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Understanding worldwide patterns of language diversity has long been a goal for evolutionary scientists, linguists and philosophers. Research over the past decade has suggested that linguistic diversity may result from differences in the social environments in which languages evolve. Specifically, recent work found that languages spoken in larger communities typically have more systematic grammatical structures. However, in the real world, community size is confounded with other social factors such as network structure and the number of second languages learners in the community, and it is often assumed that linguistic simplification is driven by these factors instead. Here, we show that in contrast to previous assumptions, community size has a unique and important influence on linguistic structure. We experimentally examine the live formation of new languages created in the laboratory by small and larger groups, and find that larger groups of interacting participants develop more systematic languages over time, and do so faster and more consistently than small groups. Small groups also vary more in their linguistic behaviours, suggesting that small communities are more vulnerable to drift. These results show that community size predicts patterns of language diversity, and suggest that an increase in community size might have contributed to language evolution.

Deficiencies in immune function increase susceptibility to infections and chronic diseases by impairing immune surveillance and tolerance mechanisms, especially in children with immature immune systems. Chronic inflammation associated with immune dysfunction can impair childhood by suppressing the GH–IGF-1. HT042 is composed of Astragalus mongholicus, Eleutherococcus senticosus, and Phlomis umbrosa, which are medicinal herbs that are traditionally utilized in East Asia to promote growth and enhance immune function; thus, HT042 itself holds potential as an immunomodulator. We evaluated the immunomodulatory effects of HT042 in a cyclophosphamide (CYP)-induced immunosuppressed mouse model, as well as in ex vivo primary splenocytes and RAW 264.7 macrophages. HT042 demonstrated remarkable immune-enhancing effects, including the restoration of weight loss and hematological parameters, as well as enhancing NK cell activity. Primary splenocytes treated with HT042 showed increased expression of CD3, CD4, and CD8, along with Th subset transcription factors (T-bet, GATA3, RORγt, Foxp3) and corresponding cytokines (IFN-γ, IL-4, IL-17, IL-10). In RAW 264.7 macrophages, HT042 increased nitric oxide production and upregulated NOS2, COX-2, and inflammatory cytokines (IL-6, IL-1β, TNF-α). It is noteworthy that HT042 enhances both innate and adaptive immune pathways, particularly via T cell modulation and macrophage activation, as this study is among the first to demonstrate such effects in the context of CYP-induced immunosuppression.

Individuals rapidly extract information about others’ social identity, including whether or not they belong to their in-group. Group membership status has been shown to affect how attentively people encode information conveyed by those others. These findings are highly relevant for the field of psycholinguistics where there exists an open debate on how words are represented in the mental lexicon and how abstract or context-specific these representations are. Here, we used a novel word learning paradigm to test our proposal that the group membership status of speakers also affects how speaker-specific representations of novel words are. Participants learned new words from speakers who either attended their own university (in-group speakers) or did not (out-group speakers) and performed a task to measure their individual in-group bias. Then, their source memory of the new words was tested in a recognition test to probe the speaker-specific content of the novel lexical representations and assess how it related to individual in-group biases. We found that speaker group membership and participants’ in-group bias affected participants’ decision biases. The stronger the in-group bias, the more cautious participants were in their decisions. This was particularly applied to in-group related decisions. These findings indicate that social biases can influence recognition threshold. Taking a broader scope, defining how information is represented is a topic of great overlap between the fields of memory and psycholinguistics. Nevertheless, researchers from these fields tend to stay within the theoretical and methodological borders of their own field, missing the chance to deepen their understanding of phenomena that are of common interest. Here we show how methodologies developed in the memory field can be implemented in language research to shed light on an important theoretical issue that relates to the composition of lexical representations.

