Support needs of Chinese immigrant cancer patients.

PURPOSE: 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. Sixty-four questions were added to the existing Portal Intake Form about the needs and preferences for Chinese-language support and survivorship services. Descriptive analysis was performed, as well as an exploratory principal component's factor analysis to determine if there were any patterns in the services and programs in which patients were interested. RESULTS: Ninety-six patients were approached for participation; 59 agreed to participate. Eighty-eight percent of participants were born in China. Ninety-seven percent preferred to speak Mandarin, Cantonese, or Fujianese in the healthcare setting. When asked about general interest in support programs, 53 % of the participants were "very interested," 27 % were "maybe interested," and 17 % were "not interested." Programs in which more participants were "very interested" included those that would provide information about obtaining financial assistance (79 %) and social assistance (74 %), information on treatment options (67 %), help in coping with the burden of illness on the family (65 %), and information about general healthcare (63 %). The factor analysis resulted in the identification of five factors: social/financial/treatment and care issues, nutrition and exercise/networking/general health care, coping with fear and stress, herbs and dietary supplements, and acupuncture and acupressure. CONCLUSION: In this study, 80 % of the participants expressed interest in programs tailored for Chinese cancer patients. The most frequently preferred topics for potential services were information-based. Findings provide a foundation for future research and the development of culturally and linguistically targeted support programs and interventions for this unique population.

Alexander disease causing mutations in the C-terminal domain of GFAP are deleterious both to assembly and network formation with the potential to both activate caspase 3 and decrease cell viability.

Alexander 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. All the mutations disrupted in vitro filament assembly. The mutations also affected the solubility and promoted filament aggregation of GFAP in transiently transfected MCF7, SW13 and U343MG cells. This correlated with the activation of the p38 stress-activated protein kinase and an increased association with the small heat shock protein (sHSP) chaperone, αB-crystallin. Of the mutants studied, D417M14X GFAP caused the most significant effects both upon filament assembly in vitro and in transiently transfected cells. This mutant also caused extensive filament aggregation coinciding with the sequestration of αB-crystallin and HSP27 as well as inhibition of the proteosome and activation of p38 kinase. Associated with these changes were an activation of caspase 3 and a significant decrease in astrocyte viability. We conclude that some mutations in the C-terminus of GFAP correlate with caspase 3 cleavage and the loss of cell viability, suggesting that these could be contributory factors in the development of Alexander disease.

Operation of emergency operating centers during mass casualty incidents in taiwan: a disaster management perspective.

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. METHODS: This study was designed to create a survey questionnaire with problem items using disaster management phases mandated by Taiwan's Emergency Medical Care Law (EMCL), use statistical methods (t test) to analyze the results and issues the EOCs encountered during the operation, and propose solutions for those problems. RESULTS: Findings showed that EOCs lacked authority to intervene or coordinate with associated agencies. Also, placing emphasis on the recovery phase should improve future prevention and response mechanisms. CONCLUSIONS: To improve the response to MCIs, the EMCL needs to be amended to give EOCs the lead during disasters; use feedback from the recovery phase to improve future disaster management and operation coordination; and establish an information-sharing platform across agencies to address all aspects of relief work.(Disaster Med Public Health Preparedness. 2014;0:1-6).

Characterization of the Hispanic or latino population in health research: a systematic review.

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. 131 articles met criteria. 56% of the articles reported only "Hispanic" or "Latino" as the characteristic of the Hispanic research population while no other characteristics were reported. 29% of the articles reported language, 27% detailed country of origin and 2% provided the breakdown of race. There is great inconsistency in reported characteristics of Hispanics in health research. The lack of detailed characterization of this population ultimately creates roadblocks in translating evidence into practice when providing care to the large and increasingly diverse Hispanic population in the US.

Caspase cleavage of GFAP produces an assembly-compromised proteolytic fragment that promotes filament aggregation.

IF (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. GFAP (glial fibrillary acidic protein), a closely related IF protein expressed mainly in astrocytes, is also a putative caspase substrate. Mutations in GFAP cause AxD (Alexander disease). The overexpression of wild-type or mutant GFAP promotes cytoplasmic aggregate formation, with caspase activation and GFAP proteolysis. In this study, we report that GFAP is cleaved specifically by caspase 6 at VELD²²5 in its L12 linker domain in vitro. Caspase cleavage of GFAP at Asp²²5 produces two major cleavage products. While the C-GFAP (C-terminal GFAP) is unable to assemble into filaments, the N-GFAP (N-terminal GFAP) forms filamentous structures that are variable in width and prone to aggregation. The effect of N-GFAP is dominant, thus affecting normal filament assembly in a way that promotes filament aggregation. Transient transfection of N-GFAP into a human astrocytoma cell line induces the formation of cytoplasmic aggregates, which also disrupt the endogenous GFAP networks. In addition, we generated a neo-epitope antibody that recognizes caspase-cleaved but not the intact GFAP. Using this antibody, we demonstrate the presence of the caspase-generated GFAP fragment in transfected cells expressing a disease-causing mutant GFAP and in two mouse models of AxD. These findings suggest that caspase-mediated GFAP proteolysis may be a common event in the context of both the GFAP mutation and excess.