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Factor IX Deficiency

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21. Ultrasound-targeted hepatic delivery of factor IX in hemophiliac mice (PubMed)

Ultrasound-targeted hepatic delivery of factor IX in hemophiliac mice Ultrasound-targeted microbubble destruction (UTMD) was used to direct the delivery of plasmid and transposase-based vectors encoding human factor IX (hFIX) to the livers of hemophilia B (FIX-/-) mice. The DNA vectors were incorporated into cationic lipid microbubbles, injected intravenously, and transfected into hepatocytes by acoustic cavitation of the bubbles as they transited the liver. Ultrasound parameters were (...) identified that produced transfection of hepatocytes in vivo without substantial damage or bleeding in the livers of the FIX-deficient mice. These mice were treated with a conventional expression plasmid, or one containing a piggyBac transposon construct, and hFIX levels in the plasma and liver were evaluated at multiple time points after UTMD. We detected hFIX in the plasma by western blotting from mice treated with either plasmid during the 12 days after UTMD, and in the hepatocytes of treated livers

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2016 Gene therapy

22. Preliminary study on non-viral transfection of F9 (factor IX) gene by nucleofection in human adipose-derived mesenchymal stem cells (PubMed)

Preliminary study on non-viral transfection of F9 (factor IX) gene by nucleofection in human adipose-derived mesenchymal stem cells Background. Hemophilia is a rare recessive X-linked disease characterized by a deficiency of coagulation factor VIII or factor IX. Its current treatment is merely palliative. Advanced therapies are likely to become the treatment of choice for the disease as they could provide a curative treatment. Methods. The present study looks into the use of a safe non-viral (...) transfection method based on nucleofection to express and secrete human clotting factor IX (hFIX) where human adipose tissue derived mesenchymal stem cells were used as target cells in vitro studies and NOD. Cg-Prkdcscid Il2rgtm1Wjl/SzJ mice were used to analyze factor IX expression in vivo studies. Previously, acute liver injury was induced by an injected intraperitoneal dose of 500 mg/kg body weight of acetaminophen. Results. Nucleofection showed a percentage of positive cells ranging between 30.7

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2016 PeerJ

23. Coagadex - human coagulation factor X. In patients with hereditary factor X deficiency

Coagadex - human coagulation factor X. In patients with hereditary factor X deficiency 30 Churchill Place ? Canary Wharf ? London E14 5EU ? United Kingdom An agency of the European Union Telephone +44 (0)20 3660 6000 Facsimile +44 (0)20 3660 5555 Send a question via our website www.ema.europa.eu/contact © European Medicines Agency, 2016. Reproduction is authorised provided the source is acknowledged. 28 January 2016 EMA/CHMP/139881/2016 Committee for Medicinal Products for Human Use (CHMP (...) Agency F1+2 Prothrombin Fragments F1 and F2 FACTOR X syn. for Coagadex FCT Fibrinogen Clotting Time FII Coagulation factor II FIX Coagulation factor IX FX Coagulation factor X FXa Activated coagulation factor X FX:Ag Factor X antigen FX:C Factor X activity FFP Fresh frozen plasma GC Gas chromatography GCP Good Clinical Practice GLP Good Laboratory Practice GMP Good Manufacturing Practice HAV Hepatitis A virus HBV Hepatitis B virus HBsAg Hepatitis B surface antigen HCV Hepatitis C virus HIV Human

2016 European Medicines Agency - EPARs

24. Turoctocog alfa (Novoeight) - haemophilia A (congenital factor VIII deficiency)

Turoctocog alfa (Novoeight) - haemophilia A (congenital factor VIII deficiency) HAS - Medical, Economic and Public Health Assessment Division 1/18 The legally binding text is the original French version T TR RA AN NS SP PA AR RE EN NC CY Y C CO OM MM MI IT TT TE EE E Opinion 2 April 2014 NOVOEIGHT 250 IU, powder and solvent for solution for injection B/1 vial of powder + 1 prefilled syringe of 4 ml solvent + 1 vial adaptor (CIP:3400958573958) NOVOEIGHT 500 IU, powder and solvent for solution (...) with haemophilia A (congenital factor VIII deficiency)” HAS - Medical, Economic and Public Health Assessment Division 2/18 Actual Benefit The actual benefit of NOVOEIGHT is substantial. Improvement in Actual Benefit NOVOEIGHT does not provide any improvement in actual benefit (level V, non-existent) in the treatment and prophylaxis of haemophilia A compared with other available treatments. Therapeutic use NOVOEIGHT is one of the first-line factor VIII concentrates used in the treatment and prophylaxis

