A Center for Academic Achievement: How Innovative Collaborations Between Faculty and Learning Center Administrators Built Model, Credit-Bearing, First-Year Courses with Embedded Support for At-Risk Students

Establishing a centralized learning assistance program to systematically address the academic challenges of all students was the first priority of the Academic Achievement Center (AAC) at Bridgewater State College when it was formed in 2001. This new, open, bright, comfortable, and inviting place has truly become the heart of the campus, for it is here that abundant human and material resources are available to support all students. In this learning environment, students can access services in advising, testing, disabilities resources, study, research, writing, communication, mathematics, adaptive technology, tutoring, and English as a second language. Primary responsibility for learning assistance lives with faculty directors who plan how to place meaningful assistance in the path of all students. This article describes the challenges and rewards in establishing and sustaining campus commitment to centralized learning assistance programs as well as some of the exciting opportunities for collaborative innovation on learning assistance that have resulted from such a commitment at Bridgewater State College. An additional discussion focuses on the administrative strategies that support this successful model, and the profound professional opportunities presented to faculty, graduate students, undergraduate student staff, and professional staff through this model. Besides the various services provided at the AAC, systemic delivery of learning assistance is meshed through academic courses for at-risk, first-year students. A description and analysis of quantitative and qualitative data point out the observed trends of student persistence and academic standing for each cohort that has benefited from this comprehensive model

A combined nucleocapsid vaccine induces vigorous SARS-CD8+ T-cell immune responses

Several studies have shown that cell-mediated immune responses play a crucial role in controlling viral replication. As such, a candidate SARS vaccine should elicit broad CD8+ T-cell immune responses. Several groups of mice were immunized alone or in combination with SARS-nucleocapsid immunogen. A high level of specific SARS-CD8+ T-cell response was demonstrated in mice that received DNA encoding the SARS-nucleocapsid, protein and XIAP as an adjuvant. We also observed that co-administration of a plasmid expressing nucleocapsid, recombinant protein and montanide/CpG induces high antibody titers in immunized mice. Moreover, this vaccine approach merits further investigation as a potential candidate vaccine against SARS

Nef Protein of Human Immunodeficiency Virus and Lipopolysaccharide Induce Expression of CD14 on Human Monocytes through Differential Utilization of Interleukin-10

We investigated the expression of membrane-bound CD14 (mCD14) on monocytes and soluble CD14 (sCD14) released into the culture supernatants of peripheral blood lymphocytes (PBMC) from human immunodeficiency virus (HIV)-infected individuals. Monocytes from HIV-positive individuals exhibited both enhanced mCD14 expression and sCD14 production in the PBMC culture supernatants compared to the levels of mCD14 and sCD14 in HIV-negative individuals. This enhanced mCD14 expression and sCD14 production in HIV-infected individuals may be due to the effects of cytokines, the bacterial product lipopolysaccharide (LPS), and/or the HIV regulatory antigens Tat and Nef. Interleukin-10 (IL-10), an immunoregulatory cytokine, as well as LPS enhanced mCD14 expression and the release of sCD14 in the culture supernatants. HIV-Nef, unlike Tat, enhanced mCD14 expression on monocytes but did not induce the release of sCD14 into the culture supernatants. Studies conducted to investigate the mechanism underlying HIV-Nef-induced mCD14 expression revealed that HIV-Nef upregulated mCD14 expression via a mechanism that does not involve endogenously produced IL-10. In contrast, LPS upregulated the expression of mCD14 and increased the release of sCD14 via a mechanism that involves, at least in part, endogenously produced IL-10. Furthermore, dexamethasone, an anti-inflammatory and immunosuppressive agent, inhibited HIV-Nef-induced CD14 expression in an IL-10-independent manner. In contrast, dexamethasone inhibited IL-10-dependent LPS-induced CD14 expression by interfering with IL-10-induced signals but not by blocking IL-10 production. These results suggest that HIV-Nef and IL-10 constitute biologically important modulators of CD14 expression which may influence immunobiological responses to bacterial infections in HIV disease