A National Study of Warden\u27s Perceptions of Prison Sex in their Institutions

A survey submitted by Christopher Hensley to the Research and Creative Productions Committee in 2001 on prison sex as perceived by wardens of penitentiaries

Transcriptional regulation of Shigella virulence plasmid-encoded genes by VirB and CRP

Shigella flexneri is a species of Gram-negative intracellular pathogens that causes bacillary dysentery in humans. Shigella relies on the precise transcriptional regulation of virulence genes, encoded by a large virulence plasmid, for invasion and infection of human colonic epithelial cells. The transcription of most identified virulence genes are regulated through a cascade controlled by the primary regulator of virulence genes, VirF, and the global transcriptional regulator, VirB. Currently, few studies have addressed how individual Shigella virulence genes are precisely regulated for optimal expression during specific stages of pathogenesis and within the constraints of the regulatory cascade. This work addresses how individual virulence genes are regulated through the study of transcriptional regulation in four Shigella virulence genes, icsP, ipaJ, phoN1, and ipaH7.8. Analysis of the icsP gene has identified multiple promoters contributing to icsP transcription and to the regulation of IcsP protein production through the use of two different translation start sites. In addition, analyses of the ipaJ, phoN1, and ipaH7.8 genes has identified that the phoN1 gene is transcriptionally regulated by the CRP, suggesting that catabolite repression is involved with the regulation of some virulence genes in Shigella. Together, these data suggest that the transcriptional regulation of virulence genes in Shigella flexneri is more complex than previously observed

Effects of Urbanization on Native Bird Species in Three Southwestern US Cities

Urbanization presents novel challenges to native species by altering both the biotic and abiotic environment. Studies have attempted to make generalizations about how species with similar traits respond to urbanization, although existing results are idiosyncratic across cities and often fail to account for seasonality. Here, we present a comparative study in three US cities: Fresno, California; Tucson, Arizona; and Phoenix, Arizona. Using presence-absence data to define regional bird species pools and urban assemblages in non-breeding (winter) and breeding (spring) seasons, we tested whether urban avian assemblages were a random subset of regional assemblages on the basis of both traits and phylogeny, and whether urbanization was associated with homogenization among avian assemblages. We found evidence for non-random trait filtering into urban assemblages, including of diet guilds, migratory status, and primary habitat, but filtering differed across cities and seasons, being strongest for diet and in Fresno. There was no evidence for non-random phylogenetic-based filtering in urban avian assemblages. Dissimilarity in species and diet guild composition within each season was higher between cities than between regional species pools. These findings show the potential for biotic differentiation as opposed to homogenization as the outcome of environmental filtering processes operating on species traits across cities and seasons

Ultrastructural study of Rift Valley fever virus in the mouse model

AbstractDetailed ultrastructural studies of Rift Valley fever virus (RVFV) in the mouse model are needed to develop and characterize a small animal model of RVF for the evaluation of potential vaccines and therapeutics. In this study, the ultrastructural features of RVFV infection in the mouse model were analyzed. The main changes in the liver included the presence of viral particles in hepatocytes and hepatic stem cells accompanied by hepatocyte apoptosis. However, viral particles were observed rarely in the liver; in contrast, particles were extremely abundant in the CNS. Despite extensive lymphocytolysis, direct evidence of viral replication was not observed in the lymphoid tissue. These results correlate with the acute-onset hepatitis and delayed-onset encephalitis that are dominant features of severe human RVF, but suggest that host immune-mediated mechanisms contribute significantly to pathology. The results of this study expand our knowledge of RVFV–host interactions and further characterize the mouse model of RVF

Notes from the Field: 10 Short Lessons on One-Shot Instruction

Librarians teach. It might not be what they planned to do when they entered the profession, or it may have been a secret hope all along. Either way, librarians teach, and one teaching scenario remains quintessential: the one-shot library instruction session. In recognition of the centrality of the one-shot, this article shares several authors\u27 notes from the field. The notes provide a range of strategies for developing pedagogically sound one-shot library instruction sessions, grouped loosely into three categories: planning, delivery, and integration. The authors offer these insights in their own words in hopes that other teaching librarians may benefit from their experiences

