Introduction: Smartphone emergency medical identification (SEMID) applications are built-in health information-storing functions that are accessible without a passcode. The utility of these applications in the real-time resuscitation of trauma patients is unknown.
Methods: We prospectively evaluated all trauma activation patients ≥16 y and unable to provide a medical history for any reason for the presence of a smartphone at our urban level I center between October 2020 and September 2021.
Objective: The objective of this study was to present the clinical, histopathologic, and radiographic findings of a unique case of intimal sarcoma (IS) embolus presenting as a large vessel occlusion causing an ischemic stroke without a detectable primary tumor site.
Methods: Extensive examinations, multimodal imaging, laboratory testing, and histopathologic analysis were used in evaluation.
Results: We report the case of a patient who presented with acute embolic ischemic stroke and was found to have IS based on a histopathologic evaluation of his embolectomy specimen.
Purpose: We studied the quality differences between the different hypo-osmotic swelling test (HOST) classes, as measured by criteria of DNA fragmentation, DNA decondensation, and nuclear architecture. The aim was to find particular HOST classes associated with good-quality metrics, which may be potentially used in ICSI (intra-cytoplasmic sperm injection).
Methods: Ten patients from the Department of Reproductive Medicine at Tenon Hospital (Paris, France) were included.
Mutations in cause intellectual disability (ID), which is often accompanied by seizures and autism. A number of studies have shown that IQSEC2 is an abundant protein in excitatory synapses and plays an important role in neuronal development as well as synaptic plasticity. Here, we review neuronal IQSEC2 signaling with emphasis on those aspects likely to be involved in autism.
View Article and Find Full Text PDFWe have recently described an A350V mutation in IQSEC2 associated with intellectual disability, autism and epilepsy. We sought to understand the molecular pathophysiology of this mutation with the goal of developing targets for drug intervention. We demonstrate here that the A350V mutation results in interference with the binding of apocalmodulin to the IQ domain of IQSEC2.
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