Student-Scientist Curriculum: Integrating Inquiry-Based Research Experiences and Professional Development Activities into an Introductory Biology Laboratory Course.

We designed a 16-week scaffolded student-scientist curriculum using inquiry-based research experiences integrated with professional development activities. This curriculum was implemented to teach undergraduate students enrolled in an introduction to biology course about enzyme activity, biochemical reactions, and alcohol fermentation. While working through the curriculum, students completed the entire scientific process by planning experiments, maintaining laboratory journals, analyzing and interpreting data, peer-reviewing research proposals, and producing and presenting a poster. The overall outcome was for students to complete a multiweek, collaborative, student-scientist project using Saccharomyces cerevisiae as the model organism. Student learning outcomes were evaluated using formative assessments (post-Research on the Integrated Science Curriculum survey and peer- and self-reflection worksheets) and summative assessments (pre/post assessments and assignment grades). Results indicated that more than 50% of the students scored 70% or higher on the collaborative student-scientist project, demonstrated several self-reported learning gains in scientific concepts and skills, and reported they would recommend this laboratory course to their peers. By providing the opportunity for students to carry out the entire scientific process, this curriculum enhanced their technical, analytical, and communication skills.

Multi-Institutional, Multidisciplinary Study of the Impact of Course-Based Research Experiences.

Numerous national reports have called for reforming laboratory courses so that all students experience the research process. In response, many course-based research experiences (CREs) have been developed and implemented. Research on the impact of these CREs suggests that student benefits can be similar to those of traditional apprentice-model research experiences. However, most assessments of CREs have been in individual courses at individual institutions or across institutions using the same CRE model. Furthermore, which structures and components of CREs result in the greatest student gains is unknown. We explored the impact of different CRE models in different contexts on student self-reported gains in understanding, skills, and professional development using the Classroom Undergraduate Research Experience (CURE) survey. Our analysis included 49 courses developed and taught at seven diverse institutions. Overall, students reported greater gains for all benefits when compared with the reported national means for the Survey of Undergraduate Research Experiences (SURE). Two aspects of these CREs were associated with greater student gains: 1) CREs that were the focus of the entire course or that more fully integrated modules within a traditional laboratory and 2) CREs that had a higher degree of student input and results that were unknown to both students and faculty.

Health-related disparities: influence of environmental factors.

Racial disparities in health cannot be explained solely on the basis of poverty, access to health care, behavior, or environmental factors. Their complex etiology is dependent on interactions between all these factors plus genetics. Scientists have been slow to consider genetics as a risk factor because genetic polymorphisms tend to be more variable within a race than between races. Now that studies are demonstrating the existence of racial differences in allelic frequencies for multiple genes affecting a single biologic mechanism, the present argument for a significant genetic role in contributing to health disparities is gaining support. Individuals vary, often significantly, in their response to environmental agents. This variability provides a high "background noise" when scientists examine human populations to identify environmental links to disease. This variability often masks important environmental contributors to disease risk and is a major impediment to efforts to investigate the causes of diseases.Fortunately, investments in the various genome projects have led to the development of tools and databases that can be used to help identify the genetic variations in environmental response genes that can lead to such wide differences in disease susceptibility. NIEHS developed the environ-mental genome project to catalog these genetic variants (polymorphisms)and to identify the ones that play a major role in human susceptibility to environmental agents. This information is being used in epidemiologic studies to pinpoint environmental contributors to disease better. The research summarized in this article is critically important for tying genetics and the environment to health disparities, and for the development of a rational approach to gauge environmental threats. Common variants in genes play pivotal roles in determining if or when illness or death result from exposure to drugs or environmental xenobiotics. Most common variants exist in all human populations, but their frequency can vary substantially,rendering individuals or groups more or less susceptible to particular environmental exposures. Such findings are consistent with the highly publicized analogy, "genetics loads the gun, but the environment pulls the trigger." That is, one can inherit the genetic predisposition to develop a disease but will do so only if or when exposed to the environmental trigger. Poor people have approximately the same genetic makeup as everyone else,but they have the unfortunate experience of living and working in environments containing multiple and high levels of carcinogens or other toxicants capable of interacting with susceptibility genes to cause disease.Furthermore, certain disadvantaged ethnic groups may have a higher incidence of certain susceptible genes that render them more vulnerable to adverse effects of the environments they inhabit. For both of these reasons,much of the nation's disease burden could likely be reduced through better environmental protection practices, especially in low-income and minority communities. Of the many implications of polymorphisms and frequency variations for public health and the practice of medicine, however, none is more urgent than the choice of drugs in therapy. Using such knowledge,randomized trials have identified race-specific drug response differences between blacks and whites [42].To date, most knowledge of the health effects of environmental factors is derived from studies of single agents. The reality, though, is that environmental contributions to health disparities are mostly from multiple agents. These simultaneous exposures to multiple risk factors, which may accumulate or interact synergistically, remain to be fully explained and defined.Finally, health disparity is a significant public health problem that cannot be solved using "business as usual" approaches for funding and priority setting. The current emphasis on basic and clinical research at the exclusion of public health and the social sciences does not provide the interdisciplinary research teams necessary to address such a complex problem as health disparities. Although the poor will always be with us, their health could be greatly improved if social, environmental, and genetic scientists could find ways to collaborate and develop more insightful and relevant ways to address the health of disadvantaged communities.

