Search

PurposeThis article unpacks the construction of authority in architectural trade journals as multimodal disciplinary communication and how librarians can use these journals to engage student's critical thinking in information and visual literacy instruction.Design/methodology/approachAn analysis of project articles was done in two consecutive issues of ten architecture print trade journals including tracking details about the building types, geographic locations, firms represented, visual coverage, and visual categorizes and conventions.FindingsThe projects represented in the analyzed trade journals were predominately public buildings built by established firms in Europe, North America and Asia. The journals employed various methods for crediting and captioning visuals, showing marked differences in conferring authority on architectural photographers and descriptive versus analytical analysis of visual communications. Overall, visuals in architecture trade journals dominate the article space, with photographs being the most prominent type; however, individual journals differ in disciplinary conventions such as presence of people, use of color and indications of scale and compass direction.Research limitations/implicationsThese findings strengthen the case for library print subscriptions to trade journals as useful when facilitating student exploration of disciplinary communication to identify markers of authority, examine bias and apply disciplinary conventions in their own scholarly output.Originality/valueBy interrogating the value of print journals in architecture, findings of this study may influence further research into the significance of print journals in other disciplines and a larger professional discussion about the implications of library trends to providing digital-only journal access.

As part of ARL’s Research Library Impact Framework initiative, a research team from the Texas Tech University (TTU) Libraries explored methods for assessing collections related to the study and research of diversity, equity, and inclusion (DEI) topics and their discoverability by users. DEI studies have increased in prominence on academic campuses along with calls to question privilege and power structures, making DEI collections assessment critical. The TTU Libraries undertook a two-part project that surveyed user needs, collections usage, cataloging and discoverability, and user behavior in searching for and evaluating DEI resources. While the researchers were not able to identify an effective method for assessing DEI in large-scale collections, key findings indicate the potential for partnering with women’s and gender studies and Mexican American and Latino/a studies and the need for increased attention on cataloging and metadata, particularly table of contents and abstract/summary fields. The research team identified that many users expressed uncertainty in searching and evaluating DEI resources and expressed interest in search enhancements for better filtering and more prominent website presence for DEI research help.

Obesity is the main risk factor behind insulin resistance and type 2 diabetes. Still, the mechanism behind adipocyte dysfunction is not yet resolved. Recently, we reported that rapid actin remodeling correlates with adipose cell size changes after short-term overfeeding. Therefore, we hypothesized that the actin-driven myocardin-related transcription factor (MRTF-A) contributes to impaired mature adipocyte function. Primary human adipocytes were subjected to adenoviral overexpression of MRTF-A or MRTF-B, followed by Western blot analysis and tracer glucose uptake assay. Further, we assessed cell size distribution, insulin response, MRTF-A localization, actin organization and degree of polymerization in adipocytes isolated from Ob/Ob mice. Overexpression of MRTF-A, but not MRTF-B, markedly suppressed PPARγ expression. Further, MRTF-A expression resulted in decreased IRS-1 level, shifted phosphorylation of Akt (pS473/pT308), IRS-1 (pS302) and AS160 (pT642), and lowered insulin-stimulated glucose uptake. Hypertrophic adipocytes from Ob/Ob mice displayed an increased proportion of polymerized actin, and increased nuclear translocation of MRTF-A compared with control (Ob/+). Similar with human adipocytes overexpressing MRTF-A, adipocytes isolated from Ob/Ob mice had reduced expression of IRS-1 and PPARγ, as well as impaired insulin response. Together, these data demonstrate that MRTF-A negatively influences insulin sensitivity and the expression of key targets in fully mature human adipocytes. This suggests that MRTF-A is poised to exert a transcriptional response in hypertrophic adipocytes, contributing to adipocyte dysfunction and insulin resistance.

This article presents the authors’ efforts to collaborate with faculty in a curriculum-mapping program that enables shared understanding of curricular objectives and goals. By collaborating and coordinating with faculty for embedded library sessions or modules, this program can be used to strengthen information and research competencies at the appropriate academic levels throughout the degree program. Curriculum mapping helps communicate opportunities to bring together teaching and learning from the lecture hall and studio to the library where students can be introduced to pertinent resources and information that will support their course work and build their understanding of research.

Diets enriched in sucrose severely impair metabolic regulation and are associated with obesity, insulin resistance and glucose intolerance. In the current study, we investigated the effect of 4 weeks high-sucrose diet (HSD) feeding in C57BL6/J mice, with specific focus on adipocyte function. Mice fed HSD had slightly increased adipose tissue mass but displayed similar hepatic triglycerides, glucose and insulin levels, and glucose clearance capacity as chow-fed mice. Interestingly, we found adipose depot-specific differences, where both the non- and insulin-stimulated glucose transports were markedly impaired in primary adipocytes isolated from the inguinal fat depot from HSD-fed mice. This was accompanied by decreased protein levels of both GLUT4 and AS160. A similar but much less pronounced trend was observed in the retroperitoneal depot. In contrast, both GLUT4 expression and insulin-stimulated glucose uptake were preserved in adipocytes isolated from epididymal adipose tissue with HSD. Further, we found a slight shift in cell size distribution towards larger cells with HSD and a significant decrease of ACC and PGC-1α expression in the inguinal adipose tissue depot. Moreover, fructose alone was sufficient to decrease GLUT4 expression in cultured, mature adipocytes. Altogether, we demonstrate that short-term HSD feeding has deleterious impact on insulin response and glucose transport in the inguinal adipose tissue depot, specifically. These changes occur before the onset of systemic glucose dysmetabolism and therefore could provide a mechanistic link to overall impaired energy metabolism reported after prolonged HSD feeding, alone or in combination with HFD.