Introduction: Beta-trace protein (BTP) is primarily used as a marker for traumatic CSF leakage. Spinal leptomeningeal cells adjacent to the spinal nerve roots are a major producer of this protein, which has prompted interest in its relevance to inflammatory polyradiculoneuropathies. BTP has not previously been investigated in patients with Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyradiculopathy (CIDP).
View Article and Find Full Text PDFBackground: The evidence on the link between cardiometabolic diseases (CMDs) and motor neuron diseases (MNDs) remains inconsistent. We aimed to determine whether there is an association of CMDs, namely, any cardiovascular disease, cardiac arrhythmia, heart failure, thromboembolic disease, hypertension, cerebrovascular disease, ischemic heart disease, diabetes mellitus type 2, and hypercholesterolemia with the risk and progression of MNDs.
Methods: We included 1463 MND patients (amyotrophic lateral sclerosis (ALS), primary lateral sclerosis (PLS), progressive spinal muscular atrophy (PSMA), and unspecified MND) diagnosed from January 1, 2015, to July 1, 2023, in Sweden according to the Swedish Motor Neuron Disease Quality Registry (i.
Acute myeloid leukaemia with NUP98 rearrangement (AML-NUP98) has been previously described in paediatric patients, and the clinical significance in adult AML patients remains largely unexplored. In this study, we identified specific partner fusion genes and examined somatic co-mutations and clonal evolution longitudinally in adult AML-NUP98 patients. Our comprehensive analysis provides an understanding of NUP98 rearrangement and co-mutations influencing clonal evolution and disease progression and offers valuable insights into potential therapeutic strategies.
View Article and Find Full Text PDFRecurrent high-grade intracranial malignancies have a grim prognosis and uniform management guidelines are lacking. Re-irradiation is underused due to concerns about irreversible side effects. Pulsed-reduced dose rate radiotherapy (PRDR) aims to reduce toxicity while improving tumor control by exploiting dose-rate effects.
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