Enhanced proliferation of functionally competent bone marrow cells in different strains of mice treated with swainsonine.

The immunomodulatory alkaloid swainsonine (8alphabeta-indolizidine-1alpha,2alpha,8beta-triol) has potential for overcoming the bone marrow suppressive effects of cancer chemotherapy and radiotherapy. An earlier study showed that multiple doses of swainsonine enhanced bone marrow cellularity in four different strains (C57BL/6; C3H-HEN; Balb/C and DBA-2 mice) of inbred mice which were not exposed to any chemotherapeutic agents or radiation. In vitro assessment of total colony formation capacity of bone marrow cells (BM CFUs) showed a 2- to 8-fold increase in swainsonine-treated mice compared to control mice that were given sham injections of physiological saline. In the current study, we have evaluated the functional competence of the bone marrow cells produced in response to swainsonine treatment of normal healthy mice. In particular, colony forming units-granulocyte-macrophage (CFU-GM), erythroid-burst forming units (BFUe) and CFU-Mix (or CFU-granulocyte-erythrocyte-monocyte-megakaryocyte (CFU-GEMM)) levels, were determined using in vitro assays. The time course of the changes in CFU-GM, BFUe and CFU-Mix (CFU-GEMM) were also followed. Our results demonstrate that swainsonine bolsters the CFU capacity of BM cells without loss of function to levels which are several folds higher than in sham-treated control mice. Swainsonine treatment caused an increase in all lineages of marrow cells without loss of function. This effect was reproduced in all four strains of inbred mice in this investigation. Examination of the peripheral blood did not reveal increase in white blood cells or changes in the hematocrit levels. The long-term effects of swainsonine treatment are not known at present. Nonetheless, swainsonine-induced increase in CFU capacity of bone marrow cells and related cells along the different differentiation paths should find clinical application in cancer treatment with chemotherapeutic agents and/or radiation.

Human pancreatic cancer fusion 2 (HPC2) 1-B3: a novel monoclonal antibody to screen for pancreatic ductal dysplasia.

BACKGROUND.: Pancreatic ductal adenocarcinoma is rarely detected early enough for patients to be cured. The objective of the authors was to develop a monoclonal antibody to distinguish adenocarcinoma and precancerous intraductal papillary mucinous neoplasia (IPMN) from benign epithelium. METHODS.: Mice were immunized with human pancreatic adenocarcinoma cells and monoclonal antibodies were screened against a panel of archived pancreatic tissue sections, including pancreatitis (23 cases), grade 1 IPMN (16 cases), grade 2 IPMN (9 cases), grade 3 IPMN (13 cases), and various grades of adenocarcinoma (17 cases). One monoclonal antibody, human pancreatic cancer fusion 2 (HPC2) 1-B3, which specifically immunostained adenocarcinoma and all grades of IPMN, was isolated. Subsequently, HPC2 1-B3 was evaluated in a retrospective series of 31 fine-needle aspiration (FNA) biopsies from clinically suspicious pancreatic lesions that had long-term clinical follow-up. RESULTS.: HPC2 1-B3 was negative in all 31 cases of chronic pancreatitis that were tested. In contrast, HPC2 1-B3 immunostained the cytoplasm and luminal surface of all 16 well- to moderately differentiated pancreatic ductal adenocarcinomas. It demonstrated only weak focal staining of poorly differentiated carcinomas. All high-grade IPMNs were found to be positive for HPC2 1-B3. The majority of low-grade to intermediate-grade IPMNs were positive (66% of cases). Immunostaining a separate series of pancreatic FNA cell blocks for HPC2 1-B3 demonstrated that the relative risk for detecting at least low-grade dysplasia (2.0 [95% confidence interval, 1.23-3.26]) was statistically significant (P = .002 by the Fisher exact test). CONCLUSIONS.: To reduce the mortality of pancreatic cancer, more effective early screening methods are necessary. The data from the current study indicate that a novel monoclonal antibody, HPC2 1-B3, may facilitate the diagnosis of early pancreatic dysplasia.