IB生物学课程中实验教学策略的启示

IB课程是欧洲背景的世界范围共同认可的系统课程,生物学科和其他实验学科一样有重要的实验教学部分并以24%占比成为内部评价构成学科总成绩。在实验选题,时间要求,指导策略,评价标准,复改制度上都有成熟的细则而且有几十年的实践。了解之后对比国内高中的实验课程情况可以提示我们能在大胆放手给学生进行研究问题自主的探究、确立分数导向,制定过程性评价细则,实行复改制度等方面参考仿效改进以期形成我们的实验课程基本教学策略。     

Little intervention,big results: intentional integration of information literacy into an introductory-level biology lab course

Abstract

Information literacy refers to a set of skills that allow its user to find appropriate resources and use them to develop, define and defend arguments. In many undergraduate programms, including biology and STEM related fields, students are expected to utilise these skills in writing lab reports, paper analyses, and in developing testable hypotheses. Here, we describe the development of a formalised information literacy module for an introductory biology laboratory course and a rubric to measure the effectiveness of this module, including suggestions for implementation. Our data show that while short-term gains were not made using previously published IL tests, application of a tailored rubric to writing assignments did show significant improvement in the students’ ability to find relevant sources, define the purpose of their work and explore that focus. The results of our evaluation demonstrate that even modest additions of formal instruction in information literacy to a course can significantly improve student gains in this area.     

Information literacy in an inquiry course for first-year science undergraduates: a simplified 3C approach

In this article, we describe a simplified approach to teach students to assess information obtained from diverse sources. Three broad categories (credibility, content, and currency; 3C) were used to evaluate information from textbooks, monographs, popular magazines, scholarly journals, and the World Wide Web. This 3C approach used in an inquiry course for freshmen in an undergraduate science program can be readily transferred to other settings.     

生物类专业课程思政教学改革初探——以生物化学为例

课程思政教学改革近两年来获得广泛关注。如何在专业课教学中融入思政元素以达到二者协同育人的目的,是值得我们思考的问题。生物化学与微生物学、细胞生物学等课程具有显著的共性和关联,是生物类专业的重要基础课程。结合本科生生物化学课堂教学中的具体例子,本文介绍了课程思政教学改革的经验,重点探讨如何发掘专业知识点的思政内涵,为相关生物类专业课程思政教学改革提供参考。     

Designing and implementing a new advanced level biology course

Salters-Nuffield Advanced Biology is a new advanced level biology course, piloted from September 2002 in England with around 1200 students. This paper discusses the reasons for developing a new advanced biology course at this time, the philosophy of the project and how the materials are being written and the specification devised. The aim of the project is to provide an up-to-date course that interests students, is considered appropriate by teachers and other professionals in biology, and takes full advantage of modern developments in biology and in teaching.     

Student-oriented learning: an inquiry-based developmental biology lecture course

In this junior-level undergraduate course, developmental life cycles exhibited by various organisms are reviewed, with special attention--where relevant--to the human embryo. Morphological features and processes are described and recent insights into the molecular biology of gene expression are discussed. Ways are studied in which model systems, including marine invertebrates, amphibia, fruit flies and other laboratory species are employed to elucidate general principles which apply to fertilization, cleavage, gastrulation and organogenesis. Special attention is given to insights into those topics which will soon be researched with data from the Human Genome Project. The learning experience is divided into three parts: Part I is a in which the Socratic (inquiry) method is employed by the instructor (GMM) to organize a review of classical developmental phenomena; Part II represents an in which students study the details related to the surveys included in Part I as they have been reported in research journals; Part III focuses on a class project--the preparation of a spiral bound on a topic of relevance to human developmental biology (e.g.,Textbook of Embryonal Stem Cells). Student response to the use of the Socratic method increases as the course progresses and represents the most successful aspect of the course.     

Integrating information literacy training into an inquiry-based introductory biology laboratory

ABSTRACT

Information literacy is an essential skill for biologists; however, most biology curricula do not intentionally integrate information literacy into classroom and laboratory exercises. There is evidence that developing information literacy skills in undergraduates improves their research skills, writing, and GPAs. Our objective was to integrate information literacy skills into a first semester introductory biology laboratory with a multi-week, inquiry-based module that leverages primary literature. Here we describe the module, which challenges students to develop and test a hypothesis related to parental care behaviour in birds. Students form hypotheses based on literature searching done during librarian-led information literacy sessions, produce an annotated bibliography, collect and analyse video data of barn swallows feeding their offspring, and present their findings. Analysis of students’ annotated bibliographies indicates that 83% of the referenced papers were appropriate for developing their specific hypotheses. The key elements ofa successful information literacy training plan include faculty-librarian collaboration, multiple classroom or laboratory sessions that introduce or utilize information literacy, and relevance ofthe information literacy training to an assignment. By introducing information literacy early inbiology curricula, departments can develop tiered information literacy plans that incorporate opportunities for students to use and refine these skills throughout their studies.     

