Simultaneous Diffusion Coating of Cr and Si on Stainless Steel using Fluoride-Free Activator

The simultaneous deposition of chromium and silicon on stainless steel using a halide-activated diffusion coating process was performed to improve oxidation properties at high temperatures. Conventional procedure in diffusion coating process uses an activator containing fluoride. Fluoride is harmful for the human body and the environment. This experimental object is a development of the fluoride-free activator in diffusion coating of chromizing-siliconizing. In this investigation, Cr-Si intermetallic compound layers were coated on stainless steel by the pack cementation to improve its oxidation resistance and the resulting properties of the obtained coatings were investigated. The pack powders used for the diffusion coating were Cr and Si as diffusion element, Al2O3 as filler, and NH4Cl and CaCl2 as fluoride-free activator or NH4Cl, NaF and AlF3 as fluoride-added activator. The diffusion coating treatment was conducted at 1323 K for 18.0 ks in an Ar atmosphere. After the simultaneous deposition of chromium and silicon on stainless steel, a modified layer was observed on the treated sample surface and fluoride-free activator could also modify the steel surface using pack cementation

Factors associated with the achievement of biological disease-modifying antirheumatic drug-free remission in rheumatoid arthritis: the ANSWER cohort study

Background: Clinical remission can be maintained after the discontinuation of biological disease-modifying antirheumatic drugs (bDMARDs) in some patients with rheumatoid arthritis (RA) (bDMARD-free remission (BFR)). It is unknown which bDMARD is advantageous for achieving BFR or under which conditions BFR can be considered. This study aimed to determine the factors associated with BFR achievement in clinical practice. Methods: Patients with RA were enrolled from a Japanese multicenter observational registry. Patients with RA who achieved clinical remission (Disease Activity Score 28-C-reactive protein 6 months), Boolean remission, no glucocorticoid use at the time of bDMARD discontinuation, and use of TNFi(mAb) or CTLA4-Ig remained as independent factors associated with BFR. Conclusions: BFR can be achieved in some patients with RA after bDMARD discontinuation in clinical practice. Use of TNFi(mAb) or CTLA4-Ig, sustained remission, Boolean remission, and no glucocorticoid use at the time of bDMARD discontinuation are advantageous for achieving BFR

Additional file 3: of Factors associated with the achievement of biological disease-modifying antirheumatic drug-free remission in rheumatoid arthritis: the ANSWER cohort study

Table S1. Types of bDMARDs and hazard ratios for bDMARD-free remission failure in bDMARD-naïve patients (univariate analysis). bDMARD-naïve patients classified into four groups based on types of bDMARDs. Hazard ratios with 95% CIs obtained using Cox’s proportional hazard model. CI confidence interval, bDMARD biological disease-modifying antirheumatic drug, TNFi(mAb) monoclonal antibodies against TNF (infliximab, adalimumab, and golimumab), TNFi(R/P) soluble TNF receptor or Fab fragments against TNF fused with polyethylene glycol (etanercept and certolizumab), CTLA4-Ig abatacept, IL-6Ri interleukin-6 receptor inhibitor (tocilizumab) (DOCX 15 kb) (DOCX 15 kb

Additional file 2: of Factors associated with the achievement of biological disease-modifying antirheumatic drug-free remission in rheumatoid arthritis: the ANSWER cohort study

Figure S2. Kaplan–Meier survival curve for maintaining bDMARD-free remission after discontinuation of different types of bDMARDs in bDMARD-naïve patients. bDMARD-naïve patients classified into four groups based on types of bDMARDs. Kaplan–Meier method used to estimate BFR maintenance time. bDMARD biological disease-modifying anti-rheumatic drug, BFR biological disease-modifying anti-rheumatic drug-free remission, TNFi(mAb) monoclonal antibodies against TNF (infliximab, adalimumab, and golimumab), TNFi(R/P) soluble TNF receptor or Fab fragments against TNF fused with polyethylene glycol (etanercept and certolizumab), CTLA4-Ig abatacept, IL-6Ri interleukin-6 receptor inhibitor (tocilizumab), CI confidence interval (PDF 80 kb) (PDF 79 kb