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This study investigates the neurocognitive underpinnings of early language learning in adults and examines the modulating effects of individual differences in prior bilingual experience and cognitive capabilities. This study used a pre/post short-term longitudinal design with a 10-day Dutch language training via Rosetta Stone. Event-Related Potentials (ERPs) were used to track neurophysiological changes during a Semantic Categorization Task (SCT), which was designed to measure the lexicalization of new words. Results showed significant reductions in N400 amplitude at post-test across all words, indicating succesful semantic integration as shown in McLaughlin et al., (2004) and Bakker et al., (2015) and rapid neural adaptation (after only 5-7 hours of learning). Higher bilingual experience predicted more reduced N400 amplitudes for cognate words, suggesting bilingualism may aid in the lexicalization of similar words across languages. Additionally, better inhibitory control (IC) predicted smaller N400s for cognates but larger N400s for non-cognates––suggesting that individuals with higher inhibitory control may manage cross-linguistic interference better for cognates, but may incur a processing cost for non-cognates. This work highlights the importance of individual differences in early language learning and advances our understanding of the interplay between language experience and neuroadaptation (Pliatsikas, 2020).

Fluent speech production remains largely preserved across adulthood, yet subtle disruptions such as pauses, repetitions, and revisions become more common with age. These disfluencies may reflect underlying cognitive and neural changes that accompany aging, particularly in executive function (EF) and large-scale brain network organization. In this study, we examined whether EF and resting-state functional connectivity (RSFC) independently or jointly explained age-related differences in naturalistic speech disfluencies in an adult lifespan sample (n = 252, ages 20-81 years). RSFC was used to assess network segregation within three systems implicated in language and cognitive control: the Language, Default Mode (DMN), and Multiple Demand (MD) networks. These task‑independent connectivity patterns provide insight into how the brain’s functional architecture impacts speech production and its age-related vulnerabilities. Our findings indicate that age was associated with increased rates of specific disfluency subtypes, such as unfilled pauses, repetitions, and revisions, as well as lower EF, lower language, MD, and DMN network segregation. Although increasing age was associated with lower EF, EF performance did not predict disfluencies or mediate their age-related increase. In contrast, higher DMN segregation predicted lower overall disfluencies, repetitions, and revisions. Age moderated the relationship between DMN segregation and repetitions, with a significant association only in younger and middle-aged adults, suggesting weaker brain-behavior relationships at older ages. DMN segregation also partially mediated the relationship between age and revisions. These findings suggest that while EF relates to planning-related disruptions, changes in functional brain organization may more directly contribute to age-related increases in self-monitoring disfluencies.

Age-related declines in cognitive function are often accompanied by changes in brain activity and network organization. This study investigated the relationship between resting state brain activity and age-related differences in speech production. We hypothesized that older adults would exhibit altered functional connectivity and activation intensity, correlating with reduced speech quality. Resting state functional MRI data were collected and a composite measure of speech complexity and fluency was calculated from younger and older adults. Results revealed significantly worse speech performance in older adults, accompanied by less segregated whole-brain networks, reduced amplitude of low-frequency fluctuations, and more heterogeneous brain states. Univariate regression analyses indicated stronger brain-behavior relationships in younger adults, while multivariate regression analyses revealed that age-related differences in resting state brain state patterns critically relate to speech production differences. Notably, the language network remained relatively stable with age, whereas whole-brain status became very important for speech performance in older adults. These findings suggest that resting state brain activity, particularly whole brain network characteristics, may serve as a stable biomarker of age-related changes in speech production.

The study of the brains’ oscillatory activity has been a standard technique to gain insights into human neurocognition for a relatively long time. However, as a complementary analysis to ERPs, only very recently has it been utilized to study bilingualism and its neural underpinnings. Here, we provide a theoretical and methodological starter for scientists in the (psycho)linguistics and neurocognition of bilingualism field(s) to understand the bases and applications of this analytical tool. Towards this goal, we provide a description of the characteristics of the human neural (and its oscillatory) signal, followed by an in-depth description of various types of EEG oscillatory analyses, supplemented by figures and relevant examples. We then utilize the scant, yet emergent, literature on neural oscillations and bilingualism to highlight the potential of how analyzing neural oscillations can advance our understanding of the (psycho)linguistic and neurocognitive understanding of bilingualism.