A subset of children with autism spectrum disorder appear to show an improvement in their behavioural symptoms during the course of a fever, a sign of systemic inflammation 1 , 2 . Here we elucidate the molecular and neural mechanisms that underlie the beneficial effects of inflammation on social behaviour deficits in mice. We compared an environmental model of neurodevelopmental disorders in which mice were exposed to maternal immune activation (MIA) during embryogenesis 3 , 4 with mouse models that are genetically deficient for contactin-associated protein-like 2 ( Cntnap2 ) 5 , fragile X mental retardation-1 ( Fmr1 ) 6 or Sh3 and multiple ankyrin repeat domains 3 ( Shank3 ) 7 . We establish that the social behaviour deficits in offspring exposed to MIA can be temporarily rescued by the inflammatory response elicited by the administration of lipopolysaccharide (LPS). This behavioural rescue was accompanied by a reduction in neuronal activity in the primary somatosensory cortex dysgranular zone (S1DZ), the hyperactivity of which was previously implicated in the manifestation of behavioural phenotypes associated with offspring exposed to MIA 8 . By contrast, we did not observe an LPS-induced rescue of social deficits in the monogenic models. We demonstrate that the differences in responsiveness to the LPS treatment between the MIA and the monogenic models emerge from differences in the levels of cytokine production. LPS treatment in monogenic mutant mice did not induce amounts of interleukin-17a (IL-17a) comparable to those induced in MIA offspring; bypassing this difference by directly delivering IL-17a into S1DZ was sufficient to promote sociability in monogenic mutant mice as well as in MIA offspring. Conversely, abrogating the expression of IL-17 receptor subunit a (IL-17Ra) in the neurons of the S1DZ eliminated the ability of LPS to reverse the sociability phenotypes in MIA offspring. Our data support a neuroimmune mechanism that underlies neurodevelopmental disorders in which the production of IL-17a during inflammation can ameliorate the expression of social behaviour deficits by directly affecting neuronal activity in the central nervous system. IL-17a induced by immune activation affects cortical neural activity and promotes social interaction in a mouse model of neurodevelopmental disorders.

Recent studies have shown that metabolic tumor volume (MTV) by positron emission tomography/computed tomography (PET/CT) is an important prognostic parameter in patients with non‐Hodgkin's lymphoma. However, it is unknown whether doxorubicin, bleomycin, vinblastine, dacarbazine (ABVD) alone in early stage Hodgkin's lymphoma would lead to similar disease control as combined modality therapy (CMT) using MTV by PET/CT. One hundred and twenty‐seven patients with early stage Hodgkin's lymphoma who underwent PET/CT at diagnosis were enrolled. The MTV was delineated on PET/CT by the area ≥SUVmax, 2.5 (standardized uptake value [SUV]). Sixty‐six patients received six cycles of ABVD only. The other 61 patients received CMT (involved‐field radiotherapy after 4–6 cycles of ABVD). The calculated MTV cut‐off value was 198 cm3. Clinical outcomes were compared according to several prognostic factors (i.e. age ≥50 years, male, performance status ≥2, stage II, B symptoms, ≥4 involved sites, extranodal site, large mediastinal mass, CMT, elevated erythrocyte sedimentation rate and high MTV). Older age (progression‐free survival [PFS], P = 0.003; overall survival [OS], P = 0.007), B symptoms (PFS, P = 0.006; OS, P = 0.036) and high MTV (PFS, P = 0.008; OS, P = 0.007) were significant independent prognostic factors. Survival of two high MTV groups treated with ABVD only and CMT were lower than the low MTV groups (PFS, P < 0.012; OS, P < 0.045). ABVD alone was sufficient to control disease in those with low MTV status. However, survival was poor, even if the CMT was assigned a high MTV status. The MTV would be helpful for deciding the therapeutic modality in patients with early stage Hodgkin's lymphoma.

Carbonic anhydrase inhibitors (CAIs) have been used for many decades in the treatment of glaucoma. Systemic CAIs were an early treatment option to lower intraocular pressure by reducing aqueous humour production; however, frequent side effects including polyuria and paresthesia contributed to the eventual development of topical CAIs. As topical drug development evolved over time, prostaglandin analogues and beta-blockers have become the gold standard of glaucoma therapies. Although prescribed less often than other classes of topical glaucoma therapies, topical CAIs continue to be used in combination therapies with beta-blockers and alpha agonists. Topical CAIs have also been demonstrated to alter biomarkers of ocular haemodynamics, which have relevance in glaucoma. The purpose of this review is to review and summarise the current state of topical CAI prescribing trends, known efficacy and suggested mechanisms and potential influence on ocular haemodynamics for the future of glaucoma management.

This study proposes a deep learning model for cortical bone segmentation in the mandibular condyle head using cone-beam computed tomography (CBCT) and an automated method for measuring cortical thickness with a color display based on the segmentation results. In total, 12,800 CBCT images from 25 normal subjects, manually labeled by an oral radiologist, served as the gold-standard. The segmentation model combined a modified U-Net and a convolutional neural network for target region classification. Model performance was evaluated using intersection over union (IoU) and the Hausdorff distance in comparison with the gold standard. The second automated model measured the cortical thickness based on a three-dimensional (3D) model rendered from the segmentation results and presented a color visualization of the measurements. The IoU and Hausdorff distance showed high accuracy (0.870 and 0.928 for marrow bone and 0.734 and 1.247 for cortical bone, respectively). A visual comparison of the 3D color maps showed a similar trend to the gold standard. This algorithm for automatic segmentation of the mandibular condyle head and visualization of the measured cortical thickness as a 3D-rendered model with a color map may contribute to the automated quantification of bone thickness changes of the temporomandibular joint complex on CBCT.

