons (IFNs) exert their effects through the induction of hundreds of IFN-stimulated genes (ISGs), many of which function by inhibiting viral replication and modulating immune responses. ISG15, a di-ubiquitin-like protein, is one of the most abundantly induced ISGs and is critical for control of certain viral and bacterial infections. Like ubiquitin, ISG15 is covalently conjugated to target proteins. In addition, free unconjugated ISG15 is present both intra- and extracellularly. Although much remains to be learned about conjugated ISG15, even less is known about the 2 free forms of ISG15. This article focuses on the role that ISG15 plays during the host response to pathogen challenge, in particular on the recent observations describing the immunomodulatory properties of free ISG15 and its potential implication in disease pathogenesis

Performance assessment tests of multi-anode photomultiplier tube at Jefferson Lab

1 online resource (170 p.) : ill., chiefly col.Includes abstract and appendices.Includes bibliographical references (p. 169-170).In nuclear physics, photomultiplier tubes (PMTs) are used to detect scintillation light resulting from high-energy reaction products for collision events passing through detector materials. The Thomas Jefferson National Accelerator Facility (JLab) in Newport News, VA received six hundred and two (602), 16-channel, Multi-Anode PMTs from Fermilab's decommissioned CDF experiment. These PMTs are being incorporated into the design and construction of a new Coordinate Detector to be located in Hall A. Of the PMTs received, one hundred and eighty six (186) were HAMAMATSU H8711 tubes, and four hundred and sixteen (416) were HAMAMATSU R5900-00-M16 tubes. To identify the best-performing PMTs, each tube was tested using a LED light source to analyze the signal response (ADC spectrum) of each of its sixteen pixels. The ADC spectrum in the absence of light, known as noise or dark current, was also characterized for every pixel in each of the PMTs. A statistical analysis algorithm was then used to fit single and double Gaussian distributions to each ADC spectrum, with the double Gaussians needed to account for cases in which the LED spectra exhibited both signal and noise responses superimposed (due to some inherent inefficiency). These fits determined the mean and standard deviation for all of the dark current (noise) and signal (LED) measurements. With this information, the actual signal response of each pixel, the average gain of each tube, and the relative responses for the 16 pixels associated with all 602 PMTs were evaluated. These results were then used to classify the overall performance of the tubes. A total of 347 PMTs were found to have uniform performance with no bad pixels, and the majority of these were found to be operating with average to high gains. Furthermore, another 107 PMTs were assessed as having non-uniform performance with at most a single bad pixel that exhibited a similar range of operational performance as the uniform tubes. These two groups of PMTs represent over 75% of the available PMTs. An additional 120 PMTs were found to have non-uniform performance with at most two to three bad pixels and exhibited average to below average operating performances. The remaining 28 PMTs had five to sixteen defective pixels, were non-uniform, and performed poorly

Human cytomegalovirus pUL79 Is an elongation factor of RNA polymerase II for viral gene transcription

In this study, we have identified a unique mechanism in which human cytomegalovirus (HCMV) protein pUL79 acts as an elongation factor to direct cellular RNA polymerase II for viral transcription during late times of infection. We and others previously reported that pUL79 and its homologues are required for viral transcript accumulation after viral DNA synthesis. We hypothesized that pUL79 represented a unique mechanism to regulate viral transcription at late times during HCMV infection. To test this hypothesis, we analyzed the proteome associated with pUL79 during virus infection by mass spectrometry. We identified both cellular transcriptional factors, including multiple RNA polymerase II (RNAP II) subunits, and novel viral transactivators, including pUL87 and pUL95, as protein binding partners of pUL79. Co-immunoprecipitation (co-IP) followed by immunoblot analysis confirmed the pUL79-RNAP II interaction, and this interaction was independent of any other viral proteins. Using a recombinant HCMV virus where pUL79 protein is conditionally regulated by a protein destabilization domain ddFKBP, we showed that this interaction did not alter the total levels of RNAP II or its recruitment to viral late promoters. Furthermore, pUL79 did not alter the phosphorylation profiles of the RNAP II C-terminal domain, which was critical for transcriptional regulation. Rather, a nuclear run-on assay indicated that, in the absence of pUL79, RNAP II failed to elongate and stalled on the viral DNA. pUL79-dependent RNAP II elongation was required for transcription from all three kinetic classes of viral genes (i.e. immediate-early, early, and late) at late times during virus infection. In contrast, host gene transcription during HCMV infection was independent of pUL79. In summary, we have identified a novel viral mechanism by which pUL79, and potentially other viral factors, regulates the rate of RNAP II transcription machinery on viral transcription during late stages of HCMV infection

