Objective: Improvement in epilepsy care requires standardized methods to assess disease severity. We report the results of implementing common data elements (CDEs) to document epilepsy history data in the electronic medical record (EMR) after 12 months of clinical use in outpatient encounters. Methods: Data regarding seizure frequency were collected during routine clinical encounters using a CDE-based form within our EMR. We extracted CDE data from the EMR and developed measurements for seizure severity and seizure improvement scores. Seizure burden and improvement was evaluated by patient demographic and encounter variables for in-person and telemedicine encounters. Results: We assessed a total of 1696 encounters in 1038 individuals with childhood epilepsies between September 6, 2019 and September 11, 2020 contributed by 32 distinct providers. Childhood absence epilepsy (n = 121), Lennox-Gastaut syndrome (n = 86), and Dravet syndrome (n = 42) were the most common epilepsy syndromes.Overall, 43% (737/1696) of individuals had at least monthly seizures, 17% (296/1696) had a least daily seizures, and 18% (311/1696) were seizure-free for >12 months.Quantification of absolute seizure burden and changes in seizure burden over time differed between epilepsy syndromes, including high and persistent seizure burden in patients with Lennox-Gastaut syndrome. Individuals seen via telemedicine or in-person encounters had comparable seizure frequencies. Individuals identifying as Hispanic/Latino, particularly from postal codes with lower median household incomes, were more likely to have ongoing seizures that worsened over time.
A new multi-scale simulation method is formulated for the study of shocked materials. The method combines molecular dynamics and the Euler equations for compressible ¤ow. Treatment of the dif£cult problem of the spontaneous formation of multiple shock waves due to material instabilities is enabled with this approach. The method allows the molecular dynamics simulation of the system under dynamical shock conditions for orders of magnitude longer time periods than is possible using the popular non-equilibrium molecular dynamics (NEMD) approach. An example calculation is given for a model potential for silicon in which a computational speedup of 10 5 is demonstrated. Results of these simulations are consistent with the recent experimental observation of an anomalously large elastic precursor on the nanosecond timescale.
Histologic patterns of tumor-bone interaction were systematically evaluated in 80 cases of metastatic lung cancer involving bone. Patterns of tumor-bone interaction varied with the histologic type of lung cancer, reflecting the biochemical and biologic differences among the different types of lung cancer. Evidence presented here suggests that destruction of bone by metastatic lung cancer is mediated neither by direct contact of tumor cells with bone matrix nor by release of diffusible substances that lyse bone matrix. Among indirect mechanisms, the most prevalent and important was the activation of bone-lining cells by metastatic tumor. Epidermoid carcinomas in particular were associated with histologic patterns of classical bone remodelling, including osteoblastic, osteoclastic, and osteocytic activity. Adenocar-cinomas showed a particularly high association with microfractures and manifested a stromal pattern consistent with release of prostaglandins. Ischemic necrosis of bone due to compression of vessels by expanding tumor mass is also a common and important mechanism. Correlation of histologic patterns with reported data on the frequency of bone metastases and syndromes of ectopic hormone production provides insight into the mechanism@) of paraneoplastic hypercalcemia in patients with lung cancer. Cancer 48:2649-2660, 1981. ETASTATIC BONE DISEASE is a major cause of M morbidity in cancer patients, commonly causing pain and limitation of motion by fractures. It may also be associated with the protean and potentially life-threatening systemic effects of hypercalcemia.' Although the prevailing clinical dictum is that such hy-percalcemia can usually be simply explained by the presence of osteolytic metastases, radiographic osteol-ysis and hypercalcemia are often strikingly disso-~ i a t e d. ~. ~ There is limited understanding of the patho-genesis of metastatic bone disease, and the efficacy of treatments proposed for the skeletal complications of cancer has been ~ariable.~.' This situation derives at least in part from the fact that the mechanism of tumor-bone interaction has not been systematically evaluated by morphologic methods. General textbooks of pathology and monographs on bone disease fail to provide any hard data on this subject.6-" Many theories have been
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