A5077733515- Prion Diseases and Protein Misfolding
- Nerve injury and regeneration
- Neurological diseases and metabolism
- Neurogenesis and neuroplasticity mechanisms
- Spinal Dysraphism and Malformations
- Cerebrospinal fluid and hydrocephalus
- Assisted Reproductive Technology and Twin Pregnancy
- Hereditary Neurological Disorders
- RNA regulation and disease
- Microtubule and mitosis dynamics
- Trace Elements in Health
- Obstructive Sleep Apnea Research
- Viral Infections and Vectors
- Tracheal and airway disorders
- Planarian Biology and Electrostimulation
- Biomedical Research and Pathophysiology
- Biochemical and Structural Characterization
- RNA Research and Splicing
- Hematological disorders and diagnostics
- Neurological and metabolic disorders
- Hedgehog Signaling Pathway Studies
- Neurological disorders and treatments
- Spinal Cord Injury Research
- Axon Guidance and Neuronal Signaling
- Parasitic infections in humans and animals
See-Spital
2023
University of Zurich
2020-2022
University Hospital of Zurich
2020-2021
Copyright Licensing Agency
2021
University of Bern
2018
Abstract Prion infections cause conformational changes of the cellular prion protein (PrP C ) and lead to progressive neurological impairment. Here we show that toxic, prion-mimetic ligands induce an intramolecular R208-H140 hydrogen bond (‘H-latch’), altering flexibility α2–α3 β2–α2 loops PrP . Expression a 2Cys mutant mimicking H-latch was constitutively whereas R207A unable form conferred resistance infection. High-affinity prevented induction repressed prion-related neurodegeneration in...
BACKGROUND CONTEXTSpinal arachnoid web (SAW) is a rare condition characterized by focal thickening of the membrane causing displacement and compression spinal cord with progressive symptoms neurological deficits. Recent reports clinical experience suggest that SAW distinct entity specific radiological findings treatment strategies distinguishable from other arachnopathies potential differential diagnoses.PURPOSETo better define diagnostic features, options outcomes surgically treated...
The adhesion G-protein coupled receptor Adgrg6 (formerly Gpr126) is instrumental in the development, maintenance and repair of peripheral nervous system myelin. prion protein (PrP) a potent activator could be used as potential therapeutic agent treating demyelinating dysmyelinating diseases. We designed dimeric Fc-fusion comprising myelinotrophic domain PrP (FT 2 Fc), which activated vitro exhibited favorable pharmacokinetic properties for vivo treatment neuropathies. While chronic FT Fc...
The cellular prion protein (PrP) is essential to the long-term maintenance of myelin sheaths in peripheral nerves. PrP activates adhesion G-protein coupled receptor Adgrg6 on Schwann cells and initiates a pro-myelination cascade molecular signals. Because crucial for development regeneration after nerve injury, we investigated role repair. We performed experimental sciatic crush injuries co-isogenic wild-type PrP-deficient mice, examined repair processes. Generation cells, macrophage...
• Video motion analysis of functional recovery in a sciatic nerve injury and repair model rats. Dynamic swimming contrast to static index. Simple setup, fast testing sessions lower costs compared other locomotion systems. Functional assessment method study new treatments improve peripheral regeneration.
Alveolar echinococcosis is a rare condition, but living or working in rural environment substantial risk factor. The liver the organ primarily affected, with additional extrahepatic manifestations approximately 25% of cases. Primary disease rare, and isolated cerebral involvement extremely unusual.The authors described an illustrative case alveolar immunocompetent farmer. Magnetic resonance imaging brain showed predominantly cystic lesion perifocal edema "bunch grapes" appearance left...
Summary Prion infections cause conformational changes of PrP C and lead to progressive neurological impairment. Here we show that toxic, prion-mimetic ligands induce an intramolecular R208-H140 hydrogen bond (“H-latch”) altering the flexibility α2-α3 β2-α2 loops . Expression a 2Cys mutant mimicking H-latch was constitutively whereas R207A unable form conferred resistance prion infection. High-affinity prevented induction repressed prion-related neurodegeneration in organotypic cerebellar...
Abstract The adhesion G-protein coupled receptor Adgrg6 (formerly Gpr126) is instrumental in the development, maintenance and repair of peripheral nervous system myelin. prion protein (PrP) a potent activator could be used as potential therapeutic agent treating demyelinating dysmyelinating diseases. We designed dimeric Fc-fusion comprising myelinotrophic domain PrP (FT 2 Fc), which activated vitro exhibited favorable pharmacokinetic properties for vivo treatment neuropathies. While chronic...
Zusammenfassung. Die eosinophile Granulomatose mit Polyangiitis (EGPA, ehemals Churg-Strauss-Syndrom) ist eine Krankheit vielen Gesichtern. Aufgrund der variablen Gefäss- und Organbeteiligung kann sich EPGA klinisch sehr unterschiedlich manifestieren. Wir berichten über einen 60-jährigen Patienten bekanntem Asthma bronchiale, Pansinusitis neu einer ausgeprägten Bluteosinophilie sowie akuten, rasch progredienten Mononeuritis multiplex. Diagnose konnte schliesslich histologisch gesichert...
Abstract The cellular prion protein (PrP) is essential to the long-term maintenance of myelin sheaths in peripheral nerves. PrP activates adhesion G-protein coupled receptor Adgrg6 on Schwann cells and initiates a pro-myelination cascade molecular signals. Because crucial for development regeneration after nerve injury, we investigated role repair. We performed experimental sciatic crush injuries co-isogenic wild-type PrP-deficient mice, examined repair processes. Generation cells,...