Numerous modern technologies are reliant on the low-phase noise and exquisite timing stability of microwave signals. Substantial progress has been made in the field of microwave photonics, whereby low-noise microwave signals are generated by the down-conversion of ultrastable optical references using a frequency comb 1 – 3 . Such systems, however, are constructed with bulk or fibre optics and are difficult to further reduce in size and power consumption. In this work we address this challenge by leveraging advances in integrated photonics to demonstrate low-noise microwave generation via two-point optical frequency division 4 , 5 . Narrow-linewidth self-injection-locked integrated lasers 6 , 7 are stabilized to a miniature Fabry–Pérot cavity 8 , and the frequency gap between the lasers is divided with an efficient dark soliton frequency comb 9 . The stabilized output of the microcomb is photodetected to produce a microwave signal at 20 GHz with phase noise of −96 dBc Hz −1 at 100 Hz offset frequency that decreases to −135 dBc Hz −1 at 10 kHz offset—values that are unprecedented for an integrated photonic system. All photonic components can be heterogeneously integrated on a single chip, providing a significant advance for the application of photonics to high-precision navigation, communication and timing systems. We leverage advances in integrated photonics to generate low-noise microwaves with an optical frequency division architecture that can be low power and chip integrated.

Hidradenitis suppurativa (HS) is a chronic inflammatory disease characterized by abscesses, nodules, dissecting/draining tunnels, and extensive fibrosis. Here, we integrate single-cell RNA sequencing, spatial transcriptomics, and immunostaining to provide an unprecedented view of the pathogenesis of chronic HS, characterizing the main cellular players and defining their interactions. We found a striking layering of the chronic HS infiltrate and identified the contribution of 2 fibroblast subtypes (SFRP4+ and CXCL13+) in orchestrating this compartmentalized immune response. We further demonstrated the central role of the Hippo pathway in promoting extensive fibrosis in HS and provided preclinical evidence that the profibrotic fibroblast response in HS can be modulated through inhibition of this pathway. These data provide insights into key aspects of HS pathogenesis with broad therapeutic implications.

