The evolution of complex brains required the incorporation of newly evolved neurons into existing circuits, yet the genetic and developmental mechanisms enabling their integration remain poorly understood. Butterflies expanded their color vision by adding a second R7 photoreceptor per ommatidium, a rare departure from the conserved insect eye ground plan. Because each R7 makes an independent stochastic fate choice, this duplication increased the number of ommatidial types from two to three. We identified the genetic basis of this expansion and demonstrated how the brain accommodates the new input. R7 duplication was achieved by converting R3/4 cells to an R1/6 fate, triggering the R7 recruitment program on both sides of the ommatidium. By manipulating transcription factor expression in Drosophila, we engineered a "butterfly-fly" that recapitulates this ancient R7 duplication and three-type stochastic mosaic. In the fly brain, two R7 subtypes connect to specific types of Dm8 neurons, which are born in excess and undergo apoptosis if they fail to find synaptic partners. In our butterfly-fly model, these surplus Dm8s are immediately rescued and form subtype-appropriate connections. These findings suggest that population-level variation maintains a reservoir of potentially interacting neurons, providing a developmental substrate that allows the brain to immediately accommodate newly evolved neurons.

Human gastrointestinal anatomy evolved under conditions of food scarcity, low-caloric-density diets, and high physical activity. In this context, a relatively gastric-accommodation stomach capacity conferred a survival advantage by allowing consumption of large volumes of fibrous, low-energy foods, buffering seasonal shortages, and maximizing intake during rare periods of abundance. Modern food environments, characterized by constant access to energy-dense foods and sedentary lifestyles, have reversed these selective pressures, creating an evolutionary mismatch between ancestral digestive physiology and contemporary diets. This narrative review explores how a digestive architecture shaped by scarcity may become maladaptive in modern high-calorie conditions and examines stomach capacity as an under-recognized contributor to obesity and metabolic disease. Evidence was synthesized from evolutionary biology, anthropology, gastroenterology, and metabolic medicine using literature identified in PubMed, Scopus, and Web of Science (1990-2024). Evolutionary and anthropological evidence suggests that increased gastric volume was advantageous in both pre-agrarian and agrarian societies. In contrast, in modern environments this trait may promote excessive energy intake, delayed satiety, and metabolic dysfunction, particularly in the presence of ultra-processed foods. Clinical observations from bariatric surgery support this framework, as surgical reduction of gastric volume induces rapid metabolic improvements, often preceding significant weight loss. Gastric accommodation capacity, once adaptive, may now contribute to metabolic disease in obesogenic environments, reframing obesity as a predictable consequence of evolutionary mismatch.

Electrochromic tungsten oxide (WO3) films suffer from gradual performance degradation during repeated ion insertion/extraction processes, while the relationship between electrolyte-dependent ion accommodation and structural stability remains insufficiently understood. Herein, magnetron-sputtered WO3 thin films were systematically investigated in H2SO4, LiClO4, ZnSO4, and Al2(SO4)3 electrolytes to clarify the coupling relationship among ion accommodation, electronic structure evolution, microstructural retention, and electrochromic durability. Combined electrochemical measurements with UV-visible spectroscopy, atomic force microscopy (AFM), scanning electron microscopy (SEM), X-ray photoelectron spectroscopy (XPS), and reflected electron energy loss spectroscopy (REELS) reveal that electrolyte chemistry regulates the balance between electrochemical activation and structural tolerance. Highly mobile H[+] and strongly interacting Al[3+] ions promote rapid ion transport and enhanced W[6+] reduction but may induce excessive structural perturbation, defect accumulation, and accelerated degradation during cycling. Zn[2+] exhibits intermediate behavior, whereas Li[+] enables balanced ion accommodation through reversible W[6+]/W[5+] conversion while preserving the WO3 framework. Consequently, the LiClO4 electrolyte achieves superior electrochromic performance with an optical modulation of 80.97% and improved cycling stability. These results demonstrate that durable electrochromic behavior is governed not by maximizing ion transport or reduction degree, but by achieving a reversible ion accommodation regime compatible with the structural tolerance of the host framework. This work provides a microstructure-oriented strategy for designing stable WO3-based electrochromic devices through electrolyte regulation.

