Publications by authors named "N Weinstock"
Background: Harm reduction, when applied to drug use, prioritizes improving patient-centered health outcomes and reducing drug-related harm. In order for harm reduction strategies to be adopted by people who inject drugs (PWID), they need to be promoted, accessible, and accepted in that population and the community-at-large. While PWID face stigma at multiple levels, less is known about how stigma influences uptake and acceptance of harm reduction services and strategies among PWID.
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- - Autoimmune pediatric neurologic diseases have diverse symptoms and different underlying mechanisms, complicating their diagnosis.
- - The study focused on autoantibodies linked to common disorders like NMDAR and LGI-1, finding distinct characteristics in their gene usage and lengths that could inform better understanding of these conditions.
- - Key findings showed that NMDAR autoantibodies had a normal length distribution while LGI-1 was skewed; also, differing isotypes such as IgG1-3 for NMDAR and IgG4 for LGI-1 were identified, which may enhance diagnostic accuracy and treatment strategies.
Article Synopsis
- Myelin is key for fast nerve signaling and protecting axons; defects in myelin can lead to further axonal damage and degeneration.* -
- Mutations in the Myelin Protein Zero (P0) gene are linked to demyelinating neuropathies, with the P0T124M mutation causing axonal neuropathy (CMT2J) without significant myelin damage, offering insight into how myelin-supporting cells can influence axons independently.* -
- Research on MpzT124M mutant mice reveals that Schwann cells struggle to support axons properly, leading to metabolic changes, axonal degeneration, and impaired motor function, mimicking symptoms seen in patients with CMT2J.*
Myalgia describes pain in the skeletal muscles. According to the current German clinical guidelines from 2020 (AWMF register number: 030/051), the initial diagnostic assessment consists of the anamnesis, clinical examination, electrophysiological examination and standard laboratory tests. Additional special examinations, such as molecular genetic investigations, special laboratory tests, medical imaging and muscle biopsy are only needed in certain cases.
View Article and Find Full Text PDFKrabbe disease is caused by a deficiency of the lysosomal galactosylceramidase (GALC) enzyme, which results in the accumulation of galactosylceramide (GalCer) and psychosine. In Krabbe disease, the brunt of demyelination and neurodegeneration is believed to result from the dysfunction of myelinating glia. Recent studies have shown that neuronal axons are both structurally and functionally compromised in Krabbe disease, even before demyelination, suggesting a possible neuron-autonomous role of GALC.
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