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Cortical reorganization following dorsal spinal injuries in newborn monkeys reveals a critical period in the development of the somatosensory cortex.
Proc Natl Acad Sci U S A
January 2025
Department of Psychology, Vanderbilt University, Nashville, TN 37240.
Lesions of the dorsal columns of the spinal cord in adult macaque monkeys lead to the loss of hand inputs and large-scale expansion of the face inputs in the hand region of the somatosensory cortex. Inputs from alternate spinal pathways do not reactivate the deafferented regions of area 3b. Here, we determined how transections of the dorsal columns done within a few days after birth affect the developing somatosensory cortex.
View Article and Find Full Text PDFImpact of Recent Translational and Therapeutic Developments on Clinical Course of BCR::ABL1-Positive and -Negative Myeloproliferative Neoplasms.
Hematol Oncol
January 2025
University of California Irvine, Irvine, California, USA.
Despite the study of BCR::ABL1-positive and -negative myeloproliferative neoplasms (MPNs) providing seminal insights into cancer biology, tumor evolution and precision oncology over the past half century, significant challenges remain. MPNs are clonal hematopoietic stem cell-derived neoplasms with heterogenous clinical phenotypes and a clonal architecture which impacts the often-complex underlying genetics and microenvironment. The major driving molecular abnormalities have been well characterized, but debate on their role as disease-initiating molecular lesions continues.
View Article and Find Full Text PDFDelayed Progression of Ataxia with a Static Cerebellar Lesion- Consider SCA27B.
Cerebellum
January 2025
Department of Neurology, Donders Institute for Brain, Cognition & Behaviour, Radboud University Medical Center, Nijmegen, The Netherlands.
Repeat expansions in the fibroblast growth factor 14 gene (FGF14), associated with spinocerebellar ataxia type 27B (SCA27B), have emerged as a prevalent cause of previously unexplained late-onset cerebellar ataxia. Here, we present a patient with residual symptom of gait ataxia after complicated meningioma surgery, who presented with progressive symptoms of oculomotor disturbances, speech difficulties, vertigo and worsening of gait imbalance, twelve years post-resection. Neuroimaging revealed a surgical resection cavity in the dorsolateral side of the left cerebellar hemisphere, accompanied by gliosis in left cerebellar hemisphere extending into the vermis, extensive non-specific supratentorial periventricular white matter abnormalities, and mild atrophy of the cerebellar vermis.
View Article and Find Full Text PDFPhysiopathological effects of entrance versus distal spread-out Bragg peak on mouse spinal cord neurons.
Sci Rep
January 2025
Department of Biomedical and Biotechnological Sciences, University of Catania, 95123, Catania, Italy.
Recent investigations into radiation-induced side effects have focused on understanding the physiopathological consequences of irradiation on late-responding tissues like the spinal cord, which can lead to chronic progressive myelopathy. Proton therapy, an advanced radiation treatment, aims to minimize damage to healthy tissues through precise dose deposition. However, challenges remain, particularly regarding the variation in dose distribution, characterized by maximum deposition at the end of the proton range, known as the distal fall-off of a spread-out Bragg peak.
View Article and Find Full Text PDFFriedreich Ataxia: An (Almost) 30-Year History After Gene Discovery.
Neurol Genet
February 2025
Department of Neurology and Neurosurgery, McGill University, Montreal, Canada.
In the late 1800s, Nikolaus Friedreich first described "degenerative atrophy of the posterior columns of the spinal cord," noting its connection to progressive ataxia, sensory loss, and muscle weakness, now recognized as Friedreich ataxia (FRDA). Renewed interest in the disease in the 1970s and 80s by the Quebec Cooperative Group and by Anita Harding led to the development of clinical diagnostic criteria and insights into associated biochemical abnormalities, although the primary defect remained unknown. In 1988, Susan Chamberlain mapped FRDA's location on chromosome 9.
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