Second language collaborative writing in face-to-face and online environments

textCollaborative writing, the joint construction of a text by two or more authors, is an instructional practice originally used in first language classrooms. More recently, it has been applied in second language (L2) learning contexts. Collaborative writing can take place in the classroom, with pairs or small groups of learners working face-to-face and interacting verbally to make decisions about the content and form of their text. It can also take place in online contexts, allowing larger groups of learners to collaborate on longer texts over a longer period of time. The aim of this paper is to explore empirical research undertaken on second language (L2) collaborative writing tasks in face-to-face and online environments. Attention is paid to the instructional contexts in which these tasks have been used, including educational settings, learners’ proficiency levels, and task types. After these elements are described, the paper integrates and analyzes research concerning the outcomes of collaborative writing tasks, namely the nature of languaging and peer scaffolding, the writing process, language learning, text quality, and learners’ perceptions of collaborative writing. The paper concludes with pedagogical implications and directions for future research.Foreign Language Educatio

ANALYSIS OF NEUROPATHOGENESIS ASSOCIATED WITH SIMIAN IMMUNODEFICIENCY VIRUS INFECTION THROUGH DIFFERENTIAL GENE EXPRESSION STUDIES

Approximately 25-30% of people infected with human immunodeficiency virus 1 (HIV-1) develop HIV-associated encephalitis and HIV-associated dementia. The underlying mechanisms leading to HIV encephalitis remain unclear. In an attempt to understand the molecular events that lead to encephalitis and subsequent dementia, I focused on identifying differentially expressed genes in the central nervous system (CNS) using SIV infected rhesus macaques as an experimental model system by using methods serial analysis of gene expression (SAGE), and microarray hybridization. I studied two different brain regions, caudate and globus pallidus, in non-infected, acutely infected, and mildly encephalitic animals. Since my analysis of macaque SAGE data utilized existing human nucleotide sequence databases, identification of the genes from which the SAGE tags were obtained proved to be challenging. I successfully identified the genes from which two of the tags were obtained. These were major histocompatibility complex class I (MHCI), differentially expressed during disease and neurogranin (Nrg), differentially expressed in caudate relative to globus pallidus. The differential expression of these two genes was confirmed by real-time RT-PCR and in situ hybridization techniques. I further characterized the localization of MHCI in the CNS tissue and found that whereas in non-infected tissues, endothelial cells were the major cell types expressing MHCI mRNA, during acute infection and mild encephalitis, when local virus replication was low or absent, all CNS cell types could express this mRNA. In addition, I observed upregulation of interferon-stimulated genes (ISGs), MxA, OAS2, and G1P3, both in the CNS and in the periphery that could be potential surrogate markers for SIV infection. Since encephalitis is observed only at end-stage disease, traditional thinking has been that the CNS remains relatively unaffected until later stages of infection. Our findings indicate that immune activation within the CNS might occur early in infection and persist in a chronic manner thereby causing continuous damage, which might affect the development of end-stage encephalitis and dementia. Therefore, early, potent, suppression of systemic viral replication could potentially inhibit the development of virus-mediated neuropathology later on. Such an approach would be of important public heath significance

Uterine Epithelial Cells Specifically Induce Interferon-Stimulated Genes in Response to Polyinosinic-Polycytidylic Acid Independently of Estradiol