Students' colleges and achievement in an advanced course

The aim of the present study was to determine whether a significant relationship exists between a student's college (Allied Health, Arts and Science, Education, and Graduate School) and achievement in an advanced-level course in human physiology (PGY 412G). The mean percentage of correct answers on four multiple-choice tests, collectively totaling 400 points, was used to assess each student's performance. A four (college)-by-three (academic year) analysis of variance was used for statistical comparisons among 660 students enrolled in PGY 412G from the fall semester of 1995 through the spring semester of 1998. Subsequent pairwise comparisons tests found that the College of Education students had a significantly lower mean percentage of correct answers (61%) compared with students in each of the other colleges (P < 0.001). No significant differences in percentage scores were found among students enrolled in Allied Health (78%), Arts and Science (78%), or the Graduate School (77%). Also, percentages of correct answers averaged across all students were significantly lower during the 1997-1998 academic year than those in either the 1996-1997 year (P < 0.001) or the 1995-1996 year (P < 0.05). Students' scores during these two earlier years did not differ significantly. Upward letter grade adjustments based on class distributions were made each semester, and more As and Bs and fewer Cs and Ds were given as course grades than expected from an absolute assessment scale. This grade inflation benefited low-scoring students from all colleges, particularly those students enrolled in the College of Education. To improve the understanding of human function of these low-scoring students may require special educational programs.     

The challenge of personalized cell biology: The example of microvillus inclusion disease

Whole exome sequencing now provides a tool for rapid analysis of patients manifesting congenital diseases. Congenital diarrheal diseases provide a critical example of the challenges of combining identification of genetic mutations responsible for disease with characterization of the cell biological and cell physiological deficits observed in patients. Recent studies exploring the cellular events associated with loss of functional Myosin 5B (MYO5B) have demonstrated the importance of cell biological and physiological analyses to provide a greater understanding of the implications of pathological mutations. Development of enteroids derived from biopsies of patients with complex congenital diarrheal diseases provides a critical resource for evaluation of the cell biological impact of specific monogenic mutations on enterocyte function. The ability to identify putative causative mutations for congenital disease now provides an opportunity to coordinate the efforts of physicians and cell biologists in an effort to provide patients with personalized cell biology analysis to improve patient diagnosis and treatment.     

Evolutionary cell biology: Lessons from diversity

Novel perspectives emerge from a recent conference on the origins of eukaryotic cells, which covered phylogenetics, population genetics and evolutionary consequences of energy requirements and host–pathogen interactions.     

