Empowering our users, educating ourselves: Getting started with critical cataloging [slides]

Slides from a presentation given October 20, 2021 for the North Carolina Library Association Biennial Conference, SEE the Future (Support. Educate. Empower.), online. Library cataloging has traditionally been directed by standards and structures that have not necessarily reflected--or even included--perspectives from or respectful descriptors for many marginalized individuals and groups. How can library cataloging and metadata personnel educate themselves on ways to address these inequities, while also helping to empower users to see--and find--accurate representations of themselves, their communities, and their areas of research in library collections? Ongoing events and conversations at the national and international levels, in the library profession at large, and within the UNC Greensboro University Libraries have led members of the Technical Services department at UNCG to look for ways to start to address and answer these questions in their own work. This presentation will offer an introduction to the origins of critical cataloging, discuss its relationship to critical librarianship, and demonstrate its relevance to libraries and library workers in and beyond metadata and cataloging fields. Presenters will offer perspectives as learners in this area--not experts--and will discuss the ongoing conversations around critical cataloging in their department and the process and progress associated with the new and developing explorations of critical cataloging practice in their institution. The session will offer resources and potential starting points to help empower attendees to think critically about their own metadata and cataloging work, as well as guidance about incorporating critical cataloging practices and concepts into the workplace

Critical cataloging: What? Why? How? [slides]

Slides from a presentation given March 17, 2022 for the Southeast Collaborative Online Conference. Critical cataloging practices can help library personnel address inequities in bibliographic description while helping library users to identify accurate representation in library collections. This session will help attendees think critically about their own metadata work, and offer resources and guidance for incorporating critical cataloging practices and concepts into the workplace

Getting started with critical cataloging [slides]

Slides from a presentation given February 10, 2022 for the Amigos Library Services Changing Standards, Local Choices: Navigating the Current Cataloging Landscape conference, online. Library cataloging has traditionally been directed by standards and structures that have not necessarily reflected - or even included - perspectives from or respectful descriptors for many marginalized individuals and groups. Critical cataloging practices offer metadata and cataloging personnel ways to address some of these inequities as well as a way to provide more accurate and respectful descriptions in bibliographic data and catalog search systems. This presentation will offer an introduction to critical cataloging and demonstrate its relevance to and potential impact on library personnel and users in contexts including name authority files, classification, subject headings, alternative vocabularies, and other aspects of resource description. Presenters will offer perspectives as learners, not experts, in this area. They will discuss their institution's exploration of critical cataloging in ongoing conversations, development of local workflows, and projects, including updating Cutter numbers and the reparative cataloging of a digital collection of public domain sheet music. The discussion of local critical cataloging projects will also address the challenges associated with taking on new initiatives during an increasingly demanding time of limited resources. This session will offer resources and potential starting points for attendees to think critically about their own metadata and cataloging work. It will also offer guidance about incorporating critical cataloging practices and concepts into the workplace

The Gly2019Ser mutation in LRRK2 is not fully penetrant in familial Parkinson's disease: the GenePD study

<p>Abstract</p> <p>Background</p> <p>We report age-dependent penetrance estimates for leucine-rich repeat kinase 2 (<it>LRRK2</it>)-related Parkinson's disease (PD) in a large sample of familial PD. The most frequently seen <it>LRRK2 </it>mutation, Gly2019Ser (G2019S), is associated with approximately 5 to 6% of familial PD cases and 1 to 2% of idiopathic cases, making it the most common known genetic cause of PD. Studies of the penetrance of <it>LRRK2 </it>mutations have produced a wide range of estimates, possibly due to differences in study design and recruitment, including in particular differences between samples of familial PD versus sporadic PD.</p> <p>Methods</p> <p>A sample, including 903 affected and 58 unaffected members from 509 families ascertained for having two or more PD-affected members, 126 randomly ascertained PD patients and 197 controls, was screened for five different <it>LRRK2 </it>mutations. Penetrance was estimated in families of <it>LRRK2 </it>carriers with consideration of the inherent bias towards increased penetrance in a familial sample.</p> <p>Results</p> <p>Thirty-one out of 509 families with multiple cases of PD (6.1%) were found to have 58 <it>LRRK2 </it>mutation carriers (6.4%). Twenty-nine of the 31 families had G2019S mutations while two had R1441C mutations. No mutations were identified among controls or unaffected relatives of PD cases. Nine PD-affected relatives of G2019S carriers did not carry the <it>LRRK2 </it>mutation themselves. At the maximum observed age range of 90 to 94 years, the unbiased estimated penetrance was 67% for G2019S families, compared with a baseline PD risk of 17% seen in the non-<it>LRRK2</it>-related PD families.</p> <p>Conclusion</p> <p>Lifetime penetrance of <it>LRRK2 </it>estimated in the unascertained relatives of multiplex PD families is greater than that reported in studies of sporadically ascertained <it>LRRK2 </it>cases, suggesting that inherited susceptibility factors may modify the penetrance of <it>LRRK2 </it>mutations. In addition, the presence of nine PD phenocopies in the <it>LRRK2 </it>families suggests that these susceptibility factors may also increase the risk of non-<it>LRRK2</it>-related PD. No differences in penetrance were found between men and women, suggesting that the factors that influence penetrance for <it>LRRK2 </it>carriers are independent of the factors which increase PD prevalence in men.</p

