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- Fagman, Erika, et al.
(författare)
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High-quality annotations for deep learning enabled plaque analysis in SCAPIS cardiac computed tomography angiography
- 2023
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Ingår i: Heliyon. - : Elsevier BV. - 2405-8440. ; 9:5
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Tidskriftsartikel (refereegranskat)abstract
- Background: Plaque analysis with coronary computed tomography angiography (CCTA) is a promising tool to identify high risk of future coronary events. The analysis process is time-consuming, and requires highly trained readers. Deep learning models have proved to excel at similar tasks, however, training these models requires large sets of expert-annotated training data. The aims of this study were to generate a large, high-quality annotated CCTA dataset derived from Swedish CArdioPulmonary BioImage Study (SCAPIS), report the reproducibility of the annotation core lab and describe the plaque characteristics and their association with established risk factors.Methods and results: The coronary artery tree was manually segmented using semi-automatic software by four primary and one senior secondary reader. A randomly selected sample of 469 subjects, all with coronary plaques and stratified for cardiovascular risk using the Systematic Coronary Risk Evaluation (SCORE), were analyzed. The reproducibility study (n = 78) showed an agreement for plaque detection of 0.91 (0.84-0.97). The mean percentage difference for plaque volumes was-0.6% the mean absolute percentage difference 19.4% (CV 13.7%, ICC 0.94). There was a positive correlation between SCORE and total plaque volume (rho = 0.30, p < 0.001) and total low attenuation plaque volume (rho = 0.29, p < 0.001).Conclusions: We have generated a CCTA dataset with high-quality plaque annotations showing good reproducibility and an expected correlation between plaque features and cardiovascular risk. The stratified data sampling has enriched high-risk plaques making the data well suited as training, validation and test data for a fully automatic analysis tool based on deep learning.
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- Goncalves, Nadia P., et al.
(författare)
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Peripheral Nerve Regeneration Is Independent From Schwann Cell p75(NTR) Expression
- 2019
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Ingår i: Frontiers in Cellular Neuroscience. - : FRONTIERS MEDIA SA. - 1662-5102. ; 13
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Tidskriftsartikel (refereegranskat)abstract
- Schwann cell reprogramming and differentiation are crucial prerequisites for neuronal regeneration and re-myelination to occur following injury to peripheral nerves. The neurotrophin receptor p75(NTR) has been identified as a positive modulator for Schwann cell myelination during development and implicated in promoting nerve regeneration after injury. However, most studies base this conclusion on results obtained from complete p75(NTR) knockout mouse models and cannot dissect the specific role of p75(NTR) expressed by Schwann cells. In this present study, a conditional knockout model selectively deleting p75(NTR) expression in Schwann cells was generated, where p75(NTR) expression is replaced with that of an mCherry reporter. Silencing of Schwann cell p75(NTR) expression was confirmed in the sciatic nerve in vivo and in vitro, without altering axonal expression of p75(NTR). No difference in sciatic nerve myelination during development or following sciatic nerve crush injury was observed, as determined by quantification of both myelinated and unmyelinated nerve fiber densities, myelinated axonal diameter and myelin thickness. However, the absence of Schwann cell p75(NTR) reduced motor nerve conduction velocity after crush injury. Our data indicate that the absence of Schwann cell p75(NTR) expression in vivo is not critical for axonal regrowth or remyelination following sciatic nerve crush injury, but does play a key role in functional recovery. Overall, this represents the first step in redefining the role of p75(NTR) in the peripheral nervous system, suggesting that the Schwann cell-axon unit functions as a syncytium, with the previous published involvement of p75(NTR) in remyelination most likely depending on axonal/neuronal p75(NTR) and/or mutual glial-axonal interactions.
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- Goncalves, Nadia P., et al.