Understanding brain function requires repeatable measurements of neural activity across multiple scales and multiple brain areas. In mice, large scale cortical neural activity evokes hemodynamic changes readily observable with intrinsic signal imaging (ISI). Pairing ISI with visual stimulation allows identification of primary visual cortex (V1) and higher visual areas (HVAs), typically through cranial windows that thin or remove the skull. These procedures can diminish long-term mechanical and physiological stability required for delicate electrophysiological measurements made weeks to months after imaging (e.g., in subjects undergoing behavioral training). Here, we optimized and directly validated an intact skull ISI system in mice. We first assessed how imaging quality and duration affect reliability of retinotopic maps in V1 and HVAs. We then verified ISI map retinotopy in V1 and HVAs with targeted, multi-site electrophysiology several weeks after imaging. Reliable ISI maps of V1 and multiple HVAs emerged with ~ 60 trials of imaging (65 ± 6 min), and these showed strong correlation to local field potential (LFP) retinotopy in superficial cortical layers (r 2  = 0.74–0.82). This system is thus well-suited for targeted, multi-area electrophysiology weeks to months after imaging. We provide detailed instructions and code for other researchers to implement this system.

The G-protein-coupled receptor GPR124, acting through the canonical Wnt pathway, is required for the maintenance of blood–brain barrier function in mouse models of stroke and glioblastoma. Although blood–brain barrier (BBB) compromise is central to the etiology of diverse central nervous system (CNS) disorders, endothelial receptor proteins that control BBB function are poorly defined. The endothelial G-protein-coupled receptor (GPCR) Gpr124 has been reported to be required for normal forebrain angiogenesis and BBB function in mouse embryos, but the role of this receptor in adult animals is unknown. Here Gpr124 conditional knockout (CKO) in the endothelia of adult mice did not affect homeostatic BBB integrity, but resulted in BBB disruption and microvascular hemorrhage in mouse models of both ischemic stroke and glioblastoma, accompanied by reduced cerebrovascular canonical Wnt–β-catenin signaling. Constitutive activation of Wnt–β-catenin signaling fully corrected the BBB disruption and hemorrhage defects of Gpr124 -CKO mice, with rescue of the endothelial gene tight junction, pericyte coverage and extracellular-matrix deficits. We thus identify Gpr124 as an endothelial GPCR specifically required for endothelial Wnt signaling and BBB integrity under pathological conditions in adult mice. This finding implicates Gpr124 as a potential therapeutic target for human CNS disorders characterized by BBB disruption.

Viral infection during pregnancy is correlated with increased frequency of neurodevelopmental disorders, and this is studied in mice prenatally subjected to maternal immune activation (MIA). We previously showed that maternal T helper 17 cells promote the development of cortical and behavioural abnormalities in MIA-affected offspring. Here we show that cortical abnormalities are preferentially localized to a region encompassing the dysgranular zone of the primary somatosensory cortex (S1DZ). Moreover, activation of pyramidal neurons in this cortical region was sufficient to induce MIA-associated behavioural phenotypes in wild-type animals, whereas reduction in neural activity rescued the behavioural abnormalities in MIA-affected offspring. Sociability and repetitive behavioural phenotypes could be selectively modulated according to the efferent targets of S1DZ. Our work identifies a cortical region primarily, if not exclusively, centred on the S1DZ as the major node of a neural network that mediates behavioural abnormalities observed in offspring exposed to maternal inflammation. The authors define a specific cortical subregion of the somatosensory cortex as a critical region of dysfunction that is causal to the emergence of abnormal social and repetitive behaviours in mice exposed to maternal inflammation. Brain patches behind behavioural defects Viral infection and activation of the maternal immune system (MIA) during pregnancy has been linked to behavioural abnormalities in the offspring. In this study, Gloria Choi, Jun Huh and colleagues identify a specific cortical subregion of the somatosensory cortex as a critical region of dysfunction, and show that the presence and size of cortical patches correlate with specific social behaviours. In a related paper published this week, Gloria Choi, Jun Huh and colleagues provide evidence that MIA-mediated abnormal behavioural phenotypes require defined gut commensal bacteria for the induction of interleukin-17 (IL-17)-producing T helper 17 (T H 17) cells, in accordance with previous studies that have demonstrated a role in this association.