Demyelination of cerebral white matter is thought to drive neuronal degeneration and permanent neurological disability in individuals with multiple sclerosis. Findings from brain MRI studies, however, support the possibility that demyelination and neuronal degeneration can occur independently. We aimed to establish whether post-mortem brains from patients with multiple sclerosis show pathological evidence of cortical neuronal loss that is independent of cerebral white-matter demyelination. Brains and spinal cords were removed at autopsy from patients, who had died with multiple sclerosis, at the Cleveland Clinic in Cleveland, OH, USA. Visual examination of centimetre-thick slices of cerebral hemispheres was done to identify brains without areas of cerebral white-matter discoloration that were indicative of demyelinated lesions (referred to as myelocortical multiple sclerosis) and brains that had cerebral white-matter discolorations or demyelinated lesions (referred to as typical multiple sclerosis). These individuals with myelocortical multiple sclerosis were matched by age, sex, MRI protocol, multiple sclerosis disease subtype, disease duration, and Expanded Disability Status Scale, with individuals with typical multiple sclerosis. Demyelinated lesion area in tissue sections of cerebral white matter, spinal cord, and cerebral cortex from individuals classed as having myelocortical and typical multiple sclerosis were compared using myelin protein immunocytochemistry. Neuronal densities in cortical layers III, V, and VI from five cortical regions not directly connected to spinal cord (cingulate gyrus and inferior frontal cortex, superior temporal cortex, and superior insular cortex and inferior insular cortex) were also compared between the two groups and with aged-matched post-mortem brains from individuals without evidence of neurological disease. Brains and spinal cords were collected from 100 deceased patients between May, 1998, and November, 2012, and this retrospective study was done between Sept 6, 2011, and Feb 2, 2018. 12 individuals were identified as having myelocortical multiple sclerosis and were compared with 12 individuals identified as having typical multiple sclerosis. Demyelinated lesions were detected in spinal cord and cerebral cortex, but not in cerebral white matter, of people with myelocortical multiple sclerosis. Cortical demyelinated lesion area was similar between myelocortical and typical multiple sclerosis (median 4·45% [IQR 2·54–10·81] in myelocortical vs 9·74% [1·35–19·50] in typical multiple sclerosis; p=0·5512). Spinal cord demyelinated area was significantly greater in typical than in myelocortical multiple sclerosis (median 3·81% [IQR 1·72–7·42] in myelocortical vs 13·81% [6·51–29·01] in typical multiple sclerosis; p=0·0083). Despite the lack of cerebral white-matter demyelination in myelocortical multiple sclerosis, mean cortical neuronal densities were significantly decreased compared with control brains (349·8 neurons per mm2 [SD 51·9] in myelocortical multiple sclerosis vs 419·0 [43·6] in controls in layer III [p=0·0104]; 355·6 [46·5] vs 454·2 [48·3] in layer V [p=0·0006]; 366·6 [50·9] vs 458·3 [48·4] in layer VI [p=0·0049]). By contrast, mean cortical neuronal densities were decreased in typical multiple sclerosis brains compared with those from controls in layer V (392·5 [59·0] vs 454·2 [48·3]; p=0·0182) but not layers III and VI. We propose that myelocortical multiple sclerosis is a subtype of multiple sclerosis that is characterised by demyelination of spinal cord and cerebral cortex but not of cerebral white matter. Cortical neuronal loss is not accompanied by cerebral white-matter demyelination and can be an independent pathological event in myelocortical multiple sclerosis. Compared with control brains, cortical neuronal loss was greater in myelocortical multiple sclerosis cortex than in typical multiple sclerosis cortex. The molecular mechanisms of primary neuronal degeneration and axonal pathology in myelocortical multiple sclerosis should be investigated in future studies. US National Institutes of Health and National Multiple Sclerosis Society

Chronic pruritus accounts for approximately 1 % of all physician visits, and providers are often confronted with how to treat patients with pruritus. Scabies is oftentimes a concern by both patients and providers, and anti-scabietic treatments are generally considered safe and effective. However, the pruritus will continue if there is an alternate etiology. We present a case of a patient empirically treated for scabies with multiple courses of anti-scabietic therapy without diagnostic confirmation of scabies. Her pruritus failed to improve, and she ultimately developed delusions of infestation (DI), a debilitating and difficult-to-treat psychocutaneous condition characterized by a fixed, false belief that one is infested with parasites. While scabies is one cause of chronic pruritus, its misdiagnosis may increase the chance that at-risk individuals, often those with prior substance abuse or psychiatric disorders, develop a persistent concern for ongoing infestation. It is possible that, in treating chronic pruritus with repeated empiric anti-scabietic treatments, the prescribing physician may contribute to the development of DI. We review the approach to a patient with chronic pruritus and ways to avoid unnecessary repeated anti-scabietic treatments.

Acute myeloid leukemia (AML) is a genetically heterogeneous, aggressive hematological malignancy induced by distinct oncogenic driver mutations. The effect of specific AML oncogenes on immune activation or suppression is unclear. Here, we examine immune responses in genetically distinct models of AML and demonstrate that specific AML oncogenes dictate immunogenicity, the quality of immune response and immune escape through immunoediting. Specifically, expression of Nras G12D alone is sufficient to drive a potent anti-leukemia response through increased MHC Class II expression that can be overcome with increased expression of Myc. These data have important implications for the design and implementation of personalized immunotherapies for patients with AML. There is increasing evidence of a functional interaction between acute myeloid leukemia (AML) and immune cells, influencing disease outcome. Here the authors study how distinct oncogenes differentially affect the host immune response to leukemic cells in preclinical models of AML.