Elekta's Monaco (Elekta AB, Stockholm, Sweden) treatment planning system (TPS) introduces script-based automation functionality. This study developed and validated a fully script-based automated radiotherapy planning solution for whole-brain radiotherapy (WBRT) based on the Monaco TPS. This approach not only enables complete automation of the planning workflow but also effectively enhances plan quality while meeting clinical dose requirements. To systematically compare dosimetric, radiobiological, and operational performance between script-generated automated plans and clinically approved manual WBRT plans on the Monaco TPS. A retrospective analysis of 20 WBRT patients was conducted. A custom C# ASP.NET script was programmed in Visual Studio 2022 for end-to-end automated template optimization. Plan quality was assessed against clinical manual plans based on a RapidPlan scoring system. Paired t-tests or Wilcoxon signed-rank tests were used to compare planning target volume (PTV) and organ-at-risk (OAR) dosimetry, beam delivery parameters, equivalent uniform dose (EUD), tumor control probability (TCP), and normal tissue complication probability (NTCP). No statistically significant inter-group differences were detected for PTV coverage metrics, majority OAR dose-volume endpoints, beam delivery parameters, or total plan quality scores (p > 0.05). Manual plans yielded significantly lower optic nerve D0.03cc (2874.42 vs 3014.61 cGy, p < 0.05), while automated plans produced significantly reduced mean doses to bilateral parotid glands (566.84 vs 675.30 cGy, p < 0.001) and cochleae (2687.25 vs 2819.73 cGy, p < 0.05). PTV EUD and TCP were nearly identical between 2 planning strategies. For radiobiological indices, automated plans demonstrated statistically elevated NTCP for hippocampi, brainstem, eyes, and optic nerves (p < 0.05). Automated batch processing drastically reduced recorded planning workflow time, though retrospective manual timestamps carry inherent measurement bias. The proposed Monaco scripting workflow reliably generates WBRT plans meeting all institutional clinical dose criteria, with favorable automated sparing of parotid and cochlear tissues. This script tool delivers consistent baseline planning and batch-processing efficiency; multicenter large-cohort validation across variable cranial anatomy is required before universal routine clinical deployment.

Why is human music rhythmically structured the way it is? One hypothesis is that the human brain is intrinsically wired to favor specific rhythmic organizations. To test this, we collected diffusion and resting-state functional MRI (fMRI) data from musically untrained participants and, weeks later, asked them to imitate randomly generated drumming sequences using finger taps. These imitations exhibited systematic biases toward temporal structures widespread in human music: predictable patterns characterized by isochronous organization (1:1) and other small integer ratios (2:1 and 3:1). Functional connectome analyses linked the increased rhythmic predictability of reproduced rhythms to intrinsic interactions between networks implicated in auditory timing (auditory basal ganglia) and executive control (task-positive and task-negative networks). Notably, the tendency toward isochrony-a feature highly conserved across species-was selectively associated with increased fiber density within a cortico-basal ganglia-thalamo-cortical network previously implicated in the perception and production of a metronomic pulse from music (the "beat"). Our findings reveal how stable neural architecture predisposes humans to produce rhythmically structured patterns. This evidence links intrinsic brain circuitry to individual cultural expressions, supporting the account of human symbolic systems, including music, as biocultural hybrids.

Communication difficulties in older adults are only partially explained by elevated hearing thresholds, suggesting that age-related changes in auditory nerve function contribute to disability beyond conventional measures of hearing sensitivity. Myelin degeneration is increasingly recognized as a fundamental feature of neural aging, yet its contribution to auditory nerve dysfunction remains poorly understood because validated in vivo biomarkers are lacking. We developed a normative physiological phenotyping framework by modeling the relationship between auditory nerve response amplitude and neural synchrony in younger adults and quantifying deviations from this relationship in older adults. Unsupervised clustering identified two auditory nerve phenotypes characterized by neural synchrony that was either as expected-or-better or poorer-than-expected relative to response amplitude, independent of age and hearing thresholds. The poorer-than-expected phenotype exhibited lower fractional anisotropy and higher radial and mean diffusivity in the auditory nerve, consistent with reduced myelin integrity. Human temporal bone diffusion MRI demonstrated changes in the same imaging metrics that corresponded with histological evidence of myelin degeneration, providing converging anatomical support for the imaging findings. Finally, the relationship between hearing loss and self-reported hearing difficulties differed between physiological phenotypes, demonstrating that poorer-than-expected neural synchrony amplifies the functional consequences of hearing loss. Together, these findings establish a physiologically defined, histologically validated biomarker of auditory nerve aging, implicate myelin degeneration as a previously underrecognized contributor to age-related communication difficulties, and introduce a general framework for identifying biologically meaningful neural aging phenotypes in living humans.

