Matthias Mietsch

This study examines natural cardiovascular aging in non-human primates, finding histological and molecular changes associated with aging, including fibrosis, inflammation, and atherosclerosis.

The paper develops a spatial contrast model to capture nonlinear spatial integration in primate retinal ganglion cells using natural and artificial stimuli, showing improved performance over linear models.

This study examines how primate retinal ganglion cells adapt their spatial processing to natural versus artificial stimuli, finding that some cell types adjust receptive fields and surrounds, but efficient coding only partially explains these changes.

The paper compares filter-based models of suppression in retinal ganglion cells across species and stimuli, finding divisive models generalize better across temporal frequencies and contrasts, while subtractive models capture slow dynamics.

The paper examines single neuron diversity in primate visual cortical areas V1 and LPFC, finding differences in morphology, electrophysiology, and intrinsic bursting that may underlie functional specialization.

This study shows that natural stimuli with species-specific gaze patterns drive correlated spiking responses in retinal ganglion cells, violating efficient coding theory.

This paper introduces STR, a method combining super-resolution and tomography to identify receptive field subunits in retinal ganglion cells, validated in primate recordings.

The paper introduces an accelerated version of spike-triggered non-negative matrix factorization to identify coordinated subunit mosaics in primate ganglion cells.

This study compares predictive models for retinal ganglion cell responses, finding that CNNs outperform LN models, while LN models show better cross-stimulus generalization.

The paper investigates how primate retinal ganglion cells respond to saccade-like image shifts, revealing distinct response patterns and functional diversity among cell types.

This study identifies LINC00607 as an endothelial-specific lncRNA that supports angiogenic function by interacting with BRG1 to regulate chromatin accessibility and ERG target gene transcription.