Progeria: Translational insights from cell biology

Cell biologists love to think outside the box, pursuing many surprising twists and unexpected turns in their quest to unravel the mysteries of how cells work. But can cell biologists think outside the bench? We are certain that they can, and clearly some already do. To encourage more cell biologists to venture into the realm of translational research on a regular basis, we would like to share a handful of the many lessons that we have learned in our effort to develop experimental treatments for Hutchinson-Gilford progeria syndrome (HGPS), an endeavor that many view as a “poster child” for how basic cell biology can be translated to the clinic.The first lesson gained from our studies of Hutchinson-Gilford progeria syndrome (HGPS) sounds simple enough: Approach any translational opportunity that may cross your path with an inquisitive mind. However, because it is nearly impossible to predict when, where, or how such opportunities might arise, the challenge is to remain open to the potential at all times and in all places.For example, the seeds of our collaboration were sown about a decade ago at a decidedly nonscientific venue: a cocktail party in Washington, D.C. During the event, the genomic researcher among us (Collins) happened to strike up a conversation with a young emergency room physician (Scott Berns) doing a White House Fellowship. The ER doctor mentioned that he and his physician-scientist wife (Gordon) had a young son with HGPS, which is a rare, genetic disease characterized by rapid, premature aging (Gordon et al., 2003). The molecular cause of HGPS was unknown at the time, making the search for potential treatments and cures all but impossible. Berns told Collins that the couple had founded The Progeria Research Foundation to encourage scientists to work on this formidable challenge. After a few more conversations, the genomic researcher was “hooked,” and agreed to help organize a workshop to help track down the genetic mutation responsible for HGPS. Pretty soon his laboratory joined in.So, what does it take to hook basic researchers on translational challenges? There are a few elements that strike us as crucial, perhaps even essential, to motivating basic scientists to apply their work toward clinical problems. Among the foremost is human need. In the case of HGPS, the need was obvious: there was no treatment for the disease, and patients died from cardiovascular disease at around age 13. Another key motivator is intellectual challenge. Nature may pose much tougher research questions than we can dream up ourselves, as we have learned time and time again in our decade of studying HGPS.We must also recognize the motivating force of technological innovation. Clinical problems once considered too difficult or time-consuming to be tackled by basic research can become amenable to solution thanks to the development of new tools and technologies. In the genomic sector, such innovation includes databases containing the reference sequence of the human genome, maps of human genetic variation, and ever-expanding catalogs of human genotype/phenotype correlations. Fueling this tsunami of genomic discovery are technologies that have dramatically cut the cost of DNA sequencing from $100 million per genome in 2001 to less than $8,000 today.Cell biology, too, has benefitted greatly from technological advances over the past decade. These advances include the development of the spinning disk and other advanced confocal microscopes that, along with higher speed cameras, make it possible to record 3D images in living cells over long periods of time (Gerlich and Ellenberg, 2003). Using the techniques of photobleaching and photoactivation, new fluorophores with a variety of excitation wavelengths have also provided additional tools to label and track how proteins behave in living cells (Lippincott-Schwartz et al., 2003; Miyawaki et al., 2003). In addition to better imaging tools, cell biologists now have access to many more wet-bench biochemical assays and kits for determining various cellular processes, including apoptosis, senescence, protein phosphorylation, ATP production, and cell stress. These types of tools have been essential for dissecting out the molecular mechanisms underlying HGPS.

Get to the root of the problem

Our second lesson is often easier said than done: get to the root of the problem. When confronted with heartbreaking human need and urgent clinical challenges, it is tempting to race ahead to exploring therapeutic possibilities before gaining a firm, or even tentative, grasp on the molecular roots of a disease. But much time, money, and, ultimately, lives may be lost if a translational research team rushes into clinical trials without a basic understanding of the molecular mechanisms underlying the disease in question.In the case of HGPS, we were fortunate that it only took us a couple of years to get the proverbial cart hooked up to the horse and heading in the right direction. In 2003, through a combination of hard work and serendipity, the Collins laboratory discovered that HGPS is caused by a C-to-T point mutation near the end of the lamin A (LMNA) gene (Eriksson et al., 2003). The point mutation activated a splice donor in the middle of an exon, leading to the production of an abnormal protein, now called progerin, that is 50 amino acids shorter than normal (Fig. 1).Open in a separate windowFigure 1.Posttranslational processing of lamin A. A farnesyl group is added to the C terminus of the lamin A protein by the enzyme farnesyltransferase, and, subsequently, the last three amino acids are cleaved by the endoprotease ZMPSTE24. ZMPSTE24 then removes the terminal 15 amino acids, a step that is blocked in HGPS because of the internal deletion of the cleavage site in the progerin protein.Since the gene discovery, understanding of HGPS has advanced at a rapid pace, fueled by basic research using both in vitro and animal models of disease. This understanding has opened many doors; some were expected, others unexpected, with some leading to exciting translational strategies and others pointing us back to the basics of human biology. How we set about exploring what lay beyond these doors leads us to our third lesson.

