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Reptiles and amphibians (herptiles) are some of the most endangered and threatened species on the planet and numerous conservation strategies are being implemented with the goal of ensuring species recovery. Little is known, however, about the gut microbiome of wild herptiles and how it relates to the health of these populations. Here, we report results from the gut microbiome characterization of both a broad survey of herptiles, and the correlation between the fungus Basidiobolus, and the bacterial community supported by a deeper, more intensive sampling of Plethodon glutinosus, known as slimy salamanders. We demonstrate that bacterial communities sampled from frogs, lizards, and salamanders are structured by the host taxonomy and that Basidiobolus is a common and natural component of these wild gut microbiomes. Intensive sampling of multiple hosts across the ecoregions of Tennessee revealed that geography and host:geography interactions are strong predictors of distinct Basidiobolus operational taxonomic units present within a given host. Co-occurrence analyses of Basidiobolus and bacterial community diversity support a correlation and interaction between Basidiobolus and bacteria, suggesting that Basidiobolus may play a role in structuring the bacterial community. We further the hypothesis that this interaction is advanced by unique specialized metabolism originating from horizontal gene transfer from bacteria to Basidiobolus and demonstrate that Basidiobolus is capable of producing a diversity of specialized metabolites including small cyclic peptides.IMPORTANCEThis work significantly advances our understanding of biodiversity and microbial interactions in herptile microbiomes, the role that fungi play as a structural and functional members of herptile gut microbiomes, and the chemical functions that structure microbiome phenotypes. We also provide an important observational system of how the gut microbiome represents a unique environment that selects for novel metabolic functions through horizontal gene transfer between fungi and bacteria. Such studies are needed to better understand the complexity of gut microbiomes in nature and will inform conservation strategies for threatened species of herpetofauna.

Outward differences between cultures are very salient, with Western and East Asian cultures as a prominent comparison pair. A large literature describes cross-cultural variation in cognition, but relatively less research has explored the developmental origins of this variation. This study helps to fill the empirical gap by replicating four prominent findings documenting cross-cultural differences in children's reasoning, visual attention, and social cognition in a cross-sectional sample of 240 3-12-year-olds from the US and China. We observe cross-cultural differences in three of the four tasks and describe the distinct developmental trajectory that each task follows throughout early and middle childhood.

Disparate impact rules are formally neutral but indirectly discriminate against protected groups (i.e., by targeting a characteristic that is more prevalent in a given group). Because these rules are not obviously malicious, they have been widely enacted to circumvent policies against explicit discrimination. In a series of four experiments, we show that adults and children are sensitive to the moral implications of disparate impact rules. However, we also find that they are more accepting of these rules when strong justification is provided, compared to rules with no justification. Crucially, demographic differences also impact people's judgments of disparate impact rules and their creators. We find that conservatives and those from groups not directly affected by the rule tend to be more accepting of it. By studying people's reasoning about disparate impact rules, this work aims to identify the mechanisms by which these rules may evade detection. Finally, we discuss how these insights may inform the development of interventions that highlight the problematic effects of indirectly discriminatory policies.

Although even infants appear to consider multiple possibilities, preschoolers often fail tasks that require reasoning about mutually exclusive alternatives. We review two explanations for this failure: (1) children have a minimal representation of possibility and fail to distinguish necessary from merely possible outcomes; and (2) children are sensitive to this distinction, but competing motivations (e.g., the tendency to explore) can lead to apparent failures. To test these hypotheses, we assessed 3- and 4-year-olds on a novel search task. Here, children searched for an object that was dropped from either a transparent (one necessary location) or opaque (two possible locations) set of inverted Y-shaped tubes. In Exp. 1, we found that children spent less time searching the first location when there were two possible candidates. Exp. 2 replicates these results in a digital task that does not require manual search.

Analogical reasoning is one of the most common ways individuals bring previous experience to bear on unfamiliar situations. Most theories describe this process as a structured comparison that involves mapping the relational properties between a familiar source and unfamiliar target. This both allows the transfer of useful inferences from the source to the target and highlights the common structure shared by both analogs, represented by an abstract schema. This schema can help with identifying and reasoning about structurally similar situations in the future. While researchers have studied how representations of source and target analogs undergo alterations as a result of this mapping process, little attention has been paid to how the abstract schemas thought to guide future analogical reasoning might similarly change with use. We explore this question in two experiments and present evidence that suggests abstract schemas do indeed drift under certain conditions.

Tuberculosis (TB) causes more deaths worldwide than any other infectious disease. Progress in reducing the global burden of TB stalled during the COVID-19 pandemic; an estimated 10.6 million persons became [...]

Type 2 diabetes (T2D) is associated with compromised identity of insulin-producing pancreatic islet β cells, characterized by inappropriate production of other islet cell-enriched hormones. Here, we examined how hormone misexpression was influenced by the MAFA and MAFB transcription factors, closely related proteins that maintain islet cell function. Mice specifically lacking MafA in β cells demonstrated broad, population-wide changes in hormone gene expression with an overall gene signature closely resembling islet gastrin+ (Gast+) cells generated under conditions of chronic hyperglycemia and obesity. A human β cell line deficient in MAFB, but not one lacking MAFA, also produced a GAST+ gene expression pattern. In addition, GAST was detected in human T2D β cells with low levels of MAFB. Moreover, evidence is provided that human MAFB can directly repress GAST gene transcription. These results support a potentially novel, species-specific role for MafA and MAFB in maintaining adult mouse and human β cell identity, respectively. Here, we discuss the possibility that induction of Gast/GAST and other non-β cell hormones, by reduction in the levels of these transcription factors, represents a dysfunctional β cell signature.

