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In 2008, University of California, San Diego (UCSD) joined the ranks of institutions offering Global Seminars, short-term study abroad programs designed and led by the institution's own faculty. In this model, an instructor teaches two courses in his or her area of expertise and guides students through a city or other location abroad for five weeks, integrating the course work with the site to enhance learning and to enrich the student experience. In the UCSD model, each Global Seminar (GS) required a minimum of 15 students for financial viability and was capped at a maximum of 30 students for manageability. In Summer 2009, the author led a program in Istanbul, teaching a lower-division world history course and an upper-division history course on Byzantium. The Istanbul program was offered again in 2010 and he will lead a fourth GS there in 2011. With the hope that this experience may be of interest or potential use to faculty or administrators at other institutions, the author offers this general introduction and overview, from program development to implementation and assessment, and discusses the integration of the site itself in history pedagogy.

A genetic polymorphism within the gene encoding the pituitary adenylate cyclase- activating polypeptide (PACAP) receptor type I (PAC1R) has recently been associated with hyper-reactivity to threat-related cues in women, but not men, with post-traumatic stress disorder (PTSD). PACAP is a highly conserved peptide, whose role in mediating adaptive physiological stress responses is well established. Far less is understood about the contribution of PACAP signaling in emotional learning and memory, particularly the encoding of fear to discrete cues. Moreover, a neurobiological substrate that may account for the observed link between PAC1R and PTSD in women, but not men, has yet to be identified. Sex differences in PACAP signaling during emotional learning could provide novel targets for the treatment of PTSD. Here we investigated the contribution of PAC1R signaling within the prefrontal cortex to the acquisition of cued fear in female and male rats. We used a variant of fear conditioning called trace fear conditioning, which requires sustained attention to fear cues and depends on working-memory like neuronal activity within the prefrontal cortex. We found that cued fear learning, but not spatial working memory, was impaired by administration of a PAC1R antagonist directly into the prelimbic area of the prefrontal cortex. This effect was specific to females. We also found that levels of mRNA for the PAC1R receptor in the prelimbic cortex were greater in females compared with males, and were highest during and immediately following the proestrus stage of the estrous cycle. Together, these results demonstrate a sex-specific role of PAC1R signaling in learning about threat-related cues. [ABSTRACT FROM AUTHOR]

Transformation of the undergraduate learning experience through evidence-based, student-centered teaching practices remains a consistent challenge for faculty and departments at large research universities with competing priorities. This paper presents a self-study of the first formalized Faculty Learning Community (FLC) at the University of California, San Diego, which united a cross-disciplinary faculty who specialize in education (at the rank of Lecturer with (Potential) Security of Employment, as part of the LSOE series) to focus on issues of student learning in large university classes. Participants in this year-long faculty development initiative gained: (1) knowledge of the norms and expectations for conducting educational research in the classroom; (2) increased awareness of curricular and pedagogical interventions to enhance student learning in large classes and greater confidence in implementing them; and (3) heightened regard for the collaborative potential of teaching assistants (TAs) in improving teaching and learning. As a result, members of this new community of teacher-scholars are better poised to serve as agents of change within their own academic units and across the campus. [ABSTRACT FROM AUTHOR]

Cerebral amyloid angiopathy (CAA) due to β-amyloid (Aβ) is one of the specific pathological features of familial Alzheimer's disease. Aβ mainly consisting of 40- and 42-mer peptides (Aβ40 and Aβ42) exhibits neurotoxicity and aggregative abilities. All of the variants of Aβ40 and Aβ42 found in CAA were synthesized in a highly pure form and examined for neurotoxicity in PC12 cells and aggregative ability. All of the Aβ40 mutants at positions 22 and 23 showed stronger neurotoxicity than wild-type Aβ40. Similar tendency was observed for Aβ42 mutants at positions 22 and 23 whose neurotoxicity was 50-200 times stronger than that of the corresponding Aβ40 mutants, suggesting that these Aβ42 mutants are mainly involved in the pathogenesis of CAA. Although the aggregation of E22G-Aβ42 and D23N-Aβ42 was similar to that of wild-type Aβ42, E22Q-Aβ42 and E22K-Aβ42 aggregated extensively, supporting the clinical evidence that Dutch and Italian patients are diagnosed as hereditary cerebral hemorrhage with amyloidosis. In contrast, A21G mutation needs alternative explanation with the exception of physicochemical properties of Aβ mutants. Attenuated total reflection-Fourier transform infrared spectroscopy spectra suggested that β-sheet content of the Aβ mutants correlates with their aggregation. However, β-turn is also a critical secondary structure because residues at positions 22 and 23 that preferably form two-residue β-turn significantly enhanced the aggregative ability. [ABSTRACT FROM AUTHOR]