2014 Haute Autorite de sante

25. Coagulation factor 9-deficient mice are protected against dextran sulfate sodium-induced colitis (PubMed)

from body-weight loss and had a reduced disease activity score. We detected decreased colonic myeloperoxidase activity and decreased CXCL1 levels in DSS-treated F9-deficient mice compared with wild-type (WT) littermate controls, indicating decreased neutrophil infiltration. Remarkably, we identified expression of coagulation factor IX (FIX) protein in small intestinal epithelial cells (MODE-K). In epithelial cell cultures, cellular FIX protein expression was increased following stimulation (...) Coagulation factor 9-deficient mice are protected against dextran sulfate sodium-induced colitis Patients with inflammatory bowel disease (IBD) are susceptible to thromboembolism. Interestingly, IBD occurs less frequently in patients with inherited bleeding disorders. Therefore, we analyzed whether F9-deficiency is protective against the onset of acute colitis in a genetic hemophilia B mouse model. In the 3.5% dextran sulfate sodium (DSS)-induced colitis model, F9-deficient mice were protected

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2018 Biology open

26. Thrombin generation assay using factor XIa to measure factors VIII and IX and their glycoPEGylated derivatives is robust and sensitive. (PubMed)

as a possible method for characterizing bleeding phenotypes in individuals with hemophilia.This study assessed the robustness and sensitivity of the TGA for measuring the activity of recombinant factor VIII (rFVIII), recombinant factor IX (rFIX) and their glycoPEGylated derivatives, N8-GP and N9-GP, in vitro.Factor-deficient plasma was spiked with 0.13-130 IU dL(-1) rFVIII or N8-GP (hemophilia A [HA] plasma), or rFIX or N9-GP (hemophilia B [HB] plasma). A calibrated automated thrombogram triggered (...) Thrombin generation assay using factor XIa to measure factors VIII and IX and their glycoPEGylated derivatives is robust and sensitive. Conventional coagulation factor assays are associated with certain limitations, as they do not always reflect the clinical heterogeneity of bleeding in hemophilic patients or correctly reflect the individual patient response to treatment with bypassing agents or novel factor concentrates. The thrombin generation assay (TGA) is currently being assessed

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2015 Journal of Thrombosis and Haemostasis

27. Riemerella anatipestifer Type IX Secretion System Is Required for Virulence and Gelatinase Secretion (PubMed)

Riemerella anatipestifer Type IX Secretion System Is Required for Virulence and Gelatinase Secretion Riemerella anatipestifer (RA), a major causative agent of septicemia anserum exsudativa in domesticated ducklings, has a protein secretion system known as the type IX secretion system (T9SS). It is unknown whether the T9SS contributes to the virulence of RA through secretion of factors associated with pathogenesis. To answer this question, we constructed an RA mutant deficient in sprT, which (...) -like serine proteases which are important virulence factors that interact with complement proteins may enable RA to evade immune surveillance in the avian innate immune system.

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2017 Frontiers in microbiology

28. The Type IX Secretion System Is Required for Virulence of the Fish Pathogen Flavobacterium columnare (PubMed)

The Type IX Secretion System Is Required for Virulence of the Fish Pathogen Flavobacterium columnare Flavobacterium columnare, a member of the phylum Bacteroidetes, causes columnaris disease in wild and aquaculture-reared freshwater fish. The mechanisms responsible for columnaris disease are not known. Many members of the phylum Bacteroidetes use type IX secretion systems (T9SSs) to secrete enzymes, adhesins, and proteins involved in gliding motility. The F. columnare genome has all (...) of the genes needed to encode a T9SS. gldN, which encodes a core component of the T9SS, was deleted in wild-type strains of F. columnare The F. columnare ΔgldN mutants were deficient in the secretion of several extracellular proteins and lacked gliding motility. The ΔgldN mutants exhibited reduced virulence in zebrafish, channel catfish, and rainbow trout, and complementation restored virulence. PorV is required for the secretion of a subset of proteins targeted to the T9SS. An F. columnare ΔporV mutant