Discovery of a Novel Series of Orally Bioavailable and CNS Penetrant Glucagon-like Peptide‑1 Receptor (GLP-1R) Noncompetitive Antagonists Based on a 1,3-Disubstituted-7-aryl-5,5-bis(trifluoromethyl)-5,8-dihydro­pyrimido[4,5‑<i>d</i>]pyrimidine-2,4(1<i>H</i>,3<i>H</i>)‑dione Core

A duplexed, functional multiaddition high throughput screen and subsequent optimization effort identified the first orally bioavailable and CNS penetrant glucagon-like peptide-1 receptor (GLP-1R) noncompetitive antagonist. Antagonist <b>5d</b> not only blocked exendin-4-stimulated insulin release in islets but also lowered insulin levels while increasing blood glucose in vivo

Speg Interacts With Myotubularin, And Its Deficiency Causes Centronuclear Myopathy With Dilated Cardiomyopathy

Centronuclear myopathies (CNMs) are characterized by muscle weakness and increased numbers of central nuclei within myofibers. X-linked myotubular myopathy, the most common severe form of CNM, is caused by mutations in MTM1, encoding myotubularin (MTM1), a lipid phosphatase. To increase our understanding of MTM1 function, we conducted a yeast two-hybrid screen to identify MTM1-interacting proteins. Striated muscle preferentially expressed protein kinase (SPEG), the product of SPEG complex locus (SPEG), was identified as an MTM1-interacting protein, confirmed by immunoprecipitation and immunofluorescence studies. SPEG knockout has been previously associated with severe dilated cardiomyopathy in a mouse model. Using whole-exome sequencing, we identified three unrelated CNM-affected probands, including two with documented dilated cardiomyopathy, carrying homozygous or compound-heterozygous SPEG mutations. SPEG was markedly reduced or absent in two individuals whose muscle was available for immunofluorescence and immunoblot studies. Examination of muscle samples from Speg-knockout mice revealed an increased frequency of central nuclei, as seen in human subjects. SPEG localizes in a double line, flanking desmin over the Z lines, and is apparently in alignment with the terminal cisternae of the sarcoplasmic reticulum. Examination of human and murine MTM1-deficient muscles revealed similar abnormalities in staining patterns for both desmin and SPEG. Our results suggest that mutations in SPEG, encoding SPEG, cause a CNM phenotype as a result of its interaction with MTM1. SPEG is present in cardiac muscle, where it plays a critical role; therefore, individuals with SPEG mutations additionally present with dilated cardiomyopathy.WoSScopu

Increased rat neonatal activity influences adult cytokine levels and relative muscle mass.

Little is known about the effect of physical activity in early life on subsequent growth and regulation of inflammation. We previously reported that exposure of muscles in growing rats to IL-6 results in decreased muscle growth apparently due to a state of resistance to growth factors such IGF-I and that running exercise could ameliorate this growth defect. Herein we hypothesized that increased activity, for a brief period during neonatal life, would pattern the adult rat towards a less inflammatory phenotype. Neonatal rats were induced to move about their cage for brief periods from day 5 to day 15 postpartum. Additional groups were undisturbed controls (CON) and handled (HAND). Sub-groups of rats were sampled at 30 and 65 days of age. Relative to CON and HAND, neonatal exercise (EX) results in decreased circulating levels of TNFα, IL-6 and IL-1β in adulthood, primarily in male rats. In addition, adult male EX rats had lower body mass and increased skeletal muscle mass suggesting a leaner phenotype. The results of this study suggest that moderate increases in activity early in life can influence the adult toward a more healthy phenotype with regard to inflammatory mediators and relative muscle mass