Search

Providing assessment validity information to decision makers in a clear and useful format is an ongoing challenge for the educational and psychological measurement community. We identify issues with a previous approach to a graphical presentation, noting that it is mislabeled as presenting incremental validity, when in fact it displays the effects of using predictors in a multiple hurdle fashion. We offer a straightforward technique for displaying incremental validity among predictors in reference to a criterion measure.

BackgroundExcessive gestational weight gain (EGWG) closely associates with postpartum obesity. However, the causal role of EGWG in postpartum obesity has not been experimentally verified. The objective of this study was to determine whether and how EGWG causes long-term postpartum obesity.MethodsC57BL/6 mice were fed with high-fat diet during gestation (HFFDG) or control chow, then their body composition and energy metabolism were monitored after delivery.ResultsWe found that HFFDG significantly increased gestational weight gain. After delivery, adiposity of HFFDG-treated mice (Preg-HF) quickly recovered to the levels of controls. However, 3 months after parturition, Preg-HF mice started to gain significantly more body fat even with regular chow. The increase of body fat of Preg-HF mice was progressive with aging and by 9 months after delivery had increased 2-fold above the levels of controls. The expansion of white adipose tissue (WAT) of Preg-HF mice was manifested by hyperplasia in visceral fat and hypertrophy in subcutaneous fat. Preg-HF mice developed low energy expenditure and UCP1 expression in interscapular brown adipose tissue (iBAT) in later life. Although blood estrogen concentrations were similar between Preg-HF and control mice, a significant decrease in estrogen receptor α (ERα) expression and hypermethylation of the ERα promoter was detected in the fat of Preg-HF mice 9 months after delivery. Interestingly, hypermethylation of ERα promoter and low ERα expression were only detected in adipocyte progenitor cells in both iBAT and WAT of Preg-HF mice at the end of gestation.ConclusionsThese results demonstrate that HFFDG causes long-term postpartum obesity independent of early postpartum fat retention. This study also suggests that HFFDG adversely programs long-term postpartum energy metabolism by epigenetically reducing estrogen signaling in both BAT and WAT.

Autism spectrum disorder (ASD) is a markedly heterogeneous condition with a varied phenotypic presentation. Its high concordance among siblings, as well as its clear association with specific genetic disorders, both point to a strong genetic etiology. However, the molecular basis of ASD is still poorly understood, although recent studies point to the existence of sex-specific ASD pathophysiologies and biomarkers. Despite this, little is known about how exactly sex influences the gene expression signatures of ASD probands. In an effort to identify sex-dependent biomarkers and characterize their function, we present an analysis of a single paired-end postmortem brain RNA-Seq data set and a meta-analysis of six blood-based microarray data sets. Here, we identify several genes with sex-dependent dysregulation, and many more with sex-independent dysregulation. Moreover, through pathway analysis, we find that these sex-independent biomarkers have substantially different biological roles than the sex-dependent biomarkers, and that some of these pathways are ubiquitously dysregulated in both postmortem brain and blood. We conclude by synthesizing the discovered biomarker profiles with the extant literature, by highlighting the advantage of studying sex-specific dysregulation directly, and by making a call for new transcriptomic data that comprise large female cohorts.

BackgroundNumerous pathologies of pregnancy originate from placental dysfunction. It is essential to understand the functions of key genes in the placenta in order to discern the etiology of placental pathologies. A paucity of animal models that allow conditional and inducible expression of a target gene in the placenta is a major limitation for studying placental development and function.ResultsTo study the platelet-derived growth factor receptor alpha (PDGFRα)-directed and tamoxifen-induced Cre recombinase expression in the placenta, PDGFRα-CreER mice were crossed with mT/mG dual-fluorescent reporter mice. The expression of endogenous membrane-localized enhanced green fluorescent protein (mEGFP) and/or dTomato in the placenta was examined to identify PDGFRα promoter-directed Cre expression. Pregnant PDGFRα-CreER;mT/mG mice were treated with tamoxifen at various gestational ages. Upon tamoxifen treatment, reporter protein mEGFP was observed in the junctional zone (JZ) and chorionic plate (CP). Furthermore, a single dose of tamoxifen was sufficient to induce the recombination.ConclusionsPDGFRα-CreER expression is restricted to the JZ and CP of mouse placentas. PDGFRα-CreER mice provide a useful tool to conditionally knock out or overexpress a target gene in these regions of the mouse placenta.