Attitudes of Homeowners in the Greater Chicago Metropolitan Region Towards Nuisance Wildlife

INHS Human Dimensions Research Program and Illinois Department of Natural Resourcesunpublishednot peer reviewedOpe

The folic acid metabolism gene mel-32/Shmt is required for normal cell cycle lengths in Caenorhabditis elegans

Neural tube defects are common and serious birth defects in which the brain and/or spinal cord are exposed outside the body. Supplementation of foods with folic acid, an essential vitamin, is linked to a lower risk of neural tube defects; however, the mechanisms by which folic acid influence neural tube defect risk are unclear. Our research seeks to identify the basic cellular roles of known folic acid metabolism genes during morphogenesis using the roundworm Caenorhabditis elegans (C. elegans) as a simple model system. Here, we used live imaging to characterize defects in embryonic development when mel-32 is depleted. mel-32 is an essential folic acid metabolism gene in C. elegans and a homolog to the mammalian enzyme serine hydroxymethyltransferase (Shmt). Disruption of mel-32 resulted in a doubling or tripling of cell cycle lengths and a lack of directed cell movement during embryogenesis. However, the order of cell divisions, as determined by lineage analysis, is unchanged compared to wild type embryos. These results suggest that mel32/Shmt is required for normal cell cycle lengths in C. elegans

Zoonotic orthopoxviruses encode a high-affinity antagonist of NKG2D

NK and T lymphocytes express both activating and inhibiting receptors for various members of the major histocompatibility complex class I superfamily (MHCISF). To evade immunologic cytotoxicity, many viruses interfere with the function of these receptors, generally by altering the displayed profile of MHCISF proteins on host cells. Using a structurally constrained hidden Markov model, we discovered an orthopoxvirus protein, itself distantly class I–like, that acts as a competitive antagonist of the NKG2D activating receptor. This orthopoxvirus MHC class I–like protein (OMCP) is conserved among cowpox and monkeypox viruses, secreted by infected cells, and bound with high affinity by NKG2D of rodents and humans (KD ∼ 30 and 0.2 nM, respectively). OMCP blocks recognition of host-encoded ligands and inhibits NKG2D-dependent killing by NK cells. This finding represents a novel mechanism for viral interference with NKG2D and sheds light on intercellular recognition events underlying innate immunity against emerging orthopoxviruses

Host Nectin-1 Promotes Chlamydial Infection in the Female Mouse Genital Tract, But is Not Required for Infection in a Novel Male Murine Rectal Infection Model

This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Chlamydia trachomatis is the most common bacterial sexually transmitted pathogen, but more than 70% of patients fail to seek treatment due to the asymptomatic nature of these infections. Women suffer from numerous complications from chronic chlamydial infections, which include pelvic inflammatory disease and infertility. We previously demonstrated in culture that host cell nectin-1 knockdown significantly reduced chlamydial titers and inclusion size. Here, we sought to determine whether nectin-1 was required for chlamydial development in vivo by intravaginally infecting nectin-1-/- mice with Chlamydia muridarum and monitoring chlamydial shedding by chlamydial titer assay. We observed a significant reduction in chlamydial shedding in female nectin-1-/- mice compared to nectin-1+/+ control mice, an observation that was confirmed by PCR. Immunohistochemical staining in mouse cervical tissue confirmed that there are fewer chlamydial inclusions in Chlamydia-infected nectin-1-/- mice. Notably, anorectal chlamydial infections are becoming a substantial health burden, though little is known regarding the pathogenesis of these infections. We therefore established a novel male murine model of rectal chlamydial infection, which we used to determine whether nectin-1 is required for anorectal chlamydial infection in male mice. In contrast to the data from vaginal infection, no difference in rectal chlamydial shedding was observed when male nectin-1+/+ and nectin-1-/- mice were compared. Through the use of these two models, we have demonstrated that nectin-1 promotes chlamydial infection in the female genital tract but does not appear to contribute to rectal infection in male mice. These models could be used to further characterize tissue and sex related differences in chlamydial infection