Publications by authors named "A H Madrid"

Purpose:  We aimed to evaluate the association between socioeconomic factors and patient-reported Western Ontario Osteoarthritis of the Shoulder (WOOS) index at 1 year after hemiarthroplasty, reverse, or anatomical total shoulder arthroplasty for osteoarthritis or cuff-tear arthropathy.

Methods:  Eligible patients were identified using linked national data from the Danish Shoulder Arthroplasty Registry and Statistics Denmark between April 2012 and April 2019. Univariable and multivariable linear regression was used to identify the association between socioeconomic factors and the WOOS index at 1 year following primary shoulder arthroplasty adjusted for age, sex, underlying diagnosis, implant design, and comorbidities.

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Introduction: Whole genome methylation sequencing (WGMS) in blood identifies differential DNA methylation in persons with late-onset dementia due to Alzheimer's disease (AD) but has not been tested in persons with mild cognitive impairment (MCI).

Methods: We used WGMS to compare DNA methylation levels at 25,244,219 CpG loci in 382 blood samples from 99 persons with MCI, 109 with AD, and 174 who are cognitively unimpaired (CU).

Results: WGMS identified 9756 differentially methylated positions (DMPs) in persons with MCI, including 1743 differentially methylated genes encoding proteins in biological pathways related to synapse organization, dendrite development, and ion transport.

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The GluA1 subunit, encoded by the putative schizophrenia-associated gene GRIA1, is required for activity-regulated AMPA receptor (AMPAR) trafficking, and plays a key role in cognitive and affective function. The cytoplasmic, carboxy-terminal domain (CTD) is the most divergent region across AMPAR subunits. The GluA1 CTD has received considerable attention for its role during long-term potentiation (LTP) at CA1 pyramidal neuron synapses.

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Diffuse pediatric-type high-grade gliomas (pedHGG), H3- and IDH-wildtype, encompass three main DNA-methylation-based subtypes: pedHGG-MYCN, pedHGG-RTK1A/B/C, and pedHGG-RTK2A/B. Since their first description in 2017 tumors of pedHGG-RTK2A/B have not been comprehensively characterized and clinical correlates remain elusive. In a recent series of pedHGG with a Gliomatosis cerebri (GC) growth pattern, an increased incidence of pedHGG-RTK2A/B (n = 18) was observed.

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