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BackgroundWhereas clinical experience in dementia indicates high risk for financial mismanagement, there has been little formal study of real world financial errors in dementia.ObjectiveWe aimed to compare caregiver-reported financial mistakes among people with Alzheimer's disease, behavioral variant frontotemporal dementia (bvFTD), and primary progressive aphasia (PPA).MethodsCaregivers reported whether participants with dementia had made financial mistakes within the last year; and if so, categorized these as resulting from: (a) being too trusting or gullible, (b) being wasteful or careless with money, or (c) trouble with memory. In a pre-registered analysis https://archive.org/details/osf-registrations-vupj7-v1), we examined the hypotheses that (1) financial mistakes due to impaired socioemotional function and diminished sensitivity to negative outcomes are more prevalent in bvFTD than in Alzheimer's disease, and (2) financial mistakes due to memory are more prevalent in Alzheimer's disease than in bvFTD. Exploratory analyses addressed vulnerability in PPA and brain-behavior relationships using voxel-based morphometry.ResultsConcordant with our first hypothesis, bvFTD was more strongly associated than Alzheimer's disease with mistakes due to being too trusting/gullible or wasteful/careless; contrary to our second hypothesis, both groups were similarly likely to make mistakes due to memory. No differences were found between Alzheimer's disease and PPA. Exploratory analyses indicated associations between financial errors and atrophy in right prefrontal and insular cortex.ConclusionsOur findings cohere with documented socioemotional and valuation impairments in bvFTD, and with research indicating comparable memory impairment between bvFTD and Alzheimer's disease.

Urothelium is a specialized multilayer epithelium that lines the urinary tract from the proximal urethra to the kidney. In addition to proliferation and differentiation during development, urothelial injury postnatally triggers a robust regenerative capacity to restore the protective barrier between the urine and tissue. Mounting evidence supports the existence of dedicated progenitor cell populations that give rise to urothelium during development and in response to injury. Understanding the cellular and molecular basis for urothelial patterning and repair will inform tissue regeneration therapies designed to ameliorate a number of structural and functional defects of the urinary tract. Here, we review the current understanding of urothelial progenitors and the signaling pathways that govern urothelial development and repair. While most published studies have focused on bladder urothelium, we also discuss literature on upper tract urothelial progenitors. Furthermore, we discuss evidence supporting existence of context-specific progenitors. This knowledge is fundamental to the development of strategies to regenerate or engineer damaged or diseased urothelium., Author(s): Ashley R. Jackson [sup.1] [sup.2] [sup.3] , Sridhar T. Narla [sup.4] , Carlton M. Bates [sup.4] [sup.5] , Brian Becknell [sup.1] [sup.2] [sup.3] Author Affiliations: (1) grid.240344.5, 0000 0004 [...]

In this article, we examine diverse forms of youth participation among Black girls through an analysis of 390 application responses for a leadership and empowerment conference. Using a counternarrative methodological approach and intersectional analytical lens, we illustrate how Black girls (a) view participation as an empowering avenue for countering harmful stereotypes that have individual and collective impacts, (b) utilize participation as an intervention for effecting change in their communities, and (c) draw upon their present participation experiences to imagine future selves and life trajectories. We contribute an expanded understanding of "youth participation" grounded in the lives of Black girls that draws from how they describe their daily lives across a diverse range of learning, religious, familial, and geographic contexts. Ultimately, we argue for studies of youth participation that are grounded in lived realities and extend beyond the limited forms of youth participation legible to society.

Background: For pandemic preparedness, researchers used online systematic searches to track unplanned school closures (USCs). We determine if Twitter provides complementary data. Methods: Twitter handles of Michigan public schools and school districts were identified. All tweets associated with these handles were downloaded. USC-related tweets were identified using 5 keywords. Descriptive statistics and multivariable logistic regression were performed in R. Results: Among 3469 Michigan public schools, 2003 maintained their own active Twitter accounts or belonged to school districts with active Twitter accounts. Of these 2003 schools, in 2015-2016 school year, at least 1 USC announcement was identified for 349 schools via the current method only, 678 schools via Twitter only, and 562 schools via both methods. No USC announcements were identified for 414 schools. Rural schools were less likely than city schools to have active Twitter coverage (adjusted relative risk [adjRR] = 0.3956, 95% confidence interval [CI] 0.3312-0.4671), and to announce USCs on Twitter (adjRR = 0.5692, 95% CI 0.4645-0.6823), but more likely to have USCs identified by the current method (adjRR = 1.4545, 95% CI 1.3545-1.5490). Conclusions: Each method identified USCs that were missed by the other. Our results suggested that identifying USCs on Twitter is complementary to the current method.

