Aim To investigate the protective effect of riboflavin on ischemia brain damage and the mecha-nism.Methods The in vivo experiments were pro-cessed in male SD rats .Rats were randomly arranged into control group , model group and riboflavin group . The rats in riboflavin group were intraperitoneally in-jected riboflavin at the dose of 1 mg? kg -1 for seven consecutive days .Then the rats in model and riboflavin groups were carried out middle cerebral artery occlu-sion( MCAO) operation.After 24 h, all rats were sacri-ficed and the brain tissue was dissected to observe the infarct area, the edema and the ultrastructure damage . The brain tissue was dyed by triphenyl tetrazolium chloride .The brain edema was observed by the weight of ischemia-side semi-brain.The ultrastructure was ob-served by electron microscope .The in vitro experiments were processed in primary culture neurons by exposed to oxygen and glycose deprivation ( OGD) .The viability of neurons was assayed by MTT method .The enzyme activity of superoxide dismutase ( SOD) , catalase ( CAT)and glutathione peroxidase ( GSH-Px ) was assayed to explore the mechanism .Results Riboflavin signifi-cantly decreased the infarct area ( P<0.01 ) , inhibited the brain edema ( P <0.01 ) and inhibited the ultra-structure damage in rats after MCAO;riboflavin protec-ted the viability ( P <0.01 ) and the ultrastructure of neurons exposed to OGD .The enzyme activity of an-tioxidant SOD1 ( P <0.01 ) , CAT ( P <0.01 ) and GSH-Px ( P <0.01 ) was protected by riboflavin in MCAO model .No difference was found in the activity of SOD2 . Conclusion Riboflavin inhibits ischemia brain damage , and the protection of the activity of an-tioxidants is involved in the mechanism .

OBJECTIVE: To explore the genetic basis for a Chinese pedigree affected with inherited afibrinogenemia. METHODS: For the proband and his family members, prothrombin time (PT), activated partial thromboplastin time (APTT), thrombin time (TT), Fibrin(ogen) degradation products (FDPs), D-dimer (D-D), plasminogen activity (PLG:A) and the TT mixed experiment with protamine sulfate were determined with a STAGO-R automatic coagulation analyzer. The activity and antigen of fibrinogen (Fg) in plasma were measured with the Clauss method and immunonephelometry method, respectively. All exons and flanking regions of the fibrinogen genes (FGA, FGB and FGG) were amplified by PCR and directly sequenced. Human Splicing Finder software was used to predict and score the change of splicing site caused by the mutation. RESULTS: The proband showed normal FDPs and D-D but significantly prolonged TT, PT and APTT. The activity and antigen of fibrinogen in plasma were significantly decreased (<0.1 g/L). His young sister and parents showed slightly prolonged TT (18.20-18.50 s) and decreased fibrinogen activity (1.27-1.54 g/L) and fibrinogen antigenic content (1.34-1.56 g/L). Genetic testing revealed that the proband has carried homozygous IVS7-12A>G (g.4147A>G) mutations of the FGG gene, for which his parents and young sister were heterozygous. As predicted by Human Splicing Finder and Mutation Taster software, the variant may generate a new splicing site which can extend the sequence of exon 7 by 11 bp, with alteration of the coding sequence. PROVEAN suggested the variant to be deleterious. CONCLUSION The afibrinogenemia of the proband may be attributed to the FGG IVS7-12A>G variant, which was unreported previously.
Adult ; Afibrinogenemia/genetics* ; Female ; Fibrinogen/genetics* ; Heterozygote ; Humans ; Male ; Mutation ; Pedigree

Objective:To investigate and compare the histologic characteristics of adenocarcinomas with mesonephric features located in different parts of the gynecologic tract.Methods:Two cases of mesonephric adenocarcinomas (MA) of the cervix and 5 cases of mesonephric-like adenocarcinomas (MLA) of the uterus and ovary were collected in Women′s Hospital, School of Medicine, Zhejiang University from January 2018 to October 2020. Hematoxylin-eosin staining, immunohistochemistry and KRAS mutation testing were performed together with review of literature.Results:MA of the cervix as well as MLA of the uterus and ovary had similar morphologic features, showing an admixture of glandular, tubular, papillary and solid growth patterns. However, both MA cases were located in cervical stroma, which demonstrated residual mesonephric ducts present at the periphery. All four uterine MLA cases extensively involved the endometrium and myometrium. The ovarian MLA case was associated with endometriosis. No residual mesonephric ducts were present in the MLA cases. Immunohistochemically, GATA3 was positive in all seven MA/MLA cases. TTF1 was expressed only in 4/5 MLA cases. ER and PR were negative and p53 was wild-type in all cases. KRAS mutation was detected in all five cases. During the 6-32 months of follow-up, one patient developed recurrence and the others were tumor-free.Conclusions:In the gynecologic tract, both MA in cervix and MLA in uterus and ovary have similar morphologic features, immunohistochemical expression and KRAS mutation. However, distinct from MA that originates from mesonephric remnant, MLA is closely related to Mullerian epithelium.