Build upon previous knowledge

U.S. President Woodrow Wilson once remarked, “I not only use all the brains I have, but all that I can borrow.” In the case of HGPS, although the earliest iteration of our team was made up primarily of genomic researchers, molecular biologists, and clinical researchers, we soon realized the need to access the impressive body of knowledge offered to us by cell biology.Once we discovered that the LMNA gene was the culprit in HGPS, nearly two decades of lamin A cell biology provided almost immediate insights about how this mutation might cause disease in a dominant fashion. Lamin A is posttranslationally modified (Fig. 1), with the addition of a farnesyl group at the C terminus that seems to assist in “zip-coding” the protein to the inner surface of the nuclear membrane. The protein then needs to be released from this tether, which is accomplished by an enzyme called ZMPSTE24. The abnormal splice event that gives rise to progerin eliminates the ZMPSTE24 cleavage, so progerin remains permanently farnesylated. To explore the cell biological consequences, we forged a rewarding collaboration with Robert Goldman, noted for his lamin A work. His laboratory helped us to document quickly the consequences of LMNA mutations at the cellular level, including abnormal nuclear morphology, premature senescence, and loss of peripheral heterochromatin (Fig. 2, A, D, and E; Goldman et al., 2004). It also became clear that we needed more cell biology expertise within our own group, and, in 2005, the Collins laboratory recruited a postdoc (Cao) with a strong background in cell biology research. The move paid off, and subsequent work showed effects of LMNA mutations on mitosis, causing incomplete disassembly of nuclear envelope, chromosome missegregation, and binucleation (Fig. 2, B and C; Cao et al., 2007; Dechat et al., 2007).Open in a separate windowFigure 2.Defects in HGPS cells. (A) Abnormal nuclear morphology (nuclear blebbing). A nucleus of a passage 17 HGPS cell (HGADFN167) was stained in green with an anti–lamin A/C antibody. (B) Mitotic defects. Nuclear disassembly is incomplete at the onset of mitosis. Progerin (green signal) forms giant aggregates in mitotic cytoplasm. DNA is stained in blue. (C) Binucleation. A binucleated HGPS cell (HGADFN167) stained with an anti-progerin antibody is shown in green. (D) Premature senescence. Senescence-associated β-galactosidase staining is shown for HGPS cells (HGADFN167) at passage 17. (E) Loss of peripheral heterochromatin and extensive nuclear disorganization of a passage 18 HGPS cell (HGADFN167). Source of cells: the Progeria Research Foundation Cell and Tissue Bank (Providence, RI). A, D, and E are courtesy of K. Cao. B and C are from Cao et al. (2007), copyright the National Academy of Sciences. Bars: (A–C and E) 5 µm; (D) 20 µm.Our pathway from bench to clinic has been illuminated by the brilliance of a diverse array of scientists, including seminal papers describing the genomic instability in HGPS (Liu et al., 2005) and the mechanical changes in the lamina of HGPS cells (Dahl et al., 2006). Likewise, several groups have generated induced pluripotent stem (iPS) cells from HGPS patients, providing all of us in the field with a powerful new tool for studying the pathogenesis of HGPS and testing new therapeutic strategies (Liu et al., 2011; Zhang et al., 2011; Progeria Research Foundation, 2012).

Clinical consequences: Time is of the essence

Like most biomedical researchers, cell biologists aspire to see their discoveries turned into better health outcomes as swiftly as possible. However, in our experience, the translational clock usually ticks faster when there is a clinician on the translational team who is acutely aware of how short the timeline is for many who suffer from lethal, progressive diseases, or when basic scientists interact with patients and their families through meetings organized by advocacy groups (Gordon et al., 2008).While our discovery of the LMNA mutation and elucidation of its mechanism of action raised a host of fascinating questions that could fuel years of basic research, we also knew that time was of the essence for children with HGPS and their families. Because HGPS is so rare, and many HGPS patients are in fragile health, there are very limited opportunities to conduct human trials of potential therapies. Consequently, we needed to select and use the scientific tools at our disposal in highly strategic ways if we were to move forward expeditiously.Theory predicted that farnesyltransferase inhibitors (FTIs) would be of potential use in HGPS by reducing the amount of permanently farnesylated progerin, so that is where we began. Tests in cell culture by the Collins laboratory and others showed that FTIs can significantly ameliorate the nuclear-shape abnormalities seen in HGPS cells (Capell et al., 2005). However, cells could only take us so far in the preclinical space. We also needed a good animal model with the precise genetic mutation seen in humans or, even better, a number of genetically precise models created via multiple strategies.Our group developed a mouse model of HGPS by reengineering human LMNA to carry the HGPS mutation, and then inserting it into the mouse germline (Varga et al., 2006). Our mice lack the skin, hair, or bone abnormalities seen in humans with HGPS, but, like the human patients, exhibit progressive loss of vascular smooth muscle cells in the media of large arteries. Tests of FTIs in this and other mouse models (Fong et al., 2006; Capell et al., 2008) complemented other data in support of an initial clinical trial that administered an FTI, lonafarnib, to HGPS patients (Fig. 3). Other work provided an evidence-based rationale (Varela et al., 2008) for a second generation of clinical trials that combined FTIs with statins and bisphosphonates.Open in a separate windowFigure 3.Children with HGPS. Participants in a clinical trial of an FTI. Photographs courtesy of The Progeria Research Foundation.Nonclinicians embarking on translational research projects would also do well to acquaint themselves with another powerful time saver: studies of the natural history of the disease in humans. Well-conducted natural history studies can define the range of manifestations and progression of rare conditions, and also identify biomarkers and other correlates of clinical outcomes that can be used to design an effective clinical trial. In the case of HGPS, such studies were limited, and so efforts to identify statistically reliable outcome measures (Gordon et al., 2007, 2011; Merideth et al., 2008; Gerhard-Herman et al., 2012) had to proceed simultaneously with the planning and implementation of treatment trials.Our therapeutic efforts may soon extend to a third generation of HGPS clinical trials. Work in cell culture supports the possibility that an analogue of rapamycin, an FDA-approved immunosuppressant drug used to prevent rejection in organ transplantation, may provide benefit if added to the current combination approach. The nuclear morphology analysis work that provided a quantitative assessment of treatment effectiveness also highlights how cell biology can serve to guide, not just support, translational strategies (Cao et al., 2011a; Driscoll et al., 2012).Readers will have noted that all of these therapeutic ideas have been based upon repurposing drugs originally developed for other purposes. But that is not the only option. Led by a better understanding of the basic biology of HGPS, concurrent investigations on high throughput assay and drug development (Auld et al., 2009), gene therapy (Scaffidi and Misteli, 2005; Osorio et al., 2011), and stem cell treatment (Wenzel et al., 2012) may all provide future opportunities for combating, and perhaps even curing, HGPS.