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2017 Applied and environmental microbiology

29. The Mechanism Underlying Activation of Factor IX by Factor XIa (PubMed)

The Mechanism Underlying Activation of Factor IX by Factor XIa Factor XI (fXI) is the zymogen of a plasma protease, factor XIa (fXIa), that contributes to thrombin generation during blood coagulation by proteolytic conversion of factor IX (fIX) to factor IXaβ (fIXaβ). There is considerable interest in fXIa as a therapeutic target because it contributes to thrombosis, while serving a relatively minor role in hemostasis. FXI/XIa has a distinctly different structure than other plasma coagulation (...) efficiency for the second cleavage is ~7-fold greater than that of the first cleavage, limiting fIXα accumulation. Residues at the N-terminus and C-terminus of the fXIa A3 domain likely form the fIX binding site. The dimeric conformation of fXIa is not required for normal fIX activation in solution. However, monomeric forms of fXI do not reconstitute fXI-deficient mice in arterial thrombosis models, indicating the dimer is required for normal function in vivo. FXI must be a dimer to be activated normal

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2014 Thrombosis research

30. Factor IX Deficiency

Factor IX Deficiency Factor IX Deficiency Toggle navigation Brain Head & Neck Chest Endocrine Abdomen Musculoskeletal Skin Infectious Disease Hematology & Oncology Cohorts Diagnostics Emergency Findings Procedures Prevention & Management Pharmacy Resuscitation Trauma Emergency Procedures Ultrasound Cardiovascular Emergencies Lung Emergencies Infectious Disease Pediatrics Neurologic Emergencies Skin Exposure Miscellaneous Abuse Cancer Administration 4 Factor IX Deficiency Factor IX Deficiency (...) Aka: Factor IX Deficiency , Christmas Disease , Hemophilia B , Plasma thromboplastin component deficiency From Related Chapters II. Pathophysiology Inherited sex linked trait Clinically indistinguishable from III. Symptoms Chronic history of since childhood Spontaneous bleeding Excessive follows: Dental procedures Surgery IV. Signs Joint deformities Muscle contractures V. Labs (PTT) prolonged Corrects with Factor IX supplementation Corrects with Normal serum VI. Management: Recombinant Factor IX

2015 FP Notebook

31. Female factor IX deficiency due to maternally inherited X-inactivation. (PubMed)

Female factor IX deficiency due to maternally inherited X-inactivation. X-chromosome inactivation is normally a random event that is regulated by the X chromosome itself. Rarely, females are affected by X-linked disorders from extremely skewed X-chromosome inactivation. Here, we report a family with hemophilia B with female expression through inherited X skewing that appears to be independent of either X chromosome. This finding suggests the possibility of a dominant autosomal contribution

2012 Clinical Genetics

32. Natural History Study of Factor IX Treatment and Complications

, Inc. Biogen/Bioverativ Swedish Orphan Biovitrum Information provided by (Responsible Party): Sharyne M. Donfield, Ph.D., Skane University Hospital Study Details Study Description Go to Brief Summary: This study will examine two groups of subjects with factor IX (FIX) deficiency: 1) those with a current or history of inhibitors to FIX, and; 2) groups of two or more affected brothers, with or without inhibitors. The overall goal is to characterize the study groups in terms of their medical history (...) , their patterns of bleeding, their care, quality of life, and complications including the development of joint disease, inhibitory antibodies to FIX, use of immune tolerance induction (ITI) and outcome. Condition or disease Intervention/treatment Factor IX Deficiency Other: Standard care with blood and urine sample collection Detailed Description: Hemophilia B, FIX deficiency, is the second most common type of hemophilia, occurring in about one in 25,000 male births. This disease is in some ways more complex

2015 Clinical Trials

33. Rate-limiting roles of tenase complex of factors VIII and IX in platelet procoagulant activity and formation of platelet-fibrin thrombi under flow. (PubMed)