Renatured β-1,3-1,6-glucan nanoparticles (r-glucan NPs) are hydrated polysaccharide nanostructures formed by alkali dissociation and neutralization-induced renaturation of glucan chains. Unlike rigid molecular hosts, their guest-accommodating environments are flexible, heterogeneous, and water-accessible. Here, aromatic guest incorporation into r-glucan NPs was investigated using resveratrol as a model guest for solvent-exchange analysis and 32 stilbene, azobenzene, and cinnamic acid derivatives as molecular probes. Solvent-exchange experiments showed that acetone-dependent loading conditions affected resveratrol retention, the transient colloidal state of r-glucan NPs, the recovered-complex state, and the chiral organization of retained resveratrol. Descriptor-based analysis revealed that guest molar fraction was positively associated with polarity- and hydrogen-bonding-related descriptors, including tPSA, OH count, and dipole moment, whereas logP and hydrophobic surface area showed negative correlations. Pairwise two-descriptor regression identified the logP/OH count model as the most chemically interpretable descriptor combination, highlighting the need to suppress excessive hydrophobic self-association while enabling hydroxy-group-derived stabilization. These results support a model in which aromatic guest incorporation is governed by kinetic selection during solvent exchange followed by stabilization within a hydrated glucan matrix. This study clarifies the inclusion characteristics of flexible hydrated polysaccharide matrices and provides descriptor-guided design principles for aromatic guest incorporation into r-glucan NPs.

Persistent postural-perceptual dizziness (PPPD) is a common chronic functional neuro-otological disorder characterized by persistent non-spinning dizziness, unsteadiness, and heightened sensitivity to upright posture, motion, and visually complex environments. Several conceptual models have been proposed to explain its persistence, including failure of readaptation after a destabilizing event, maladaptive multisensory integration with excessive visual or somatosensory weighting, and prediction-actual sensory mismatch with amplified prediction errors. This narrative review synthesizes neuroimaging, behavioral, psychophysical, and clinical evidence to examine attentional dysfunction as a candidate organizing mechanism that may link these partly overlapping pathways. Structural and functional alterations involving the dorsolateral prefrontal cortex (DLPFC), anterior cingulate cortex (ACC), posterior insula, precuneus, visual cortex, vestibular cortical regions, and large-scale attention, salience, sensorimotor, visual, and default-mode networks suggest distributed functional reorganization rather than a single lesional substrate. Behavioral studies indicate that postural control and self-motion perception may become excessively attention-dependent in subsets of patients, with dual-task effects, altered visual exploration, stiffened postural strategies, and abnormal sensory-perceptual scaling. Clinical studies further show balance vigilance, attentional bias, and heterogeneous symptom phenotypes, including visual intolerance, quiet standing or sitting intolerance, passive motion intolerance, and active motion intolerance. We propose a revised active-inference model in which attention contributes to dysregulated precision weighting across visual, vestibular, somatosensory, interoceptive, and postural prediction-error signals. This model is hypothesis-generating rather than definitive. It accommodates patients with or without a clear preceding vestibular disorder and patients whose symptoms occur without overt body motion. The framework highlights testable targets for future studies using event-related potentials, computational modeling, dual-task paradigms, and phenotype-stratified treatment trials.

Predicting cooperative behavior and thermodynamic nonideality in heterogeneous molecular solids remains challenging because activity coefficients and collective phase behavior are typically treated within separate theoretical frameworks. Here, we show that both quantities can be interpreted as manifestations of a common boundary mismatch free energy associated with local structural incompatibility within the correlated crystalline environments. Using a minimal coarse-grained statistical-mechanical framework, the energetic penalty associated with boundary formation is shown to govern both excess chemical potential and correlation length, thereby linking activity coefficients to the cooperative domain size. Triacylglycerol (TAG) molecular solids are used as an experimentally accessible model system, because solid-state activity coefficients and cooperative melting behavior can be independently extracted from equilibrium melting transitions. Reanalysis of previously reported thermodynamic data reveals a crossover from entropy-dominated to mismatch-controlled behavior together with scaling consistent with an exponential dependence of cooperativity on the boundary mismatch free energy. The results suggest that activity coefficients in heterogeneous molecular solids encode information not only about thermodynamic nonideality but also about correlated structural organization, domain connectivity, and structural accommodation. More broadly, the framework provides a physical interpretation of cooperative behavior in terms of interfacial mismatch energetics and suggests that activity coefficients may serve as experimentally accessible probes of correlations and collective organization in hierarchical matter.

