Mouse Anti-Human Fibrinogen (α chain) monoclonal antibody, clone 7D7

It is well-known in the literature that internal defects play a major role in the Very-High-Cycle Fatigue (VHCF) response of metallic materials. Generally, VHCF failures nucleate from internal defects characterized by a limited size. Unexpectedly, it has been found that cracks can grow from the initial defect even if the Stress Intensity Factor (SIF) is quite below the characteristic threshold for crack growth. Even though researchers unanimously accept this singular experimental evidence, they still dispute about its physical justification. Different micromechanical explanations have been proposed in the literature: local grain refinement, carbide decohesion, matrix fragmentation, hydrogen embrittlement, numerous cyclic pressure and formation of persistent slip bands are the most famous proposals. Regardless of the specific micromechanical explanation, it is generally acknowledged that a weakening mechanism occurs around the initial defect, thus permitting crack growth below the SIF threshold. The present paper proposes an innovative approach for the quantitative modeling of the weakening process around the initial defect. The proposed model considers an additional SIF that reduces the SIF threshold of the material. Starting from a very general formulation for the additional SIF, possible scenarios for crack growth from the initial defect are also identified and described. It is theoretically demonstrated that, depending on the scenario, a VHCF limit may also be present and its final formulation recalls the well-known expression previously proposed by Murakami. Copyright (C) 2017 The Authors. Published by Elsevier B.V.

Purpose Early diagnosis is crucial to increase the chances of conservation treatment for patients with steroid-induced osteonecrosis of the femoral head (SIONFH). This study aimed to identify serum peptides as potential biomarkers to diagnose SIONFH. Experimental Design The serum proteome of 32 SIONFH patients and 24 healthy controls are analyzed using magnetic bead-based weak cation exchange (MB-WCX) and matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF-MS). Next, candidate biomarkers are identified using liquid chromatography-electrospray ionization-tandem mass spectrometry (LC-ESI-MS/MS). Candidate biomarkers are then validated using ELISA and western blotting. Results 39 peaks are identified and the expression fold changes of seven peaks in the two groups are greater than 1.5. Three peaks (m/z: 1077.84 Da; m/z: 1061.78 Da; m/z: 1099.56 Da) tend to be upregulated, while four peaks (m/z: 3973.92 Da; m/z: 7766.53 Da; m/z: 3957.31 Da; m/z: 4212.02 Da) tend to be down-regulated in SIONFH patients. The peak for a 1077.84 Da peptide is identified as Isoform 1 of the Fibrinogen alpha chain precursor (FGA). ELISAs and western blot analyses reveal that the expression of FGA is significantly higher in SIONFH patients than healthy controls. Conclusion and Clinical Relevance FGA is overexpressed in SIONFH patients, and thus, is a novel potential biomarker for SIONFH.