Interferon β (IFNβ) is an antiviral cytokine secreted in response to pathogenic exposure that creates a restrictive intracellular environment through the action of downstream interferon-stimulated genes (ISG). The objective of this study was to examine the expression of IFNβ and ISG in both human uterine epithelial cells (UEC) and the ECC-1 uterine epithelial cell line and determine if expression changes with TLR stimulation and hormone exposure. Stimulation of primary uterine epithelial cells and ECC-1 cells with the TLR3 agonist poly (I∶C) induced the mRNA expression of IFNβ, MxA, OAS2 and PKR. Other TLR agonists including imiquimod and CpG had no effect on either IFNβ or ISG expression. In contrast to ECC-1 cell responses which were slower, maximal IFNβ upregulation in UEC occurred 3 hours post-stimulation and preceded the ISG response which peaked approximately 12 hours after poly (I∶C) exposure. Unexpectedly, estradiol, either alone or prior to treatment with poly (I∶C), had no effect on IFNβ or ISG expression. Blockade of the IFN receptor abrogated the upregulation of MxA, OAS2 and PKR. Furthermore, neutralizing antibodies against IFNβ partially inhibited the upregulation of all three ISG. Estradiol, directly and in the presence of poly (I∶C) had no effect on IFNβ and ISG expression. These results indicate that uterine epithelial cells are important sentinels of the innate immune system and demonstrate that uterine epithelial cells are capable of mounting a rapid IFN-mediated antiviral response that is independent of estradiol and is therefore potentially sustained throughout the menstrual cycle to aid in the defense of the uterus against potential pathogens

Nuclear Localization of the Protein from the Open Reading Frame x1 of the Borna Disease Virus Was through Interactions with the Viral Nucleoprotein

AbstractPrevious studies have predicted the presence of a small open reading frame (ORFx1) located between ORF-1 and ORF-2 of the Borna disease viral (BDV) genome. The ORFx1 is expressed as a p10 protein that is localized in the nucleus and cytoplasm of BDV-infected cells. In this study, we cloned the nucleotide sequence of ORFx1 into expression vectors and showed that it is expressed as p10. An anti-p10 serum gave nuclear and cytoplasmic staining of cells persistently infected with BDV. Immunoprecipitation of p10 from BDV-infected cells coprecipitated the p40 nucleoprotein N and the 24-kDa viral phosphoprotein P. Transient transfection of noninfected cells showed that p10 and p40 can be coprecipitated and revealed that p10 localized in the cytoplasm was imported into the nucleus in the presence of the BDV p40 N.In vitroprotein–protein interaction studies on solid phase showed the direct interaction of the p10 with the BDV N protein. The subcellular distribution of p10 and its interaction with p40 suggest that this protein may play a role in the nuclear replication and/or transcription of BDV

Anti-HIV Activity in Cervical-Vaginal Secretions from HIV-Positive and -Negative Women Correlate with Innate Antimicrobial Levels and IgG Antibodies

We investigated the impact of antimicrobials in cervicovaginal lavage (CVL) from HIV(+) and HIV(−) women on target cell infection with HIV. Since female reproductive tract (FRT) secretions contain a spectrum of antimicrobials, we hypothesized that CVL from healthy HIV(+) and (−) women inhibit HIV infection. indicated that each was present in CVL from HIV(+) and HIV(−) women. HBD2 and MIP3α correlated with anti-HIV activity as did anti-gp160 HIV IgG antibodies in CVL from HIV(+) women.These findings indicate that CVL from healthy HIV(+) and HIV(−) women contain innate and adaptive defense mechanisms that inhibit HIV infection. Our data suggest that innate endogenous antimicrobials and HIV-specific IgG in the FRT can act in concert to contribute toward the anti-HIV activity of the CVL and may play a role in inhibition of HIV transmission to women

Selective Impact of HIV Disease Progression on the Innate Immune System in the Human Female Reproductive Tract