This study describes how nine university professors managed their teaching when a shift from lecturing to inquiry-based learning was mandated in a large enrollment course, linear algebra for math majors. We describe the tensions that emerged and how they were resolved, in part via the production of worksheets that were used in teaching. We describe the way in which professional obligations towards the discipline and towards the institution shaped the tensions and the ways in which they were resolved by this group of faculty. We offer a conceptualization of the enactment of instruction that was prompted by the study and implications for continued investigation of change strategies in undergraduate mathematics.

Urothelium forms a distensible yet impermeable barrier, senses and transduces stimuli, and defends the urinary tract from mechanical, chemical, and bacterial injuries. Biochemical and genetic labeling studies support the existence of one or more progenitor populations with the capacity to rapidly regenerate the urothelium following injury, but slow turnover, a low mitotic index, and inconsistent methodologies obscure progenitor identity. The progenitor properties of basal keratin 5 urothelial cells (K5-UCs) have been previously investigated, but those studies focused on embryonic or adult bladder urothelium. Urothelium undergoes desquamation and apoptosis after birth, which requires postnatal proliferation and restoration. Therefore, we mapped the fate of bladder K5-UCs across postnatal development/maturation and following administration of cyclophosphamide to measure homeostatic and reparative progenitor capacities, respectively. In vivo studies demonstrate that basal K5-UCs are age-restricted progenitors in neonates and juveniles, but not in adult mice. Neonatal K5-UCs retain a superior progenitor capacity in vitro, forming larger and more differentiated urothelial organoids than adult K5-UCs. Accordingly, K5-UC transcriptomes are temporally distinct, with enrichment of transcripts associated with cell proliferation and differentiation in neonates. Induction of urothelial proliferation is sufficient to restore adult K5-UC progenitor capacity. Our findings advance the understanding of urothelial progenitors and support a linear model of urothelial formation and regeneration, which may have significant impact on therapeutic development or tissue engineering strategies. NEW & NOTEWORTHY: Fate mapping reveals an important linear relationship, whereby bladder basal urothelial cells give rise to intermediate and superficial cells in an age-restricted manner and contribute to tissue repair. Neonatal basal cells reprise their role as superior progenitors in vitro and display distinct transcriptional signatures, which suggest progenitor function is at least partially cell intrinsic. However, the urothelium progenitor niche cannot be overlooked, since FGF7 rescues adult basal cell progenitor function. [ABSTRACT FROM AUTHOR]

Myocardin (MYOCD) is the founding member of a class of transcriptional coactivators that bind the serum-response factor to activate gene expression programs critical in smooth muscle (SM) and cardiac muscle development. Insights into the molecular functions of MYOCD have been obtained from cell culture studies, and to date, knowledge about in vivo roles of MYOCD comes exclusively from experimental animals. Here, we defined an often lethal congenital human disease associated with inheritance of pathogenic MYOCD variants. This disease manifested as a massively dilated urinary bladder, or megabladder, with disrupted SM in its wall. We provided evidence that monoallelic loss-of-function variants in MYOCD caused congenital megabladder in males only, whereas biallelic variants were associated with disease in both sexes, with a phenotype additionally involving the cardiovascular system. These results were supported by cosegregation of MYOCD variants with the phenotype in 4 unrelated families by in vitro transactivation studies in which pathogenic variants resulted in abrogated SM gene expression and by the finding of megabladder in 2 distinct mouse models with reduced Myocd activity. In conclusion, we have demonstrated that variants in MYOCD result in human disease, and the collective findings highlight a vital role for MYOCD in mammalian organogenesis., Introduction Urinary tract and kidney malformations often result in termination of pregnancy after being detected on ultrasound screening, and these anomalies are also a major cause of renal failure in [...]