Students bring with them rich cultural and linguistic ways of knowing and communicating when engaged in figuring out explanations of phenomena. However, it is a challenge for teachers to support bi/multilingual learners in language-intensive science and engineering practices when they don't share a common language. When we position students' bi/multilingualism as an asset rather than an obstacle, we can support bi/multilingual students' equitable sensemaking. To support bi/multilingual learners' equitable sensemaking, we offer two tools: language surveys and the multiple ways of communicating strategies sheet. We describe how a teacher (second author) used these resources to adapt an investigation about air resistance and contact forces for his bi/multilingual students. The tools and examples provided can help educators better understand their students and make principled changes to science instruction, to expand how we use language in science. We hope the tools aid teachers in this challenging work but also reframe how educators see what students are saying and doing as assets for developing their ideas and learning. [ABSTRACT FROM AUTHOR]

Binocular diplopia limits quality of life by hampering visual function. There are several treatment options with individual advantages and drawbacks. Contact lenses have recently emerged as an attractive treatment delivery mechanism due to advances in lens manufacturing and imaging modalities. Contact lenses can offer better comfort, efficacy, and cosmetic appeal compared to alternative treatments such as spectacles. They also present unique challenges due to risks of inflammation, infection, and intolerability. This review will explore the management of binocular diplopia using several types of contact lenses including base down prism in contact lenses, scleral lenses, occlusive lenses, and monovision lenses. Increased awareness of differing contact lens will help providers and patients make better informed decisions about diplopia management. [ABSTRACT FROM AUTHOR]

This article explores the electrocardiographic manifestations of cardiac disorders in rheumatological conditions, focusing on two case studies of patients with systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). It emphasizes the importance of early recognition and diagnosis of cardiac involvement in autoimmune diseases to enable appropriate interventions. The article provides an overview of common rhythm and conduction disorders seen in systemic autoimmune diseases and suggests that ECG abnormalities should prompt further cardiac imaging for treatment guidance. Managing cardiac involvement in autoimmune diseases requires a multidisciplinary approach, including reducing inflammation, optimizing cardiovascular risk factors, and following evidence-based guidelines. Early detection and intervention can have prognostic implications for patients with cardiac involvement in autoimmune diseases. [Extracted from the article]

Lafora disease (LD) is a syndrome of progressive myoclonic epilepsy and cumulative neurocognitive deterioration caused by recessively inherited genetic lesions of EPM2A (laforin) or NHLRC1 (malin). Neuropsychiatric symptomatology in LD is thought to be directly downstream of neuronal and astrocytic polyglucosan aggregates, termed Lafora bodies (LBs), which faithfully accumulate in an age‐dependent manner in all mouse models of LD. In this study, we applied home‐cage monitoring to examine the extent of neurobehavioral deterioration in a model of malin‐deficient LD as a means to identify robust preclinical endpoints that may guide the selection of novel genetic treatments. At 6 weeks, ∼6–7 months, and ∼12 months of age, malin‐deficient mice ("KO") and wild‐type (WT) littermates underwent a standardized home‐cage behavioral assessment designed to non‐obtrusively appraise features of rest/arousal, consumptive behaviors, risk aversion, and voluntary wheel‐running. At all timepoints, and over a range of metrics that we report transparently, WT and KO mice were essentially indistinguishable. In contrast, within WT mice compared across the same timepoints, we identified age‐related nocturnal hypoactivity, diminished sucrose preference, and reduced wheel‐running. Neuropathological examinations in subsets of the same mice revealed expected age‐dependent LB accumulation, gliosis, and microglial activation in cortical and subcortical brain regions. At 12 months of age, despite the burden of neocortical LBs, we did not identify spontaneous seizures during an electroencephalographic (EEG) survey, and KO and WT mice exhibited similar spectral EEG features. However, in an in vitro assay of neocortical function, paroxysmal bursts of network activity (UP states) in KO slices were more prolonged at 3 and 6 months of age, but similar to WT at 12 months. KO mice displayed a distinct response to pentylenetetrazole, with a greater incidence of clonic seizures and a more pronounced postictal suppression of movement, feeding, and drinking behavior. Together, these results highlight the clinicopathologic dissociation in a mouse model of LD, where the accrual of LBs may latently modify cortical circuit function and seizure threshold without clinically meaningful changes in home‐cage behavior. Our findings allude to a delay between LB accumulation and neurobehavioral decline in LD: one that may provide a window for treatment, and whose precise duration may be difficult to ascertain within the typical lifespan of a laboratory mouse. [ABSTRACT FROM AUTHOR]

The parenting practices of both transracially adopted Korean American adults and multiracial families are often overlooked in developmental science, yet are important to address, given that the majority of Korean adoptees are now adults with families of their own and given rapid increases in the multiracial population. This qualitative study examined the cultural socialization beliefs and practices among transracially adopted Korean Americans who are parents of multiracial Asian-White children. Drawing upon interviews with 31 Korean adoptee parents (29 female; M[subscript age] = 41.26), we identified four themes that capture parents' understanding of their children's multiracial identities, how that understanding subsequently shapes their cultural socialization practices, and how parents' socialization beliefs and practices vary by developmental stage. These themes described the ways that parents' cultural socialization practices were shaped by their children's phenotypes, parents' understanding of their children's multiracial identities, geographic location, and the multiracial family context. This study also demonstrated how multiracial couples in our sample engaged in cultural socialization together. Results suggest that Korean adoptee parents largely acknowledged their children's multiracial identities through labels, but primarily socialized children as monoracial minorities.