We have previously demonstrated intrinsic anti-HIV activity in cervicovaginal lavage (CVL) from HIV-infected women with high CD4 counts and not on antiretroviral therapy. However, the impact of HIV disease progression on CVL innate immune responses has not been delineated.CVL from 57 HIV-infected women not on antiretroviral therapy were collected by washing the cervicovaginal area with 10 ml of sterile normal saline. We characterized subject HIV disease progression by CD4 count strata: >500 cells/µl, 200–500 cells/µl, or <200 cells/µl of blood. To assess CVL anti-HIV activity, we incubated TZM-bl cells with HIV plus or minus CVL. Antimicrobials, cytokines, chemokines and anti-gp160 HIV IgG antibodies were measured by ELISA and Luminex.CVL exhibited broad anti-HIV activity against multiple laboratory-adapted and transmitted/founder (T/F) viruses, with anti-HIV activity ranging from 0 to 100% showing wide variation between viral strains. Although there was broad CVL inhibition of most both laboratory-adapted and T/F virus strains, there was practically no inhibition of T/F strain RHPA.c, which was isolated from a woman newly infected via heterosexual intercourse. HIV disease progression, measured by declining CD4 T cell counts, resulted in a selective reduction in intrinsic anti-HIV activity in CVL that paralleled CVL decreases in human beta-defensin 2 and increases in Elafin and secretory leukocyte protease inhibitor. HIV disease progress predicted decreased CVL anti-HIV activity against both laboratory-adapted and T/F strains of HIV. Anti-HIV activity exhibited close associations with CVL levels of fourteen cytokines and chemokines.Amid a multifaceted immune defense against HIV-1 and other sexually transmitted pathogens, HIV disease progression is associated with selective disturbances in both CVL anti-HIV activity and specific innate immune defenses in the human female reproductive tract (FRT). Overall, these studies indicate that innate immune protection in the FRT is compromised as women progress to AIDS

Uterine Epithelial Cell Regulation of DC-SIGN Expression Inhibits Transmitted/Founder HIV-1 Trans Infection by Immature Dendritic Cells

Sexual transmission accounts for the majority of HIV-1 infections. In over 75% of cases, infection is initiated by a single variant (transmitted/founder virus). However, the determinants of virus selection during transmission are unknown. Host cell-cell interactions in the mucosa may be critical in regulating susceptibility to infection. We hypothesized in this study that specific immune modulators secreted by uterine epithelial cells modulate susceptibility of dendritic cells (DC) to infection with HIV-1.Here we report that uterine epithelial cell secretions (i.e. conditioned medium, CM) decreased DC-SIGN expression on immature dendritic cells via a transforming growth factor beta (TGF-β) mechanism. Further, CM inhibited dendritic cell-mediated trans infection of HIV-1 expressing envelope proteins of prototypic reference. Similarly, CM inhibited trans infection of HIV-1 constructs expressing envelopes of transmitted/founder viruses, variants that are selected during sexual transmission. In contrast, whereas recombinant TGF- β1 inhibited trans infection of prototypic reference HIV-1 by dendritic cells, TGF-β1 had a minimal effect on trans infection of transmitted/founder variants irrespective of the reporter system used to measure trans infection.Our results provide the first direct evidence for uterine epithelial cell regulation of dendritic cell transmission of infection with reference and transmitted/founder HIV-1 variants. These findings have immediate implications for designing strategies to prevent sexual transmission of HIV-1

The Economic Burden of Malaria Cases Imported from Hispaniola to other Non- Endemic Countries in the Western Hemisphere (2007- 2013)

Background / Objectives: Hispaniola is the only island endemic for malaria in the Caribbean region. Widening income disparity and natural disasters have hindered malaria control. Routine travel between Hispaniola and other non- endemic countries in the western hemisphere could pose a risk for the re-introduction of malaria in non-endemic countries. Given the paucity of information on the cost of imported cases to non-endemic countries in the Americas, this study sought to estimate the cost and evaluate the economic burden of malaria cases imported from Hispaniola to non-endemic countries in Americas. Methods: Epidemiologic data on imported malaria cases came from reports from the US Centers for Disease Control and Prevention, Public Health Agency of Canada, the Canadian Malaria Network, the World Health Organization and the Pan American Health Organization. Calculation of costs per disability adjusted life-year (DALY), were based upon the WHO burden of disease estimates of DALY loss due to malaria in non-endemic countries in Americas, and the costs of diagnosis and treatment of malaria. Results: During 2007-2013, the estimated number of malaria cases, imported from Hispaniola, to non-endemic countries in North America ranged between 30 and 192. Disease management costs varied between $100,018 and$1,229,320; the Cost/DALY range was $121,377 to$1,079,557. Between 2011 and 2013, 24 cases from Haiti reported in non-endemic Caribbean Islands; they cost $53,076, with no loss of DALY reported. Conclusion: Understanding the economic and human impact of malaria on endemic countries as well as on their non-endemic neighbors helps strengthen the case for worldwide malaria elimination