RESUMO
BACKGROUND: The Rapid Emergency Medicine Score (REMS) and Worthing Physiological Scoring system (WPS) have been developed for predicting in-hospital mortality in nonsurgical emergency department (ED) patients. The prognostic performance of the scoring systems in independent populations has not been clear. The aim of the study is to evaluate the prognostic accuracy of REMS and WPS systems in the estimation of 30-day mortality risk among medical patients in ED. METHODS: The study was designed as a prospective investigation, with the setting being the ED of the National Hospital of Can Tho, Vietnam. We enrolled medical patients aged 16+ years who met the study entry criteria. Clinical data were obtained as required for each scoring system. The primary outcome was mortality within 30 days since hospitalization. The association between each scoring system and mortality was assessed by the hazard ratio (HR) of the Cox's proportional hazard model. RESULTS: The study involved 1746 patients, average age 65.9 years (SD 17). During the period of follow-up, 172 patients (9.9 %) died. The risk of 30-day mortality was increased by 30 % for each additional REMS unit (HR: 1.28; 95 % confidence interval (CI): 1.23-1.34) and by 60 % for each additional WPS unit (HR: 1.6; 95 % CI: 1.5-1.7). The AUC of the REMS was 0.71 (95 % CI: 0.67-0.76) which was significantly lower than that of the WPS (0.80; 95 % CI: 0.76-0.83). CONCLUSIONS: Both REMS and WPS have good prognostic value in the prediction of death in ED patients. The WPS appeared to have a better prognostic performance than the REMS system.
RESUMO
Dysregulated fibroblast growth factor (FGF) signaling has been implicated in the pathogenesis of human cancers. Aberrant activation of FGF receptor 2 (FGFR2) signaling, through overexpression of FGFR2 and/or its ligands, mutations, and receptor amplification, has been found in a variety of human tumors. We generated monoclonal antibodies against the extracellular ligand-binding domain of FGFR2 to address the role of FGFR2 in tumorigenesis and to explore the potential of FGFR2 as a novel therapeutic target. We surveyed a broad panel of human cancer cell lines for the dysregulation of FGFR2 signaling and discovered that breast and gastric cancer cell lines harboring FGFR2 amplification predominantly express the IIIb isoform of the receptor. Therefore, we used an FGFR2-IIIb-specific antibody, GP369, to investigate the importance of FGFR2 signaling in vitro and in vivo. GP369 specifically and potently suppressed ligand-induced phosphorylation of FGFR2-IIIb and downstream signaling, as well as FGFR2-driven proliferation in vitro. The administration of GP369 in mice significantly inhibited the growth of human cancer xenografts harboring activated FGFR2 signaling. Our findings support the hypothesis that dysregulated FGFR2 signaling is one of the critical oncogenic pathways involved in the initiation and/or maintenance of tumors. Cancer patients with aberrantly activated/amplified FGFR2 signaling could potentially benefit from therapeutic intervention with FGFR2-targeting antibodies.