This paper analyses the workplace as a critical site where overdiagnosis is institutionally reconfigured. Drawing on ethnographic fieldwork in three workspaces hosting technology startups and creative agencies in Lisbon, Portugal, including participant observation and in-depth interviews with twelve neurodivergent employees and three HR managers, the paper traces how the neurodiversity movement's ethos of "difference, not deficit" is absorbed into organisational governance. It explores how initiatives framed as inclusive often intensify institutional demands for formal diagnosis as a prerequisite for accommodations, recognition, and employability itself. For employees, diagnosis operates ambivalently as both a gateway to support and a mechanism of surveillance tying legitimacy to a medical label; for HR managers, diagnostic categories function as managerial tools that render difference legible, predictable, and optimisable. The paper identifies two institutional logics driving this expansion: a gatekeeping logic, in which diagnosis is still required to access protection, and a celebratory logic, largely absent from existing accounts of institutional diagnosis, in which certified difference is marketed as a productive organisational value, intensifying rather than easing diagnostic demand. Together, these logics extend theories of institutional classification to the workplace as a distinctive site and show that norms of able-bodiedness operate through incorporation as much as exclusion. Overdiagnosis thus emerges less as a matter of clinical excess than as a socio-institutional phenomenon. The Portuguese case offers a Southern European perspective on dynamics of diagnostic expansion examined primarily in Anglo-American contexts, with implications for identity, governance, and the definition of the legitimate worker.

Antifluorite oxides containing ordered tetrahedral voids provide a structurally flexible platform for Li-ion transport; however, experimentally identifying and controlling the defect configurations that activate these voids remains challenging. Here, Li-excess defect engineering is demonstrated in orthorhombic Li5AlO4 to regulate its Li-ion transport behavior. High-resolution time-of-flight neutron powder diffraction (TOF-NPD), combined with Rietveld refinement and Fourier difference nuclear-density mapping, resolves the underlying Li-related defect architecture. The refinement results reveal that excess Li is accommodated through the coupled formation of Al/Li antisite occupancy at the 2a Wyckoff site and newly occupied interstitial Li at the intrinsically vacant 2b site, accompanied by systematic lattice expansion and local structural relaxation. BVSE-guided CI-NEB calculations reveal a multistep Li-ion migration network, in which the three-dimensional bottleneck decreases from 0.43 eV in pristine Li5AlO4 to 0.40 eV in the coupled-defect model, while the local migration segments directly involving the occupied 2b site exhibit larger barrier reductions. Consistently, electrochemical impedance spectroscopy shows an increase in the room-temperature bulk ionic conductivity to 3.33 × 10-7 S cm-1 for the Li-excess sample. These findings establish an experimentally validated correlation between Li-related defect chemistry and ion transport in Li5AlO4, providing guidance for defect-enabled transport design in antifluorite oxide conductors.

Memantine is a primary pharmacological treatment for moderate-to-severe Alzheimer's disease but its efficacy and brain delivery remain limited. Lipid bicontinuous cubic phases and their nanoparticle dispersions (cubosomes) offer platforms for enhancing central nervous system drug delivery, yet the rigid adamantane scaffold of memantine can destabilise lipid organisation. This study resolves how an amphiphilic, adamantane-containing drug interacts with non-lamellar lipid bilayers using monoolein-based bulk cubic mesophases and cubosomes formulated with biomimetic lipid compositions and multiple stabilisers. SAXS revealed that lipid composition primarily governed mesophase structure, while memantine induced only modest structural changes in bulk cubic phases. Following memantine incorporation, cubosomes retained cubic symmetry and colloidal stability across stabilisers, although they were more susceptible than bulk phases to additive-induced disorder, with cryo-TEM showing transitions toward less ordered, lower curvature sponge-like structures. Bulk mesophases exhibited 3-5-fold higher apparent drug retention than nanoparticle dispersions. Under excess hydration, however, even bulk phases released memantine rapidly, losing ∼65% of the drug within 24 h. SANS and molecular dynamics simulations revealed a mobile state of memantine with predominantly interfacial localisation rather than stable burial within the hydrophobic tails, providing a mechanistic explanation for its mesophase-dependent structural effects and its limited retention. These findings show that the adamantane scaffold alone is insufficient to ensure efficient incorporation into cubic phases. Localisation, accommodation, and retention are governed by the balance between hydrophobic anchoring and the hydration demands of attached functionalities, establishing a mechanistic framework for predicting the behaviour of amphiphilic adamantane-containing therapeutics in non-lamellar lipid nanocarriers.