The amplitudes of the human compound action potential (CAP) and auditory brainstem response (ABR) are influenced by the cochlear traveling wave. To synchronize auditory nerve (AN) firing, short, rising-frequency chirps have been used to compensate for traveling wave delays; however, for high presentation levels, basal spread of excitation may disrupt AN synchrony. Further, unintended spread of excitation over the time course of the chirp may adapt basal AN fibers, thereby reducing CAP and ABR amplitudes-opposite of the objective of using chirps. Previous work has altered the rate of frequency change as a function of chirp level to maximize AN synchrony. Here, we evaluated, in normal-hearing adults (N = 12, six males), an alternative approach of attenuating low-frequency chirp energy and hypothesized this manipulation would increase CAP and ABR amplitudes relative to the original, flat-spectrum chirp for high stimulus levels. Low-frequency-attenuated chirps produced larger CAP and ABR wave amplitudes than clicks and the original chirp for nearly all stimulus levels. To explore mechanisms underlying these results, we derived AN firing distributions for chirps and clicks. The distributions for low-frequency-attenuated chirps were consistent with greater AN synchrony compared to those for clicks and the original chirp. ABR waveforms were reasonably simulated by convolving the derived AN firing distributions with an impulse response waveform associated with the ABR electrode montage. These findings suggest that low-frequency-attenuated chirps and predicted AN firing distributions may be useful in evaluating human AN function, including the effects of AN fiber loss, and other disease states.

A 36-year-old with refractory otorrhea, otalgia, and facial palsy had HRCT bony erosion. Microsoft Copilot flagged malignancy; biopsy confirmed T1N0M0 squamous cell carcinoma. Curative resection achieved clear margins. Cranial nerve involvement demands biopsy regardless of age; AI aids but cannot replace clinical judgment.

Sensorineural hearing loss is driven by disruption of cochlear homeostasis, where dysregulated redox, ionic, and metabolic factors lead to hair cell degeneration and synaptic injury. Current strategies lack the capacity to restore the enzymatic clearance of reactive oxygen species or penetrate the blood-labyrinth barrier. Here, we report a cell-inspired dual-tandem catalytic nanoreactor (HSC@Se) integrating GPx-mimetic diselenide with superoxide dismutase and catalase to reconstruct the detoxification cascade. We show that the albumin scaffold stabilizes the nanoarchitecture and enables active blood-labyrinth barrier penetration of neutrophil-adhesive transport and megalin-mediated uptake, facilitating cochlear delivery to hair cells and spiral ganglion neurons. In noise-induced mouse models, we demonstrate that HSC@Se restores redox equilibrium, suppresses ferroptosis, normalizes iron handling, preserves hair-cell integrity, maintains ribbon synapses, and reduces auditory threshold shifts. We perform transcriptomics to reveal activation of antioxidative and metabolic repair pathways. This work presents cell-inspired nanoreactors that emulate natural antioxidant networks to rebalance cochlear redox homeostasis and drive hearing protection.

Type 2 diabetes mellitus (T2DM) is increasingly recognized as a disorder affecting both the peripheral and central nervous systems. Although diabetic neuropathy has traditionally been associated with peripheral nerve damage, accumulating evidence suggests that central auditory pathways are also vulnerable to chronic hyperglycaemia. This narrative review synthesizes current evidence regarding auditory brainstem response (ABR) abnormalities in adults with T2DM, with emphasis on their pathophysiological basis, characteristic electrophysiological alterations, clinical associations, and potential diagnostic significance. A structured search of PubMed/MEDLINE, Scopus, and Google Scholar identified 10 observational studies published between 2000 and 2024 that evaluated ABR parameters in adults with T2DM. Across the included studies, the most consistent findings were prolonged wave III and wave V absolute latencies together with extended interpeak intervals (I-III, III-V, and I-V), while wave I latency remained normal in most patients, indicating predominant central auditory pathway dysfunction. A smaller proportion of studies demonstrated additional peripheral auditory nerve involvement, suggesting mixed neuropathic changes. Higher glycated haemoglobin (HbA1c) levels and longer duration of diabetes were generally associated with greater ABR abnormalities, supporting the role of cumulative metabolic injury in central neural conduction delay. Despite methodological heterogeneity and predominantly cross-sectional study designs, the evidence consistently indicates that the auditory brainstem is an early target of diabetes-related neural injury. ABR represents a non-invasive and reproducible tool with potential utility for detecting subclinical central diabetic neuropathy before overt auditory impairment becomes clinically evident. Further multicentre longitudinal studies using standardized ABR protocols are required to validate its diagnostic and prognostic value in routine clinical practice.