Strengthening mechanisms of reduced activation ferritic/martensitic steels:A review

This review summarizes the strengthening mechanisms of reduced activation ferritic/martensitic(RAFM)steels.High-angle grain boundaries,subgrain boundaries,nano-sized M_(23)C_(6),and MX carbide precipitates effectively hinder dislocation motion and increase high-temperature strength.M23C6 carbides are easily coarsened under high temperatures,thereby weakening their ability to block dislocations.Creep properties are improved through the reduction of M23C6 carbides.Thus,the loss of strength must be compensated by other strengthening mechanisms.This review also outlines the recent progress in the development of RAFM steels.Oxide dispersion-strengthened steels prevent M23C6 precipitation by reducing C content to increase creep life and introduce a high density of nano-sized oxide precipitates to offset the reduced strength.Severe plastic deformation methods can substantially refine subgrains and MX carbides in the steel.The thermal deformation strengthening of RAFM steels mainly relies on thermo-mechanical treatment to increase the MX carbide and subgrain boundaries.This procedure increases the creep life of TMT(thermo-mechanical treatment)9Cr-1W-0.06Ta steel by~20 times compared with those of F82H and Eurofer 97 steels under 550℃/260 MPa.

Fibroblast Growth Factor Receptor 1 Gene Amplification in Nonsmall Cell Lung Cancer

Objective： To review the prevalence and prognostic significance of fibroblast growth factor receptor 1 （FGFRI） amplification and to establish an association between FGFRI amplification and the clinical characteristics of nonsmall cell lung cancer （NSCLC）. Data Sources： We searched PubMed for English-language studies published between January 2010 and May 2016. Study Selection： We included all relevant articles, with no limitation of study design. Results： FGFRI amplification was reported in 8.7-20.0% of NSCLC cases and was significantly more frequent in squamous cell carcinomas （SCCs） （9.7-28.3%） than in adenocarcinomas （ADCs） （0-15.0%）. The rates of FGFRI amplification were as follows： males, 13.9-22.1%; females, 0-20.1%; Stage 1 NSCLC, 9.3-24.1%; Stage II NSCLC, 12.9-25.0%; Stage 111 NSCLC, 8.2-19.5%： Stage IV NSCLC, 0-12.5%; current smokers, 13.3-29.0%; former smokers, 2.5-23.0%; and nonsmokers, 0-22.2%. Overall survival was 43.9-70.8 months in patients with FGFRI amplification and 42.4-115.0 months in patients with no FGFRI amplification; disease-free survival was 22.5-58.5 months and 52.4-94.6 months, respectively. Conclusions： FGFR1 amplification is more frequent in SCCs than in ADCs. The association between FGFRI amplification and clinical characteristics （gender, smoking status, and disease stage） and the prognostic significance of FGFRI amplification in NSCLC remain controversial.