Wind-farm planning requires practical methods for identifying potential ecological conflicts before detailed project-level surveys. Existing seabird sensitivity assessments are less suitable for species whose breeding distributions shift among years and whose marine use areas are difficult to delineate, because space use depends on colony location and central-place foraging constraints. Here, we present a screening framework for such species, using Little Tern Sternula albifrons in Japan as a case study. The framework integrates three components: (1) MaxEnt-based nesting suitability from 95 occupied 500-m grid cells, (2) energetically constrained foraging accessibility derived from a central-place foraging model parameterised with field observations and prey-energy data, and (3) wind-turbine response quantified from three-dimensional flight tracking. The MaxEnt model identified bare land as the strongest positive predictor of suitable nesting area, highlighting extensive high-potential coastal habitat. The foraging model estimated a maximum one-way foraging distance of 8.92 km from nesting colonies under the median prey-energy scenario, allowing marine use areas to be mapped from suitable nesting sites. Mapped areas overlapped with offshore wind projects under environmental impact assessment, and with government-designated pre-EIA planning areas. Ornithodolite tracking showed clear horizontal turbine avoidance, with significantly fewer approaches at radii of 60–140 m from turbine tower centres and no trajectories recorded within 70 m. Together, these components provide a first-pass spatial screen of potential conflict between offshore wind development and breeding Little Terns, identifying areas requiring detailed site-specific surveys. The framework is intended for early-stage screening and does not estimate collision mortality or population-level consequences.
The anterior cingulate cortex (ACC), crucial for executive function, is frequently impaired in progressive supranuclear palsy (PSP), yet mechanisms underlying this selective vulnerability remain unclear. Given the integration of astrocytes into neural circuits, we hypothesized that astrocyte dysfunction and altered astrocyte–neuron crosstalk contribute to functional abnormalities in the ACC in PSP. To test this hypothesis, we conducted a multimodal analysis integrating SWATH-MS-based proteomics, histopathology, and in vivo magnetic resonance spectroscopy (MRS) in postmortem and living brains of patients with PSP and healthy controls (HCs). The astrocytic markers glial fibrillary acidic protein (GFAP) and aquaporin-4 (AQP4) were significantly elevated in the ACC of patients with PSP compared with those in HCs. Enhanced astrocytic Ca2⁺ signaling through the IP3-Ca2⁺ cascade was suggested in the ACC of patients with PSP, consistent with elevated myo-inositol levels on MRS. Proteomic data revealed reduced expression of pyruvate dehydrogenase complex components (DLD and PDHX) and oxidative phosphorylation-related proteins, including astrocyte-enriched genes such as ETFDH and UQCRC1. MRS also revealed significantly increased levels of lactate and glutamate in the ACC of patients with PSP compared with those in HCs. Notably, myo-inositol, lactate, and glutamate levels were positively correlated, indicating astrocyte-associated metabolic dysfunction. Expression of glutamate–glutamine cycle-related molecules and neuronal markers was negatively correlated with GFAP and AQP4 levels, suggesting that astrocytic dysfunction is associated with alterations in the excitatory/inhibitory balance in the ACC of patients with PSP. These findings demonstrate that multiple aspects of astrocyte–neuron crosstalk, including AQP4-mediated glymphatic clearance, energy metabolism, and neurotransmitter cycling, are altered in the ACC of patients with PSP. Such disruptions may contribute to neuronal dysfunction. Our study highlights astrocyte dysfunction as a central feature of the PSP pathophysiology.
p62/SQSTM1 self-assembles with polyubiquitin into liquid-like condensates ("p62 bodies") that function as stress-signaling hubs and selective autophagy cargo. We show that TBK1-dependent phosphorylation at Ser403 acts as a threshold-dependent modulator of a condensate's physical properties and promotes their rapid autophagic clearance. Phosphorylation within p62 bodies drives a transition from large, fluid droplets to compact, gel-like condensates that efficiently capture LC3-positive isolation membranes and accelerate the autophagic removal of ubiquitinated proteins. PP2A holoenzymes containing PPP2R5A/B/E, recruited via a KEAP1 bridge, counteract TBK1 by dephosphorylating Ser403. Homozygous p62S403E/S403E knock-in embryonic stem cells differentiate into post-mitotic neurons enriched in miniaturized, gel-like p62 bodies. Consistently, phosphorylation-mimetic knock-in mice show similar remodeling of p62 condensates in vivo, demonstrating that this phosphorylation-driven mechanism maintains proteostasis across scales. We propose that Ser403 phosphorylation functions as a molecular switch that couples the material state of p62 condensates to their stability and serves as a central control point for p62-mediated protein degradation.
To define the clinical spectrum and treatment responses of anti-Kelch-like protein 11 (KLHL11) IgG-associated neurological syndromes by screening a large, expanded cohort of patients with suspected autoimmune cerebellar ataxia (ACA), autoimmune encephalitis (AE), and related neurological disorders. In this retrospective, observational study, serum samples from 930 patients collected from over 100 medical institutions across Japan between 2002 and 2025 were screened. The study population was categorized into five cohorts: cerebellar ataxia (CA) of unknown etiology (n = 778), AE (n = 49), brainstem encephalitis (n = 2), myelitis (n = 12), and multiple system atrophy (MSA) (n = 89). Anti-KLHL11 antibodies were detected using a fixed cell-based assay with HEK293T cells. Cerebrospinal fluid was analyzed in all serum-positive cases. Anti-KLHL11 antibodies were identified in four cases, three males and one female with a mean onset age > 60 years, all showing dual positivity in serum and cerebrospinal fluid. The clinical phenotypes consisted of predominantly CA (n = 2), combined limbic encephalitis (LE) and CA (n = 1), and isolated LE associated with small-cell lung cancer (n = 1). Notably, none of the cases were associated with testicular tumor. While typical paraneoplastic presentations were observed, one patient had no detectable malignancy and improved with immunotherapy alone, and another showed neurological recovery following treatment of a non-testicular tumor. Anti-KLHL11 antibodies were absent in all disease controls with MSA. Expanding our initial findings, this nationwide study indicates that anti-KLHL11 antibody-associated ACA and AE are rare but increasingly recognized in Japan and may be under-recognized globally. The clinical spectrum of anti-KLHL11 antibody-associated neurological diseases is broad, including females and individuals without a detectable testicular tumor. Importantly, patients presenting with AE may show more favorable responses to immunotherapy or tumor-directed treatment than those with isolated CA, highlighting the importance of early recognition and phenotype-specific management.
In this study, the structural, compositional, and electrical properties of nanocrystalline silicon/silicon oxide (nc-Si/SiOx) composite films fabricated by plasma-enhanced chemical vapor deposition were investigated for high-performance Si solar cells. The Si-rich layers in the composite layer precursor were deposited using various [CO2]/([SiH4] + [CO2]) flow rate ratios and post-deposition annealing was performed to induce nc-Si formation. Auger electron spectroscopy confirmed that the Si/O ratio of the Si-rich layers can be tuned by the gas flow rate ratio. Cross-sectional transmission electron microscope images revealed nc-Si formation was promoted and its areal density increased by decreasing the gas flow rate ratio. The passivation performance exhibited a clear optimum at an oxygen concentration of similar to 5 at.%, whereas both higher and lower O contents degraded the effective carrier lifetime. In contrast, the electrical resistance increased monotonically with O concentration, suggesting improved carrier transport in Si-rich films with higher nc-Si density. No trade-off was observed between conductivity and passivation, demonstrating that both can be independently optimized. These results show that controlling the gas flow rate ratio and annealing enables simultaneous improvement of passivation and carrier conduction in nc-Si/SiOx layers.
