Barriers and opportunities for integrating social science into natural resource management: lessons from National Estuarine Research Reserves.

The need for cross-disciplinary scientific inquiries that facilitate improved natural resource management outcomes through increased understanding of both the biophysical and human dimensions of management issues has been widely recognized. Despite this broad recognition, a number of obstacles and barriers still sometimes challenge the successful implementation of cross-disciplinary approaches. Improving understanding of these challenges and barriers will help address them and thereby foster appropriate and effective utilization of cross-disciplinary approaches to solve natural resource management challenges. This research uses a case study analysis of the United States National Estuarine Research Reserve System to improve understanding of the critical factors that influence practitioners' decisions related to incorporating social science into their natural resource management work. The case study research is analyzed and evaluated within a Theory of Planned Behavior framework to (1) determine and describe the factors that predict practitioners' intent to incorporate social science into their natural resource related activities and (2) recommend potential strategies for encouraging and enabling cross-disciplinary approaches to natural resource management. The results indicate that National Estuarine Research Reserve practitioners' decisions related to incorporating social science are primarily influenced by (1) confidence in their own capability to incorporate social science into their work and (2) beliefs about whether the outcomes of incorporating social science into their work would be valuable or beneficial.

Analysis of adenovirus infections in synchronized cells.

Adenoviruses (Ads) are small DNA tumor viruses that have played a pivotal role in understanding eukaryotic cell biology and viral oncogenesis. Among other cellular pathways, Ad usurps cell cycle progression following infection. Likewise, progression of the viral infection is influenced by the host cell cycle. We describe here methods developed for synchronizing dividing cell populations and for analysis of cell cycle synchrony by flow cytometry. Furthermore, three methods used to evaluate the outcome of Ad infection in synchronized cell populations are described. These include two assays for infectious centers and an assay for analyzing production of progeny virus by transmission electron microscopy. These methods have been used to demonstrate that Ads that fail to direct synthesis of the E1B 55-kDa or E4orf6 proteins replicate most effectively upon infecting cells in S phase.

E4orf3 is necessary for enhanced S-phase replication of cell cycle-restricted subgroup C adenoviruses.

E1B-55K-mutant or E4orf6-mutant adenoviruses replicate more effectively after infecting cells in S phase than after infecting cells in G(1). Enhanced S-phase replication of the E4orf6-mutant viruses requires the E4orf3 gene. This report demonstrates that the E4orf3 gene is also required for enhanced S-phase replication of the E1B-55K-mutant virus.

Diverse roles for E4orf3 at late times of infection revealed in an E1B 55-kilodalton protein mutant background.

Species C human adenovirus mutants that fail to express open reading frame 3 of early region 4 (E4orf3) are phenotypically indistinguishable from the wild-type virus when evaluated in cells cultured in vitro. However, E4orf3 gene function has been productively studied in the context of additional viral mutations. This study identifies diverse roles for the E4orf3 protein that are evident in the absence of early region 1B 55-kDa protein (E1B-55K) function. In an E1B-55K-deficient background, the E4orf3 protein promotes viral replication by increasing both the burst size and the probability that an infected cell will produce virus. Early viral gene expression is not impaired in E1B-55K/E4orf3 double mutant virus-infected cells. Cells infected with the double mutant virus accumulated concatemers of viral DNA. However, the E1B-55K/E4orf3 double mutant virus did not replicate any better in MO59J cells, in which viral DNA concatemers did not accumulate, than in MO59K cells, in which viral DNA concatemers were produced, suggesting that viral DNA concatenation is not the primary growth defect of the E1B-55K/E4orf3 double mutant virus. Accumulation of viral mRNA in the nucleus and cytoplasm of E1B-55K/E4orf3 double mutant virus-infected cells was severely reduced compared to that on wild-type virus-infected cells. Thus, in an E1B-55K mutant background, the E4orf3 protein promotes the accumulation of late viral RNA and enhances late gene expression. Finally, within the context of an E1B-55K mutant virus, the E4orf3 protein acts to suppress host cell translation and preserve the viability of cells at moderately late times of infection.