Excessive hypercholesterolemia (eHC) in pregnancy is associated with complications such as preeclampsia, yet its impact on maternal cardiac adaptation and long-term cardiovascular health remains unclear. We hypothesized that eHC impairs maternal cardiac structure and function during pregnancy and that these effects persist postpartum. Sprague Dawley rats were fed either a control diet (CTL) or high-cholesterol diet (eHC) from gestational day (GD) 6-20 (term = 22 days). Echocardiography was performed before pregnancy, at GD20, and 3 mo postpartum. Plasma and left ventricular tissue were collected at GD20 and postpartum for molecular analyses. CTL dams demonstrated normal pregnancy-associated cardiac adaptations, including increased diastolic left ventricular internal diameter, stroke volume, cardiac output, and diastolic left ventricular volume in late pregnancy, with normalization postpartum. These adaptations were attenuated in eHC dams. In late pregnancy, eHC dams exhibited reduced stroke volume and cardiac output compared with CTL, along with alterations in diastolic function, including reduced mitral valve A' velocity. Postpartum, eHC dams showed changes in diastolic indices, including reduced mitral valve A-wave velocity and E'/A' ratio. Measures of systolic performance (ejection fraction and fractional shortening) were unchanged between groups. Molecular analyses revealed increased cardiomyocyte size, altered collagen remodeling characterized by an increased type I collagen (COL1)-to-type I collagen 3 (COL3) ratio, and elevated CD31 expression in eHC dams during pregnancy. Postpartum, collagen remodeling was evident, but now with reduced COL1 and increased COL3 expression. Together, these findings demonstrate that eHC disrupts normal maternal cardiac adaptation during pregnancy and promotes adverse remodeling and cardiac dysfunction postpartum, with potential implications for long-term cardiovascular disease risk.NEW & NOTEWORTHY Excessive hypercholesterolemia impairs the adaptive cardiac remodeling normally associated with pregnancy and postpartum recovery, indicating reduced cardiac plasticity. Although systolic function remained preserved, altered hemodynamic responses, diastolic parameters, and tissue markers indicate early subclinical maladaptive remodeling. These findings suggest that excessive hypercholesterolemia compromises the maternal heart's ability to accommodate the physiological demands of pregnancy.

Background and Clinical Significance: Hemophagocytic lymphohistiocytosis (HLH) is a life-threatening hyperinflammatory syndrome characterized by excessive activation of the immune system. Case Presentation: We present the case of an eight-month-old infant with influenza A(H1N1) who presented with seizures, hepatosplenomegaly, cytopenias, and markedly elevated levels of ferritin, IL-18, and CXCL9, raising concern for HLH. Despite initiation of HLH-directed and antiviral therapy, she succumbed to cardiorespiratory failure. Genetic testing revealed heterozygous variants in LYST and NLRC4, suggesting a potential genetic predisposition. Conclusions: This case underscores the challenge of distinguishing primary from secondary HLH and highlights the importance of balancing aggressive immunosuppression with infection control. Early genetic and cytokine profiling may assist in guiding personalized treatment strategies, enabling targeted interventions that avoid excessive immunosuppressive treatment in cases of reactive hyperinflammation while facilitating timely escalation of therapy in true or refractory HLH.

Excessive moisture sensitivity of pristine HKUST-1 often causes rapid framework collapse and burst release under highly humid conditions, limiting its use as a humidity-triggered carrier for volatile antimicrobials. Here, we report a hierarchically porous composite aerogel constructed by in situ growth of HKUST-1 within a poly (vinyl alcohol)/carboxymethyl chitosan/TEMPO-oxidised cellulose nanofiber network, followed by carvacrol (CAR) loading to obtain PCTH@CAR. This confined growth architecture regulated metal organic framework (MOF) distribution, helped moderate moisture-induced structural disruption, and coupled polymer-derived macropores with MOF micropores, thereby improving cargo accommodation and release control. The cumulative CAR release reached 54.32% after 12 d even at 15% RH, while at 98% RH it reached 34.61% after 2 d and 81.99% after 12 d, with release sustained throughout storage rather than concentrated at the initial stage. The aerogel also showed effective vapour phase antimicrobial activity against Escherichia coli, Staphylococcus aureus, and Botrytis cinerea. In strawberry packaging, PCTH@CAR delayed visible spoilage and reduced weight loss from 20.45% to 2.04% after 8 d, whereas untreated strawberries had already lost marketability by day 4 owing to evident mould growth and softening. These results support in situ grown HKUST-1 within a hierarchically porous biopolymer aerogel as a practical route to non-contact, humidity-adaptive active packaging for postharvest preservation.