(författare)
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Schwann cell p75 neurotrophin receptor modulates small fiber degeneration in diabetic neuropathy
- 2020
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Ingår i: Glia. - : WILEY. - 0894-1491 .- 1098-1136. ; 68:12, s. 2725-2743
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Tidskriftsartikel (refereegranskat)abstract
- Diabetic neuropathy has an incidence as high as 50% of diabetic patients and is characterized by damage to neurons, Schwann cells and blood vessels within the peripheral nervous system. The low-affinity neurotrophin receptor p75 (p75(NTR)), particularly expressed by the Schwann cells in the peripheral nerve, has previously been reported to play a role in developmental myelination and cell survival/death. Increased levels of p75(NTR), in the endoneurium and plasma from diabetic patients and rodent models of disease, have been observed, proposing that this receptor might be involved in the pathogenesis of diabetic neuropathy. Therefore, in this study, we addressed this hypothesis by utilizing a mouse model of selective nerve growth factor receptor (Ngfr) deletion in Schwann cells (SC-p75(NTR)-KO). Electron microscopy of sciatic nerves from mice with high fat diet induced obesity demonstrated how loss of Schwann cell-p75(NTR)aggravated axonal atrophy and loss of C-fibers. RNA sequencing disclosed several pre-clinical signaling alterations in the diabetic peripheral nerves, dependent on Schwann cell p75(NTR)signaling, specially related with lysosome, phagosome, and immune pathways. Morphological and biochemical analyses identified abundant lysosomes and autophagosomes in the C-fiber axoplasm of the diabetic SC-p75(NTR)-KO nerves, which together with increased Cathepsin B protein levels corroborates gene upregulation from the phagolysosomal pathways. Altogether, this study demonstrates that Schwann cell p75(NTR)deficiency amplifies diabetic neuropathy disease by triggering overactivation of immune-related pathways and increased lysosomal stress.
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- Townsend, Simon William, et al.
(författare)
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Exorcising Grice's ghost : an empirical approach to studying intentional communication in animals.
- 2017
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Ingår i: Biological Reviews. - : Wiley-Blackwell Publishing Inc.. - 1464-7931 .- 1469-185X. ; 92:3, s. 1427-1433
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Tidskriftsartikel (refereegranskat)abstract
- Language's intentional nature has been highlighted as a crucial feature distinguishing it from other communication systems. Specifically, language is often thought to depend on highly structured intentional action and mutual mindreading by a communicator and recipient. Whilst similar abilities in animals can shed light on the evolution of intentionality, they remain challenging to detect unambiguously. We revisit animal intentional communication and suggest that progress in identifying analogous capacities has been complicated by (i) the assumption that intentional (that is, voluntary) production of communicative acts requires mental-state attribution, and (ii) variation in approaches investigating communication across sensory modalities. To move forward, we argue that a framework fusing research across modalities and species is required. We structure intentional communication into a series of requirements, each of which can be operationalised, investigated empirically, and must be met for purposive, intentionally communicative acts to be demonstrated. Our unified approach helps elucidate the distribution of animal intentional communication and subsequently serves to clarify what is meant by attributions of intentional communication in animals and humans.less thanbr /greater than (© 2016 Cambridge Philosophical Society.)
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- Ulrichsen, Maj, et al.
(författare)
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Sortilin Modulates Schwann Cell Signaling and Remak Bundle Regeneration Following Nerve Injury
- 2022
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Ingår i: Frontiers in Cellular Neuroscience. - : Frontiers Media SA. - 1662-5102. ; 16
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Tidskriftsartikel (refereegranskat)abstract
- Peripheral nerve regeneration relies on the ability of Schwann cells to support the regrowth of damaged axons. Schwann cells re-differentiate when reestablishing contact with the sprouting axons, with large fibers becoming remyelinated and small nociceptive fibers ensheathed and collected into Remak bundles. We have previously described how the receptor sortilin facilitates neurotrophin signaling in peripheral neurons via regulated trafficking of Trk receptors. This study aims to characterize the effects of sortilin deletion on nerve regeneration following sciatic crush injury. We found that Sort1(-)(/)(-) mice displayed functional motor recovery like that of WT mice, with no detectable differences in relation to nerve conduction velocities and morphological aspects of myelinated fibers. In contrast, we found abnormal ensheathment of regenerated C-fibers in injured Sort1(-)(/)(-) mice, demonstrating a role of sortilin for Remak bundle formation following injury. Further studies on Schwann cell signaling pathways showed a significant reduction of MAPK/ERK, RSK, and CREB phosphorylation in Sort1(-)(/)(-) Schwann cells after stimulation with neurotrophin-3 (NT-3), while Schwann cell migration and myelination remained unaffected. In conclusion, our results demonstrate that loss of sortilin blunts NT-3 signaling in Schwann cells which might contribute to the impaired Remak bundle regeneration after sciatic nerve injury.
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