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Fischmeister, F.

Publications and source records attributed to Fischmeister, F..

2 recordsLinked to original sources

Beyond the Resection: Surgical White Matter Disruption alters Non-Resected Brain Anatomy

Resective neurosurgery is a cornerstone treatment for many neurological conditions. Although traditionally viewed as localised procedure, increasing evidence from advanced magnetic resonance imaging (MRI) shows that also non-resected anatomy can degenerate following surgery. The relationship between local tissue removal and these postoperative changes remains thus far speculative. Here, we investigate the hypothesis that degenerative changes to surgically preserved grey and white matter are mediated by transneuronal degeneration, a deterioration of intact neuronal populations due to lost axonal input. Using a robust structural and diffusion MRI framework, we first identify widespread postoperative atrophy: pronounced cortical thickness decreases near the resection, and extensive white matter impairments across the ipsilateral hemisphere. Importantly, we then link these alterations to surgical white matter disruption, revealing a sequential network atrophy following neurosurgery. Beyond degenerative effects, we also demonstrate often reported structural network reorganisations as an artefact of image processing, indicating limited capacity for macroscale plasticity post-resection. Key PointsO_LIResective neurosurgery can lead to postoperative atrophy of non-resected grey and white matter. Utilising a robust longitudinal neuroimaging framework, we evaluate these changes as consequences of transneuronal degeneration, demonstrating a sequential atrophy of brain anatomy following the loss of surgically disrupted white matter. C_LIO_LIThe majority of severed connections projected to atrophic cortices near the resection, indicating them to be short association fibers. Consecutive white matter atrophy however affected extensive ipsilateral pathways, highlighting a cascading network effect of resective brain surgery. C_LIO_LIWe did not find evidence to support often reported structural reorganisations of large-scale brain networks post-resection. Yet, we demonstrate that evidence typically interpreted as such can be replicated when using non-robust reconstruction methods. C_LI

neuroscience↗

Methane emission of humans is explained by dietary habits, host genetics, local formate availability and a uniform archaeome

Archaea are responsible for methane production in the human gastrointestinal tract. Twenty percent of the Western populations exhale substantial amounts of this gas. The underlying principle determining high or low methane emission and its effect on human health was still not sufficiently understood. In this study, we analysed the gastrointestinal microbiome, archaeome, metagenome, metabolome, and eating behaviour of 100 healthy young adults. We correlated high levels of human methane emission (5-75 ppm) with a 1000-fold increase in Methanobrevibacter smithii. This archaeon co-occurred with a bacterial community specialised on dietary fibre degradation, which included members of the Ruminococcaceae and Christensenellaceae. Methane production was negatively affected by high vitamin B12 and fat intake of the subjects, and was positively associated with increased formate concentrations in the gut. Overall, methane emission is explained by dietary habits, host genetics, local metabolite availability and microbiome/archaeome composition, emphasizing the unique biology of high methane-emitters which has potentially positive impact on human health. O_FIG O_LINKSMALLFIG WIDTH=171 HEIGHT=200 SRC="FIGDIR/small/423794v1_ufig1.gif" ALT="Figure 1"> View larger version (79K): org.highwire.dtl.DTLVardef@16eb91org.highwire.dtl.DTLVardef@c3b928org.highwire.dtl.DTLVardef@1b11fa5org.highwire.dtl.DTLVardef@194bed2_HPS_FORMAT_FIGEXP M_FIG O_FLOATNOGraphical abstract:C_FLOATNO C_FIG

microbiology↗