Youth services: Promoting health, inclusion, and resiliency through libraries and library education

The ALISE Youth Services Special Interest Group (SIG) presents a panel that explores the ways in which youth services in libraries support health, inclusion, and youth resiliency. The session will begin with presentations of two papers (25 minutes each), followed by a Q&A. Attendees with then be able to share their own works in progress on these topics. The two presentations include research from Dr. Maria Cahill, Dr. Denice Adkins, and Dr. Bobbie Bushman focusing on library services for young children with disabilities and research from Dr. Denice Adkins, Dr. Beth Brendler, and Kerry Townsend on how school librarians can support youth mental health. The work of Dr. Cahill, Dr. Adkins, and Dr. Bushman will include a review of the existing literature examining library services for young children with disabilities and/or developmental delays. This review attempts to identify large gaps in the current knowledge base and instigate a call to action for the field. Dr. Adkins, Dr. Brendler, and Dr. Townsend will present preliminary findings from an IMLS-funded, mixed-methods research project, including an introduction to scalable strategies for rural public and school libraries who wish to support community health needs, an example of which is the creation of an elective course offered at the University of Missouri designed to help future librarians support teen mental health through young adult literature. The COVID-19 pandemic, subsequent interruption to in-person schooling, and existing economic and health inequalities among young people have all served to contribute to an emerging crisis in young people’s mental health and disability support services. This presentation and the subsequent attendee discussion will begin to explore the ways that the LIS field can work to address this crisis

Understanding Victim Cooperation in Cases of Nonfatal Gun Assaults

Victims play a central role in criminal case processing, but research suggests many victims do not report crimes to police or cooperate in a police investigation. This study extends the literature on victim cooperation by examining the effect of incident-level variables and neighborhood characteristics on victim cooperation in nonfatal shooting incidents. The sample includes 1,054 nonfatal shooting victims from two Midwestern cities. Results using binary logistic regression suggest that incident and victim characteristics are significantly associated with cooperation, but race conditions the effect of injury severity and motive on cooperation. The willingness to cooperate among Whites is contingent on injury severity while non-White victims do not become markedly more cooperative when confronted with serious injury. Race also moderates the relationship between crime motive and cooperation. This work demonstrates the need to incorporate nonfatal firearm violence into studies of victim cooperation and gun crime more broadly

The Difference Between Living and Dying: Victim Characteristics and Motive Among Nonfatal Shootings and Gun Homicides

Using both official and unofficial data sources, researchers examined nonfatal (n = 617) and fatal shooting (n = 159) victim characteristics over an 18-month period in Indianapolis. This research revealed that the typical shooting victim was male, non-White, almost 29 years old, had been arrested prior to inclusion in this study, and had been shot more than once. Interestingly, this research supports the notion that nonfatal shooting and homicide victims are different, especially as they relate to victim age, gunshot wound severity, and shooting motive. It highlights the need for better gun violence data collection beyond what currently exists. Striving for improved, more comprehensive cross-sector data collection has implications beyond just police policy and practice to include public health and prevention efforts

Human GUCY2C-Targeted Chimeric Antigen Receptor (CAR)-Expressing T Cells Eliminate Colorectal Cancer Metastases.

One major hurdle to the success of adoptive T-cell therapy is the identification of antigens that permit effective targeting of tumors in the absence of toxicities to essential organs. Previous work has demonstrated that T cells engineered to express chimeric antigen receptors (CAR-T cells) targeting the murine homolog of the colorectal cancer antigen GUCY2C treat established colorectal cancer metastases, without toxicity to the normal GUCY2C-expressing intestinal epithelium, reflecting structural compartmentalization of endogenous GUCY2C to apical membranes comprising the intestinal lumen. Here, we examined the utility of a human-specific, GUCY2C-directed single-chain variable fragment as the basis for a CAR construct targeting human GUCY2C-expressing metastases. Human GUCY2C-targeted murine CAR-T cells promoted antigen-dependent T-cell activation quantified by activation marker upregulation, cytokine production, and killing of GUCY2C-expressing, but not GUCY2C-deficient, cancer cells in vitro. GUCY2C CAR-T cells provided long-term protection against lung metastases of murine colorectal cancer cells engineered to express human GUCY2C in a syngeneic mouse model. GUCY2C murine CAR-T cells recognized and killed human colorectal cancer cells endogenously expressing GUCY2C, providing durable survival in a human xenograft model in immunodeficient mice. Thus, we have identified a human GUCY2C-specific CAR-T cell therapy approach that may be developed for the treatment of GUCY2C-expressing metastatic colorectal cancer

Binding of Soluble Yeast β-Glucan to Human Neutrophils and Monocytes is Complement-Dependent

The immunomodulatory properties of yeast β-1,3/1,6 glucans are mediated through their ability to be recognized by human innate immune cells. While several studies have investigated binding of opsonized and unopsonized particulate β-glucans to human immune cells mainly via complement receptor 3 (CR3) or Dectin-1, few have focused on understanding the binding characteristics of soluble β-glucans. Using a well-characterized, pharmaceutical grade, soluble yeast β-glucan, this study evaluated and characterized the binding of soluble β-glucan to human neutrophils and monocytes. The results demonstrated that soluble β-glucan bound to both human neutrophils and monocytes in a concentration-dependent and receptor-specific manner. Antibodies blocking the CD11b and CD18 chains of CR3 significantly inhibited binding to both cell types, establishing CR3 as the key receptor recognizing the soluble β-glucan in these cells. Binding of soluble β-glucan to human neutrophils and monocytes required serum and was also dependent on incubation time and temperature, strongly suggesting that binding was complement-mediated. Indeed, binding was reduced in heat-inactivated serum, or in serum treated with methylamine or in serum reacted with the C3-specific inhibitor compstatin. Opsonization of soluble β-glucan was demonstrated by detection of iC3b, the complement opsonin on β-glucan-bound cells, as well as by the direct binding of iC3b to β-glucan in the absence of cells. Binding of β-glucan to cells was partially inhibited by blockade of the alternative pathway of complement, suggesting that the C3 activation amplification step mediated by this pathway also contributed to binding