Translational research may yield basic insights

Although the primary goal of translational research is helping patients, basic researchers going after this goal may also find themselves rewarded with unexpected insights into fundamental biological processes. In our case, the translation-oriented discovery of the HGPS mutation paved the way for a series of cell biology studies that demonstrated that progerin is also made in normal cells. The splice site activated in HGPS to create progerin is actually used at a low level in normal cells, and becomes more active as cell senescence approaches (Scaffidi and Misteli, 2006; McClintock et al., 2007; Olive et al., 2010). This splice site even may play a role in normal development, such as in closure of the ductus arteriosus (Bökenkamp et al., 2011). Most recently, our work suggests that use of this splice site is somehow triggered by shortened telomeres, hastening the irreversible process of cellular senescence (Cao et al., 2011b). These findings establish HGPS as a valid model system for future basic research into aging.The example of HGPS should make it clear that translational science is not just a one-way street, with basic research discoveries flowing from the bench toward more applied research in the clinic. Rather, the translational process is a virtuous circle, in which basic science benefits clinical research and vice versa. In the span of a decade, HGPS has gone from being a rare and mostly ignored disorder to being “hot science” in both basic and clinical journals. If clinical researchers had not persuaded basic researchers to devote significant effort to solving the translational riddle posed by HGPS, the entire biology community might have missed out on a valuable window into development, senescence, and aging.

You can do it too!

Although this is still a work in progress, we think HGPS is a translational success story worth repeating, and we would like to encourage more cell biologists to give it a try. With more than 4,500 human conditions now having their molecular causes defined, many scientists working on basic research into particular genes, proteins, or pathways may have new opportunities to make these translational connections. For cell biologists who are considering heading down the translational pathway, we suggest checking out the Online Mendelian Inheritance in Man database (http://www.omim.org/) to see what disorders might now connect to their work. We also encourage cell biologists to reach out to clinicians and patient advocacy organizations to seek potential collaborations, as well as to welcome the occasions when they reach out.It is true that serendipity played a significant role for HGPS, and that does not always happen. But we do view our experience as a beacon of hope that shows what basic and clinical researchers can accomplish when they join together to tackle a translational challenge. The scientific opportunities have never been better. We look forward to seeing what cell biology can do in the next few years to help us light up more of these beacons for the millions of people awaiting treatments and cures.     

Student construction of phylogenetic trees in an introductory biology course

Background

Phylogenetic trees have become increasingly essential across biology disciplines. Consequently, learning about phylogenetic trees has become an important component of biology education and an area of interest for biology education research. Construction tasks, in which students generate phylogenetic trees from some type of data, are often used for instruction. However, the impact of these exercises on student learning is uncertain, in part due to our fragmented knowledge of what students construct during the tasks. The goal of this project was to develop a more robust method for describing student-generated phylogenetic trees, which will support future investigations that attempt to link construction tasks with student learning.

