Background Millions of people pass through U.S. jails annually. Conducting research about these public institutions is critical to understanding on-the-ground policies and practices, especially health care services, affecting millions of people. However, there is no existing database of the number, location, or contact information of jails. We created the National Jails Compendium to address this gap. In this paper, we detail our comprehensive methodology for identifying jail locations and contact information. We then describe the first research project to use the Compendium, a survey assessing jails’ treatment practices for incarcerated pregnant people with opioid use disorder. Results This study sent surveys electronically or in paper form to all 2986 jails in the Compendium, with 1139 surveys returned. We outline the process for using the Compendium, highlighting challenges in reaching contacts through case examples, cataloging responses and non-responses, and defining what counts as a jail. Conclusion We aim to provide tools for future researchers to use the Compendium as well as a pathway for keeping it current. The Compendium provides transparency that aids in understanding jail policies and practices. Such information may help devise interventions to ensure humane, evidence-based treatment of incarcerated people.
Intercellular propagation of aggregated protein inclusions along actin-based tunneling nanotubes (TNTs) has been reported as a means of pathogenic spread in Alzheimer’s, Parkinson’s, and Huntington’s diseases. Propagation of oligomeric-structured polyglutamine-expanded ataxin-1 (Atxn1[154Q]) has been reported in the cerebellum of a Spinocerebellar ataxia type 1 (SCA1) knock-in mouse to correlate with disease propagation. In this study, we investigated whether a physiologically relevant polyglutamine-expanded ATXN1 protein (ATXN1[82Q]) could propagate intercellularly. Using a cerebellar-derived live cell model, we observed ATXN1 aggregates form in the nucleus, subsequently form in the cytoplasm, and finally, propagate to neighboring cells along actin-based intercellular connections. Additionally, we observed the facilitation of aggregate-resistant proteins into aggregates given the presence of aggregation-prone proteins within cells. Taken together, our results support a pathogenic role of intercellular propagation of polyglutamine-expanded ATXN1 inclusions.
Intercellular propagation of aggregated protein inclusions along actin-based tunneling nanotubes (TNTs) has been reported as a means of pathogenic spread in Alzheimer’s, Parkinson’s and Huntington’s Disease. Propagation of oligomeric-structured polyglutamine-expanded ataxin-1 (Atxn1[154Q]) has been reported in the cerebellum of a Spinocerebellar ataxia type 1 (SCA1) knock-in mouse to correlate with disease propagation. In this study, we investigated whether a physiologically-relevant polyglutamine-expanded ATXN1 protein (ATXN1[82Q]) could propagate intercellularly. Using a cerebellar-derived live cell model, we observed ATXN1 aggregates form in the nucleus, export out of the nucleus into the cytoplasm, and finally, propagate to neighboring cells along actin-based intercellular connections. Additionally, we observed the facilitation of aggregate-resistant proteins into aggregates given the presence of aggregation-prone proteins within a cell. Taken together, our results support a pathogenic role of intercellular propagation of polyglutamine-expanded ATXN1 inclusions.
The retinogeniculate synapse transmits information from retinal ganglion cells (RGC) in the eye to thalamocortical relay neurons in the visual thalamus, the dorsal lateral geniculate nucleus (dLGN). Studies in mice have identified genetic markers for distinct classes of RGCs encoding different features of the visual space, facilitating the dissection of RGC subtype-specific physiology and anatomy. In this study, we examine the morphological properties of axon arbors of the BD-RGC class of ON-OFF direction selective cells that, by definition, exhibit a stereotypic dendritic arbor and termination pattern in the retina. We find that axon arbors from the same class of RGCs exhibit variations in their structure based on their target region of the dLGN. Our findings suggest that target regions may influence the morphologic and synaptic properties of their afferent inputs.
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