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Factor IX Deficiency

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1201. Botrocetin/VWF-induced signaling through GPIb-IX-V produces TxA2 in an αIIbβ3- and aggregation-independent manner (Full text)

Botrocetin/VWF-induced signaling through GPIb-IX-V produces TxA2 in an αIIbβ3- and aggregation-independent manner Binding of von Willebrand factor (VWF) to the platelet membrane glycoprotein (GP) Ib-IX-V complex initiates a signaling cascade that causes alphaIIbbeta3 activation and platelet aggregation. Previous work demonstrated that botrocetin (bt)/VWF-mediated agglutination activates alphaIIbbeta3 and elicits adenosine triphosphate (ATP) secretion in a thromboxane A2 (TxA2)- and Ca2 (...) wortmannin, and mouse platelets deficient in Lyn, Src, Syk, Src homology 2 (SH2) domain-containing leukocyte protein 76 (SLP-76), phospholipase Cgamma2 (PLCgamma2), linker for activation of T cells (LAT), or Fc receptor gamma-chain (FcRgamma-chain) were used for these studies. LAT and FcRgamma-chain were found not to be required for agglutination-driven TxA2 production or activation of alphaIIbbeta3, but were required for granule secretion and aggregation. The results also clearly demonstrate that bt/VWF

2005 Blood PubMed

1202. Carbonic anhydrase IX expression and tumor oxygenation status do not correlate at the microregional level in locally advanced cancers of the uterine cervix. (Full text)

IX immunostaining with direct oxygenation measurements using pO2 microsensors have thus far yielded contradictory results.Because tumor heterogeneity may be among the factors responsible for the discrepancy between the two methods, CA IX expression in tissue samples originating from oxygen microelectrode tracks of locally advanced cervical cancers was assessed in this study. Seventy-seven biopsy specimens were analyzed immunohistochemically using an anti-CA IX rabbit polyclonal antibody (...) not correlate with the oxygenation status may be due to the degree to which other factors, such as nutrient (e.g., glucose) deficiency or the action of oncogenic mutations, can modulate the in vivo expression of this protein, rendering a strict association with tumor hypoxia too unreliable for clinical use.

2005 Clinical Cancer Research PubMed

1203. Pseudoxanthoma elasticum-like phenotype with cutis laxa and multiple coagulation factor deficiency represents a separate genetic entity. (Full text)

Pseudoxanthoma elasticum-like phenotype with cutis laxa and multiple coagulation factor deficiency represents a separate genetic entity. Data on six patients with a Pseudoxanthoma Elasticum (PXE)-like phenotype, characterized by excessive skin folding (resembling cutis laxa) and a deficiency of the vitamin K-dependent clotting factors (II, VII, IX, and X) are presented. A comparison is made between the clinical, ultrastructural, and molecular findings in these patients and those seen in classic (...) , and no decrease in visual acuity. Moreover, detailed electron microscopic analyses revealed that alterations of elastic fibers as well as their mineralization were slightly different from those in classic PXE. Molecular analysis revealed neither causal mutations in the ABCC6 gene (ATP-binding cassette subfamily C member 6), which is responsible for PXE, nor in VKORC1 (vitamin K 2,3 epoxide reductase), known to be involved in vitamin K-dependent factor deficiency. However, the GGCX gene (gamma-glutamyl

2007 Journal of Investigative Dermatology PubMed

1204. Effects of coagulation factor deficiency on plasma coagulation kinetics determined via thrombelastography: critical roles of fibrinogen and factors II, VII, X and XII. (PubMed)

, VIII, IX, X, XI, XII, or XIII activated with celite (0.28 mg ml(-1)) or tissue factor (TF, 0.1%) (n = 6 per condition). Additional fibrinogen concentration activity (75-345 mg dl(-1)) and Factor II, VII, X and XII activity-response relationships (1%, 6.25%, 12.5%, 25%, 50% and 100% activity) were obtained (n = 8 per condition). Thrombelastography parameters included reaction time (R), angle (alpha), and clot strength (A, amplitude; G, elastic modulus).Celite activation of FXII-deficient plasma, TF (...) Effects of coagulation factor deficiency on plasma coagulation kinetics determined via thrombelastography: critical roles of fibrinogen and factors II, VII, X and XII. Thrombelastography (TEG) is used to assess coagulopathy. However, a comprehensive characterization of the effects of specific coagulation factor deficiencies and mode of activation on TEG data does not exist.Thrombelastography was performed for 15 min with control plasma and plasmas deficient (<1% activity) in Factors II, V, VII

2005 Acta Anaesthesiologica Scandinavica

1205. Association of congenital deficiency of multiple vitamin K-dependent coagulation factors and the phenotype of the warfarin embryopathy: clues to the mechanism of teratogenicity of coumarin derivatives. (Full text)

Association of congenital deficiency of multiple vitamin K-dependent coagulation factors and the phenotype of the warfarin embryopathy: clues to the mechanism of teratogenicity of coumarin derivatives. We have evaluated a boy who had excessive bleeding and bruising from birth and showed markedly prolonged prothrombin times, partially correctable by oral vitamin K administration. Additional laboratory studies demonstrated decreased activities of plasma factors II, VII, IX, and X; near normal (...) levels of immunologically detected and calcium binding-independent prothrombin; undercarboxylation of prothrombin; excess circulating vitamin K epoxide; decreased excretion of carboxylated glutamic acid residues; and abnormal circulating osteocalcin. These results all are consistent with effects resulting from decreased posttranslational carboxylation secondary to an inborn deficiency of vitamin K epoxide reductase. This individual also had nasal hypoplasia, distal digital hypoplasia, and epiphyseal