Two Remarkably Luminous Galaxy Candidates at z≈11−13z\approx11-13 Revealed by JWST

The first few hundred Myrs at $z>10$ mark the last major uncharted epoch in the history of the Universe, where only a single galaxy (GNz11 at $z\approx11$) is currently spectroscopically confirmed. Here we present a search for luminous $z>10$ galaxies with $JWST$/NIRCam photometry spanning $\approx1-5\mu$m and covering 49 arcmin$^{2}$ from the public $JWST$ Early Release Science programs (CEERS and GLASS). Our most secure candidates are two $M_{\rm{UV}}\approx-21$ systems: GLASS-z13 and GLASS-z11. These galaxies display abrupt $\gtrsim2.5$ mag breaks in their spectral energy distributions, consistent with complete absorption of flux bluewards of Lyman-$\alpha$ that is redshifted to $z\approx13$ and $z\approx11$. Lower redshift interlopers such as dusty quiescent galaxies with strong Balmer breaks would be comfortably detected at $>5\sigma$ in multiple bands where instead we find no flux. From SED modeling we infer that these galaxies have already built up $\sim 10^9$ solar masses in stars over the $\lesssim300-400$ Myrs after the Big Bang. The brightness of these sources enable morphological constraints. Tantalizingly, GLASS-z11 shows a clearly extended exponential light profile, potentially consistent with a disk galaxy of $r_{\rm{50}}\approx0.7$ kpc. These sources, if confirmed, join GNz11 in defying number density forecasts for luminous galaxies based on Schechter UV luminosity functions, which require a survey area $>10\times$ larger than we have studied here to find such luminous sources at such high redshifts. They extend evidence from lower redshifts for little or no evolution in the bright end of the UV luminosity function into the cosmic dawn epoch, with implications for just how early these galaxies began forming. This, in turn, suggests that future deep $JWST$ observations may identify relatively bright galaxies to much earlier epochs than might have been anticipated.Comment: Submitted to ApJL. Figs. 1 and 2 summarize the candidates, Fig. 3 places the brightness of these systems in context, Fig. 4 shows the morphology, Fig. 5 explores implications for the UVLF. Comments warmly welcome

Clinical and genetic aspects of KBG syndrome.

KBG syndrome is characterized by short stature, distinctive facial features, and developmental/cognitive delay and is caused by mutations in ANKRD11, one of the ankyrin repeat-containing cofactors. We describe 32 KBG patients aged 2-47 years from 27 families ascertained via two pathways: targeted ANKRD11 sequencing (TS) in a group who had a clinical diagnosis of KBG and whole exome sequencing (ES) in a second group in whom the diagnosis was unknown. Speech delay and learning difficulties were almost universal and variable behavioral problems frequent. Macrodontia of permanent upper central incisors was seen in 85%. Other clinical features included short stature, conductive hearing loss, recurrent middle ear infection, palatal abnormalities, and feeding difficulties. We recognized a new feature of a wide anterior fontanelle with delayed closure in 22%. The subtle facial features of KBG syndrome were recognizable in half the patients. We identified 20 ANKRD11 mutations (18 novel: all truncating) confirmed by Sanger sequencing in 32 patients. Comparison of the two ascertainment groups demonstrated that facial/other typical features were more subtle in the ES group. There were no conclusive phenotype-genotype correlations. Our findings suggest that mutation of ANKRD11 is a common Mendelian cause of developmental delay. Affected patients may not show the characteristic KBG phenotype and the diagnosis is therefore easily missed. We propose updated diagnostic criteria/clinical recommendations for KBG syndrome and suggest that inclusion of ANKRD11 will increase the utility of gene panels designed to investigate developmental delay. © 2016 The Authors. American Journal of Medical Genetics Part A Published by Wiley Periodicals, Inc.This article is freely available via Open Access. Click on the Additional Link above to access the full-text via the publisher's site

Prevalence and architecture of de novo mutations in developmental disorders.

The genomes of individuals with severe, undiagnosed developmental disorders are enriched in damaging de novo mutations (DNMs) in developmentally important genes. Here we have sequenced the exomes of 4,293 families containing individuals with developmental disorders, and meta-analysed these data with data from another 3,287 individuals with similar disorders. We show that the most important factors influencing the diagnostic yield of DNMs are the sex of the affected individual, the relatedness of their parents, whether close relatives are affected and the parental ages. We identified 94 genes enriched in damaging DNMs, including 14 that previously lacked compelling evidence of involvement in developmental disorders. We have also characterized the phenotypic diversity among these disorders. We estimate that 42% of our cohort carry pathogenic DNMs in coding sequences; approximately half of these DNMs disrupt gene function and the remainder result in altered protein function. We estimate that developmental disorders caused by DNMs have an average prevalence of 1 in 213 to 1 in 448 births, depending on parental age. Given current global demographics, this equates to almost 400,000 children born per year