* Context.--Mast cells are essential components of the immune system and play crucial pathogenetic roles in several digestive diseases, including mastocytic enterocolitis and eosinophilic gastrointestinal disorders. Pathologists have rarely been asked to evaluate the distribution and density of mast cells in gastrointestinal (GI) biopsy specimens. However, such requests are becoming more common because of an increasing awareness of the role of mast cells in functional GI disease and in both esophageal and nonesophageal eosinophilic gastrointestinal disorders. Objective.--To provide pathologists with tools to incorporate the assessment of mast cells in the evaluation of esophageal, gastric, and intestinal specimens by developing a systematic approach to their evaluation, counting, and reporting. Design.--This study consisted of a review of the literature followed by multiple consensus sessions to decide where to count mast cells and what a countable mast cell is. Results.--We reviewed 135 papers addressing the content of mast cells in the digestive tract, selected 21 that detailed how cells were counted (microscope lens, area of high-power fields, locations evaluated, type of cells considered as countable), and summarized their data in a table. Then, drawing from both the acceptable literature and our own extensive experience, we reached a tentative consensus on: (1) the normal numbers in the different segments of the GI tract; (2) the morphology of countable mast cells; and (3) the locations and strategies for counting them. Conclusions.--The result is a set of suggestions for reporting mast cell counts, their distribution, and their location in a way clinicians can understand and use for management decisions. (Arch Pathol Lab Med. 2024; 148:e25-e35; doi: 10.5858/arpa.2023-0070-OA), The discovery of mast cells and the gradual understanding of their role in the immune system have been described in fascinating detail by Blank et al. (1) First reported by [...]

Disruptive behavior disorders in childhood are increasingly pervasive and associated with numerous, negative long-term outcomes. The current study examined whether adding a brief, home-visitation intervention to an existing, multi-component (child and teacher) intervention, would improve social-emotional and behavioral outcomes for young children with challenging behavior in home and school settings who required intensive support. A total of 379 teacher-parent-student triads were screened for elevated levels of behavioral risk in school and home settings and then randomly assigned to school only intervention (i.e., teacher and student components), home only intervention (i.e., parent), both combined, or business-as-usual control conditions. We examined baseline and posttest outcomes across prosocial behavior, problem behavior, and academic domains. The results demonstrated substantial support for the teacher and child-focused condition and combined conditions, and modest support for the parent-focused condition. The study advances the literature by increasing the knowledge base related to these interventions implemented alone and in combination.

PurposeModel-constrained reconstruction with Fourier-based undersampling (MoReFUn) is introduced to accelerate the acquisition of dynamic MRI using hyperpolarized [1-13 C]-pyruvate.MethodsThe MoReFUn method resolves spatial aliasing using constraints introduced by a pharmacokinetic model that describes the signal evolution of both pyruvate and lactate. Acceleration was evaluated on three single-channel data sets: a numerical digital phantom that is used to validate the accuracy of reconstruction and model parameter restoration under various SNR and undersampling ratios, prospectively and retrospectively sampled data of an in vitro dynamic multispectral phantom, and retrospectively undersampled imaging data from a prostate cancer patient to test the fidelity of reconstructed metabolite time series.ResultsAll three data sets showed successful reconstruction using MoReFUn. In simulation and retrospective phantom data, the restored time series of pyruvate and lactate maintained the image details, and the mean square residual error of the accelerated reconstruction increased only slightly (

To make accurate causal inferences about social-group inequalities, people must consider structural causes. Structural causes are a distinct type of extrinsic cause-they are stable, interconnected societal forces that systematically advantage some social groups and disadvantage others. We propose a new cognitive framework to specify how people attribute inequality to structural causes. This framework is rooted in counterfactual theories of causal judgment and suggests that people will recognize structural factors as causal when they are perceived as "difference-making" for inequality above and beyond any intrinsic causes. Building on this foundation, our framework makes the following contributions. First, we propose specific types of evidence that support difference-making inferences about structural factors: within-group change (i.e., observing that disadvantaged groups' outcomes improve under better societal conditions) and well-matched between-group comparisons (i.e., observing that advantaged group members, who have similar baseline traits to the disadvantaged group, experience more favorable societal conditions and life outcomes). Second, we consider contextual, cognitive, and motivational barriers that may complicate the availability and acceptance of this evidence. We conclude by exploring how the framework might be applied in future research examining people's causal inferences about inequality.

Prolactin (PRL) is elevated in B-cell-mediated lymphoproliferative diseases and promotes B-cell survival. Whether PRL or PRL receptors drive the evolution of B-cell malignancies is unknown. We measure changes in B cells after knocking down the pro-proliferative, anti-apoptotic long isoform of the PRL receptor (LFPRLR) in vivo in systemic lupus erythematosus (SLE)- and B-cell lymphoma-prone mouse models, and the long plus intermediate isoforms (LF/IFPRLR) in human B-cell malignancies. To knockdown LF/IFPRLRs without suppressing expression of the counteractive short PRLR isoforms (SFPRLRs), we employ splice-modulating DNA oligomers. In SLE-prone mice, LFPRLR knockdown reduces numbers and proliferation of pathogenic B-cell subsets and lowers the risk of B-cell transformation by downregulating expression of activation-induced cytidine deaminase. LFPRLR knockdown in lymphoma-prone mice reduces B-cell numbers and their expression of BCL2 and TCL1. In overt human B-cell malignancies, LF/IFPRLR knockdown reduces B-cell viability and their MYC and BCL2 expression. Unlike normal B cells, human B-cell malignancies secrete autocrine PRL and often express no SFPRLRs. Neutralization of secreted PRL reduces the viability of B-cell malignancies. Knockdown of LF/IFPRLR reduces the growth of human B-cell malignancies in vitro and in vivo. Thus, LF/IFPRLR knockdown is a highly specific approach to block the evolution of B-cell neoplasms.