Anti-Oxidized Fibrinogen polyclonal antibody

Background: The present study aimed to determine serum markers for cervical cancer (CC) and to provide valuable references for clinical diagnosis and treatment. Material/Methods: Serum samples were collected from age-matched healthy control women, and from female CC patients before and after surgery. Serum biomarkers were selected by comparing serum peptides profiles among the 3 groups by magnetic bead-based weak cation - exchange chromatography fractionation combined with matrix-assisted laser desorption/ionization-time of flight mass spectrometry. Probable serum biomarkers for cervical cancer were then further identified by liquid chromatography-electrospray ionization-tandem mass spectrometry system and the identified proteins were verified by enzyme-linked immunosorbent assay (ELISA). Results: Three peptide biomarkers were identified for distinguishing CC patients from normal individuals, and distinguishing preoperative CC patients from postoperative CC patients. Of these 3 identified protein peptide regions, 2 peptide regions - TKT (Peak 2, 2435.63 m/z, 499-524) and FGA (Peak 4, 2761.79 m/z, 603-629) - were identified as upregulated markers, and peptide region of APOA1 (Peak 9, 2575.3 m/z, 245-260) was identified as a downregulated biomarker in preoperative CC patients compared with healthy women. Conclusions: The present study provides a new method for identifying potential serum biomarkers for CC patients.

Objectives Inherited dysfibrinogenemia is a rare disorder, for which clinical studies related to the risk of bleeding or thrombosis and the type of causative mutation are scanty. Materials and Methods We analyzed the laboratory, clinical, and genotypic features of 50 patients with inherited dysfibrinogenemia belonging to 19 unrelated families. Results In all the index cases, fibrinogen activity by Clauss method was below the normal range, while it was observed in 57.9% only by PT-derived method. In three families, hypodysfibrinogenemia was evident, associated with three novel mutations (Ter492Gln in FGB, Cys365Asp, and Leu370Phe in FGG). Three additional novel mutations were also identified (Arg114Lys in FGA, Ile131Thr and Trp234Arg in FGG). Bleeding symptoms assessed by ISTH-BAT scored at least 1 in 30% of patients and, significant bleeding symptoms were mainly present in female patients, especially associated with pregnancy. Two patients with FGB Arg44Cys suffered from venous thromboembolism, and two with FGA Arg35His had ischemic stroke at older age. Conclusions This study confirms the heterogeneity of clinical features in inherited dysfibrinogenemia, due to the wide spectrum of the causative mutations. Larger multicenter studies are needed to assess the definitive correlation of some mutations with bleeding or thrombosis.