Disaster Med Public Health Prep
October 2014
Objective: On April 27, 2011, a train derailed and crashed in Taiwan, causing a mass casualty incident (MCI) that was similar to a previous event and with similar consequences. In both disasters, the emergency operating centers (EOCs) could not effectively integrate associated agencies to deal with the incident. The coordination and utilization of resources were inefficient, which caused difficulty in command structure operation and casualty evacuation.
View Article and Find Full Text PDFIF (intermediate filament) proteins can be cleaved by caspases to generate proapoptotic fragments as shown for desmin. These fragments can also cause filament aggregation. The hypothesis is that disease-causing mutations in IF proteins and their subsequent characteristic histopathological aggregates could involve caspases.
View Article and Find Full Text PDFPurpose: To enable better psychosocial, informational, and practical support of Chinese patients with cancer, this study was conducted to identify the specific support needs of Chinese immigrant cancer patients.
Methods: The Cancer Portal Project at Memorial Sloan-Kettering Cancer Center's Center for Immigrant Health and Cancer Disparities is a patient navigation program that assists underserved and minority cancer patients in obtaining social and economic assistance at ten New York City cancer clinics. This need assessment was conducted as part of the Portal Project.
The size and diversity of the Hispanic population in the United States has dramatically increased, with vast implications for health research. We conducted a systematic review of the characterization of the Hispanic population in health research and described its implications. Relevant studies were identified by searches of PubMed, Embase Scopus, and Science/Social Sciences Citation Index from 2000 to 2011.
View Article and Find Full Text PDFAlexander disease is a primary genetic disorder of astrocyte caused by dominant mutations in the astrocyte-specific intermediate filament glial fibrillary acidic protein (GFAP). While most of the disease-causing mutations described to date have been found in the conserved α-helical rod domain, some mutations are found in the C-terminal non-α-helical tail domain. Here, we compare five different mutations (N386I, S393I, S398F, S398Y and D417M14X) located in the C-terminal domain of GFAP on filament assembly properties in vitro and in transiently transfected cultured cells.
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