Rate-limiting roles of tenase complex of factors VIII and IX in platelet procoagulant activity and formation of platelet-fibrin thrombi under flow. The importance of factor Xa generation in thrombus formation has not been studied extensively so far. Here, we used mice deficient in either factor VIII or factor IX to determine the role of platelet-stimulated tenase activity in the formation of platelet-fibrin thrombi on collagen. With tissue factor present, deficiency in factor VIII or IX (...) markedly suppressed thrombus growth, fibrin formation and platelet procoagulant activity (phosphatidylserine exposure). In either case, residual fibrin formation was eliminated in the absence of tissue factor. Effects of factor deficiencies were antagonized by supplementation of the missing coagulation factor. In wild-type thrombi generated under flow, phosphatidylserine-exposing platelets bound (activated) factor IX and factor X, whereas factor VIII preferentially co-localized at sites of von

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2015 Haematologica

34. A Safety and Efficacy Extension Study of a Recombinant Fusion Protein Linking Coagulation Factor IX With Albumin (rIX-FP) in Patients With Hemophilia B

A Safety and Efficacy Extension Study of a Recombinant Fusion Protein Linking Coagulation Factor IX With Albumin (rIX-FP) in Patients With Hemophilia B A Safety and Efficacy Extension Study of a Recombinant Fusion Protein Linking Coagulation Factor IX With Albumin (rIX-FP) in Patients With Hemophilia B - Full Text View - ClinicalTrials.gov Hide glossary Glossary Study record managers: refer to the if submitting registration or results information. Search for terms x × Study Record Detail Saved (...) Studies Save this study Warning You have reached the maximum number of saved studies (100). Please remove one or more studies before adding more. A Safety and Efficacy Extension Study of a Recombinant Fusion Protein Linking Coagulation Factor IX With Albumin (rIX-FP) in Patients With Hemophilia B The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. of clinical

2014 Clinical Trials

35. Measurement of factor IX activity in plasma-derived and recombinant concentrates: insights from thrombin generation and activation-based assays. (PubMed)

Measurement of factor IX activity in plasma-derived and recombinant concentrates: insights from thrombin generation and activation-based assays. Hemophilia B, resulting from a deficiency of coagulation factor IX, is treated effectively with either recombinant FIX (r-FIX) or plasma-derived FIX (pd-FIX) concentrates, although differences in pharmacokinetics are observed. FIX is activated in vivo by both activated FXI (FXIa) and tissue factor (TF)-activated FVII (FVIIa); however, conventional

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2014 Journal of Thrombosis and Haemostasis

36. Immune Tolerance Induction to Factor IX through B Cell Gene Transfer: TLR9 Signaling Delineates between Tolerogenic and Immunogenic B Cells (PubMed)

Immune Tolerance Induction to Factor IX through B Cell Gene Transfer: TLR9 Signaling Delineates between Tolerogenic and Immunogenic B Cells A subset of patients with severe hemophilia B, the X-linked bleeding disorder resulting from absence of coagulation factor IX (FIX), develop pathogenic antibody responses during replacement therapy. These inhibitors block standard therapy and are often associated with anaphylactic reactions to FIX. Established clinical immune tolerance induction protocols (...) be blocked by toll-like receptor 9 (TLR9) inhibition. While innate responses to TLR4 activation or to retrovirus were minimal in B cells, plasmid DNA activated TLR9, resulting in CpG-dependent NF-κB activation/IL-6 expression and adaptor protein 3 dependent, CpG-independent induction of IFN-I. Neither response was seen in TLR9-deficient B cells. Therefore, TLR9 signaling in B cells, in particular in response to plasmid vector, is highly immunogenic and has to be avoided in design of tolerance protocols.