Interferon-β 1a and SARS Coronavirus Replication

A global outbreak of severe acute respiratory syndrome (SARS) caused by a novel coronavirus began in March 2003. The rapid emergence of SARS and the substantial illness and death it caused have made it a critical public health issue. Because no effective treatments are available, an intensive effort is under way to identify and test promising antiviral drugs. Here, we report that recombinant human interferon (IFN)-β 1a potently inhibits SARS coronavirus replication in vitro

Biochemical and biophysical characterization of cell-free synthesized Rift Valley fever virus nucleoprotein capsids enables in vitro screening to identify novel antivirals

Cell fractionation indicates that the compounds access the nucleus. The most potent compounds were exposed to HEK cells at a concentration of 1 ΟM for 24 h, after which the nucleus was separated from the cytoplasm. The concentration of these two blue compounds could be observed by the relative higher intensity in the nucleus compared to that in the cytoplasm. (PDF 3721 kb

Human pDCs preferentially sense enveloped hepatitis A virions

Unlike other picornaviruses, hepatitis A virus (HAV) is cloaked in host membranes when released from cells, providing protection from neutralizing antibodies and facilitating spread in the liver. Acute HAV infection is typified by minimal type I IFN responses; therefore, we questioned whether plasmacytoid dendritic cells (pDCs), which produce IFN when activated, are capable of sensing enveloped virions (eHAV). Although concentrated nonenveloped virus failed to activate freshly isolated human pDCs, these cells produced substantial amounts of IFN-α via TLR7 signaling when cocultured with infected cells. pDCs required either close contact with infected cells or exposure to concentrated culture supernatants for IFN-α production. In isopycnic and rate-zonal gradients, pDC-activating material cosedimented with eHAV but not membrane-bound acetylcholinesterase, suggesting that eHAV, and not viral RNA exosomes, is responsible for IFN-α induction. pDC activation did not require virus replication and was associated with efficient eHAV uptake, which was facilitated by phosphatidylserine receptors on pDCs. In chimpanzees, pDCs were transiently recruited to the liver early in infection, during or shortly before maximal intrahepatic IFN-stimulated gene expression, but disappeared prior to inflammation onset. Our data reveal that, while membrane envelopment protects HAV against neutralizing antibody, it also facilitates an early but limited detection of HAV infection by pDCs

Recombinant Simian Varicella Virus-Simian Immunodeficiency Virus Vaccine Induces T and B Cell Functions and Provides Partial Protection against Repeated Mucosal SIV Challenges in Rhesus Macaques

HIV vaccine mediated efficacy, using an expanded live attenuated recombinant varicella virus-vectored SIV rSVV-SIVgag/env vaccine prime with adjuvanted SIV-Env and SIV-Gag protein boosts, was evaluated in a female rhesus macaques (RM) model against repeated intravaginal SIV challenges. Vaccination induced anti-SIV IgG responses and neutralizing antibodies were found in all vaccinated RMs. Three of the eight vaccinated RM remained uninfected (vaccinated and protected, VP) after 13 repeated challenges with the pathogenic SIVmac251-CX-1. The remaining five vaccinated and infected (VI) macaques had significantly reduced plasma viral loads compared with the infected controls (IC). A significant increase in systemic central memory CD4+ T cells and mucosal CD8+ effector memory T-cell responses was detected in vaccinated RMs compared to controls. Variability in lymph node SIV-Gag and Env specific CD4+ and CD8+ T cell cytokine responses were detected in the VI RMs while all three VP RMs had more durable cytokine responses following vaccination and prior to challenge. VI RMs demonstrated predominately SIV-specific monofunctional cytokine responses while the VP RMs generated polyfunctional cytokine responses. This study demonstrates that varicella virus-vectored SIV vaccination with protein boosts induces a 37.5% efficacy rate against pathogenic SIV challenge by generating mucosal memory, virus specific neutralizing antibodies, binding antibodies, and polyfunctional T-cell responses