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Introduction: The envelope proteins syncytin-1 and pHERV-W from the Human Endogenous Retroviral family 'W' (HERV-W) have been identified as potential risk factors in multiple sclerosis (MS). This study aims to evaluate both humoral and cell-mediated immune response to antigenic peptides derived from these proteins across different clinical forms and inflammatory phases of MS.

Methods: Indirect enzyme-linked immunosorbent assay (ELISA) was employed to measure immunoglobulin G (IgG) responses to syncytin-1 and pHERV-W peptides in MS patients.

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Background: Avascular necrosis (AVN) of the femoral head is a degenerative condition characterized by ischemic bone death, resulting in pain and impaired mobility. Core decompression, a surgical intervention, is widely performed for stage II AVN to alleviate symptoms and delay disease progression. While clinical and radiological outcomes are well-documented, the psychosocial dimensions of recovery remain underexplored.

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Background: Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by motor and nonmotor symptoms, with a significant genetic component. Early-onset Parkinson's disease (EOPD), manifesting before age 45, is often linked to mutations in genes such as PARK2, PINK1, and PARK7, the latter coding for the protein DJ-1.

Objective: We present the first reported cases of EOPD carrying a previously undescribed homozygous PARK7 mutation, p.

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Approximately 800,000 total knee arthroplasties and 450,000 total hip arthroplasties are performed annually in the United States. These procedures provide significant pain relief and restore function in patients with advanced osteoarthritis, rheumatoid arthritis, and other degenerative joint conditions. Patient evaluation before surgery includes a history, physical examination, laboratory tests, and imaging.

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Friedreich 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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