Results

Through iterative examination of data from an introductory biology course, we developed a method for describing student-generated phylogenetic trees in terms of style, conventionality, and accuracy. Students used the diagonal style more often than the bracket style for construction tasks. The majority of phylogenetic trees were constructed conventionally, and variable orientation of branches was the most common unconventional feature. In addition, the majority of phylogenetic trees were generated correctly (no errors) or adequately (minor errors only) in terms of accuracy. Suggesting extant taxa are descended from other extant taxa was the most common major error, while empty branches and extra nodes were very common minor errors.

Conclusions

The method we developed to describe student-constructed phylogenetic trees uncovered several trends that warrant further investigation. For example, while diagonal and bracket phylogenetic trees contain equivalent information, student preference for using the diagonal style could impact comprehension. In addition, despite a lack of explicit instruction, students generated phylogenetic trees that were largely conventional and accurate. Surprisingly, accuracy and conventionality were also dependent on each other. Our method for describing phylogenetic trees constructed by students is based on data from one introductory biology course at one institution, and the results are likely limited. We encourage researchers to use our method as a baseline for developing a more generalizable tool, which will support future investigations that attempt to link construction tasks with student learning.

     

Microscopy images as interactive tools in cell modeling and cell biology education

The advent of genomics, proteomics, and microarray technology has brought much excitement to science, both in teaching and in learning. The public is eager to know about the processes of life. In the present context of the explosive growth of scientific information, a major challenge of modern cell biology is to popularize basic concepts of structures and functions of living cells, to introduce people to the scientific method, to stimulate inquiry, and to analyze and synthesize concepts and paradigms. In this essay we present our experience in mixing science and education in Brazil. For two decades we have developed activities for the science education of teachers and undergraduate students, using microscopy images generated by our work as cell biologists. We describe open-air outreach education activities, games, cell modeling, and other practical and innovative activities presented in public squares and favelas. Especially in developing countries, science education is important, since it may lead to an improvement in quality of life while advancing understanding of traditional scientific ideas. We show that teaching and research can be mutually beneficial rather than competing pursuits in advancing these goals.     

专业素质与法律素养融合教育的探索——以“微生物学”课程为例

高校是培养高素质创新创业人才的基地,大学生的法律素养成为高校素质教育的重要组成部分。培养大学生法制观念和法律意识,需要多渠道、多层次、多模式地渗透到专业课程的教学中。微生物学是一门涉及法律法规较多的学科,在微生物学的教学过程中,采用生动的语言、真实的案例和情境讨论将相关法律法规渗透于专业知识中,使学生对日常生活及专业相关的法律法规产生具体形象的认识;基于考核方法改革,引导学生设计微生物产品并撰写项目可行性报告,全面考虑产品及行业相关法律法规,提高项目执行力;结合实习、实践活动,了解企业运行法律法规框架,从企业可持续发展的高度认识法律法规的重要性。促使学生从自身实际出发,思考并运用法律法规为自己的人生规划服务,切实有效地推动大学生的综合素质教育,为创新创业人才培养奠定坚实的基础。     

Expanding course goals beyond disciplinary boundaries: physiology education in an undergraduate course on psychoactive drugs

The topic of psychoactive drugs is one of inherent interest to college students. We used this insight to design and implement a multidisciplinary undergraduate course with psychoactive drugs as the central theme. The Medical Science of Psychoactive Drugs examines the biological mechanisms underlying all major effects of psychoactive drugs, including the effects on the brain and other organs and tissues. Physiological principles, molecular mechanisms, and genetic factors involved in drug-induced therapeutic and adverse effects are emphasized. The course is open to undergraduate students at all levels and carries no prerequisites, and enrollment is limited to approximately 50 students. Major teaching modes include lecture, short homework papers on topics related to the previous class meeting, small-group discussions at several points during each class, and whole class discussions. Because of the diversity of students' knowledge of basic science, we employ a variety of methods designed to help students grasp the necessary scientific concepts. Our methods are intended to be inquiry based and highly interactive. Our goals are 1) to foster the development of an organized knowledge base about psychoactive drugs that will have practical applicability in the daily lives of the students; 2) to promote the rational application of this knowledge in thinking about current medical, social, legal, and ethical issues involving psychoactive drugs; and 3) to cultivate science literacy, critical thinking, and communication skills among students.