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2014 Molecular Therapy

37. Involvement of the Type IX Secretion System in Capnocytophaga ochracea Gliding Motility and Biofilm Formation (PubMed)

Involvement of the Type IX Secretion System in Capnocytophaga ochracea Gliding Motility and Biofilm Formation Capnocytophaga ochracea is a Gram-negative, rod-shaped bacterium that demonstrates gliding motility when cultured on solid agar surfaces. C. ochracea possesses the ability to form biofilms; however, factors involved in biofilm formation by this bacterium are unclear. A type IX secretion system (T9SS) in Flavobacterium johnsoniae was shown to be involved in the transport of proteins (e.g (...) ., several adhesins) to the cell surface. Genes orthologous to those encoding T9SS proteins in F. johnsoniae have been identified in the genome of C. ochracea; therefore, the T9SS may be involved in biofilm formation by C. ochracea. Here we constructed three ortholog-deficient C. ochracea mutants lacking sprB (which encodes a gliding motility adhesin) or gldK or sprT (which encode T9SS proteins in F. johnsoniae). Gliding motility was lost in each mutant, suggesting that, in C. ochracea, the proteins

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2016 Applied and environmental microbiology

38. The transformation of hemostatic platelet plugs in normal and Factor IX deficient dogs. (PubMed)

The transformation of hemostatic platelet plugs in normal and Factor IX deficient dogs. 5675266 1968 10 28 2018 11 13 0002-9440 53 3 1968 Sep The American journal of pathology Am. J. Pathol. The transformation of hemostatic platelet plugs in normal and Factor IX deficient dogs. 355-73 Hovig T T Dodds W J WJ Rowsell H C HC Mustard J F JF eng Journal Article United States Am J Pathol 0370502 0002-9440 9001-31-4 Fibrin AIM IM Animals Blood Coagulation Blood Platelets Cell Membrane Permeability (...) Cytoplasm Dogs Fibrin Hemophilia A etiology pathology Hemophilia B pathology Microscopy, Electron Organoids Time Factors 1968 9 1 1968 9 1 0 1 1968 9 1 0 0 ppublish 5675266 PMC2013462 Blood. 1966 Feb;27(2):167-86 5901983 Am J Pathol. 1967 Nov;51(5):681-719 4168026 Blood. 1967 Nov;30(5):636-68 6073859 Acta Med Scand. 1958 Nov 27;162(5):361-74 13605613 Br J Haematol. 1960 Jul;6:259-66 13727144 Acta Pathol Microbiol Scand. 1964;60:55-82 14114329 Br J Exp Pathol. 1964 Oct;45:467-74 14213053 Acta Pathol

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1968 The American journal of pathology

39. Factor IX (Overview)

Factor IX (Overview) Factor IX Deficiency (Hemophilia B): Practice Essentials, Background, Pathophysiology Edition: No Results No Results Please confirm that you would like to log out of Medscape. If you log out, you will be required to enter your username and password the next time you visit. https://profreg.medscape.com/px/getpracticeprofile.do?method=getProfessionalProfile&urlCache=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvMTk5MDg4LW92ZXJ2aWV3 processing > Factor IX Deficiency (...) (Hemophilia B) Updated: Apr 02, 2018 Author: Robert A Schwartz, MD, MPH; Chief Editor: Srikanth Nagalla, MBBS, MS, FACP Share Email Print Feedback Close Sections Sections Factor IX Deficiency (Hemophilia B) Overview Practice Essentials Factor IX (FIX) deficiency or dysfunction, or hemophilia B, is an X-linked inherited bleeding disorder, usually manifested in males and transmitted by females who carry the causative mutation on the X chromosome. Hemophilia B results from a variety of defects in the FIX

2014 eMedicine.com

40. Factor IX (Diagnosis)

Factor IX (Diagnosis) Factor IX Deficiency (Hemophilia B): Practice Essentials, Background, Pathophysiology Edition: No Results No Results Please confirm that you would like to log out of Medscape. If you log out, you will be required to enter your username and password the next time you visit. https://profreg.medscape.com/px/getpracticeprofile.do?method=getProfessionalProfile&urlCache=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvMTk5MDg4LW92ZXJ2aWV3 processing > Factor IX Deficiency (...) (Hemophilia B) Updated: Apr 02, 2018 Author: Robert A Schwartz, MD, MPH; Chief Editor: Srikanth Nagalla, MBBS, MS, FACP Share Email Print Feedback Close Sections Sections Factor IX Deficiency (Hemophilia B) Overview Practice Essentials Factor IX (FIX) deficiency or dysfunction, or hemophilia B, is an X-linked inherited bleeding disorder, usually manifested in males and transmitted by females who carry the causative mutation on the X chromosome. Hemophilia B results from a variety of defects in the FIX

2014 eMedicine.com

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