1987 American Journal of Human Genetics PubMed

1206. Acquired Antibody to Factor XI in a Patient with Congenital Factor XI Deficiency (Full text)

as that of patients with severe Factor VIII or IX deficiency. This suggests that physiologic activation of Factors XI and IX does not occur exclusively in series because deficiency of factors XII, XI, VIII, and IX should then have similar hemostatic consequences. We propose that independent mechanisms for bypass of Factors XII and XI are important in physiologic activation of coagulation. (...) Acquired Antibody to Factor XI in a Patient with Congenital Factor XI Deficiency The results of studies in a patient with congenital deficiency of Factor XI who developed an inhibitor are presented. The patient presented with a severe, apparently spontaneous bleed into the thigh, which progressed despite infusion of fresh frozen plasma, but which responded promptly to activated prothrombin complex. During therapy with plasma his clotting time and Factor XI level were unresponsive and a Factor

1982 Journal of Clinical Investigation PubMed

1207. Regional localization on the human X chromosome and polymorphism of the coagulation factor IX gene (hemophilia B locus). (Full text)

Regional localization on the human X chromosome and polymorphism of the coagulation factor IX gene (hemophilia B locus). Hemophilia B is an X-linked disease caused by a functional deficiency in coagulation factor IX. A cDNA clone corresponding to factor IX has been used to detect homologous sequences in the human genome. All DNA fragments hybridizing to the probe, under medium- or high-stringency conditions, are X-linked, and the patterns obtained suggest that a single large (greater than

1984 Proceedings of the National Academy of Sciences of the United States of America PubMed

1208. Molecular basis of hemophilia B: a defective enzyme due to an unprocessed propeptide is caused by a point mutation in the factor IX precursor. (Full text)

of the factor IX, indicating the importance of the leader sequence in substrate recognition by the vitamin K-dependent carboxylase. This represents an example of an enzyme defect due to the presence of a point mutation in a precursor protein (preproenzyme) that is the cause of a human hereditary disease. This defect will serve as a prototype for understanding the molecular basis of some forms of hemophilia and other hereditary enzyme deficiencies. (...) Molecular basis of hemophilia B: a defective enzyme due to an unprocessed propeptide is caused by a point mutation in the factor IX precursor. A mutant factor IX, designated factor IXCambridge, was isolated from a patient with hemophilia B. This protein includes an 18-residue propeptide attached to the NH2 terminus of factor IX. A point mutation at residue -1, from an arginine to a serine, precludes cleavage of the propeptide by a processing protease and interferes with gamma-carboxylation

1986 Proceedings of the National Academy of Sciences of the United States of America PubMed

1209. An intragenic deletion of the factor IX gene in a family with hemophilia B. (Full text)

. The deletion included two exons (exons V and VI) coding for the amino acid sequence from number 85 to 195 of the factor IX protein. The deleted portion of the gene contained the entire factor IX activation peptide. The length of the deletion was estimated to be 10 +/- 0.3 kilobase pairs. This specific gene has been named FIXSeattle. In this family both the deletion and a Taq 1 restriction fragment length polymorphism can be used as a useful marker for accurate detection of female carriers of the deficient (...) An intragenic deletion of the factor IX gene in a family with hemophilia B. A family of seven patients severely afflicted with hemophilia B has been studied for their factor IX genes through the use of factor IX cDNA and genomic DNA probes. The patients had detectable (less than 10% of normal) factor IX antigen in urine and no detectable inhibitors in sera to factor IX protein. Based on the DNA hybridization analysis, these patients showed a partial intragenic deletion in their factor IX gene

1985 Journal of Clinical Investigation PubMed

1210. Ulnar artery pseudoaneurysm in a patient with factor IX deficiency (hemophilia B) (Full text)

Ulnar artery pseudoaneurysm in a patient with factor IX deficiency (hemophilia B) The hypothenar hammer syndrome describes a constellation of symptoms resulting from repetitive trauma to the hypothenar eminence, often due to the use of the hand as a hammer. Sequelae of this syndrome include both true and false aneurysms, as well as thrombosis of the ulnar artery due to its vulnerability to blunt trauma as it exits Guyon's canal. Although this is a relatively well-documented phenomenon (...) , an extensive review of the literature revealed that no cases have been described involving a patient with hemophilia. The present case describes a 46-year-old farmer with factor IX deficiency (hemophilia B) presenting with a 5 cm x 7 cm pseudoaneurysm of the ulnar artery of the right hand.

2007 The Canadian Journal of Plastic Surgery PubMed

1211. Prophylaxis in factor IX deficiency product and patient variation. (PubMed)

Prophylaxis in factor IX deficiency product and patient variation. To determine the dosing needed to maintain a prophylactic level of factor IX (FIX) >/=2%, 15 non-inhibitor severe (deficient subjects participated in a double-blind, two-period crossover study to assess the pharmacokinetics of two FIX concentrates, Mononine (pd-FIX), an ultra-high-purity plasma-derived concentrate, and BeneFix (r-FIX), a recombinant product. The median recovery in the pd-FIX group was 1.67 IU dL(-1

2003 Haemophilia : the official journal of the World Federation of Hemophilia

1212. A simple technique to reduce epistaxis and nasopharyngeal trauma during nasotracheal intubation in a child with factor IX deficiency having dental restoration. (Full text)

A simple technique to reduce epistaxis and nasopharyngeal trauma during nasotracheal intubation in a child with factor IX deficiency having dental restoration. Epistaxis and airway trauma are often associated with nasotracheal intubation. We describe a patient with Factor IX deficiency who required nasotracheal intubation. An inexpensive, nonproprietary, rapid technique was used to reduce the trauma of intubation.

2004 Anesthesia and Analgesia PubMed

1213. Acute hepatitis in a patient with mild factor IX deficiency after anesthesia with isoflurane. (Full text)

Acute hepatitis in a patient with mild factor IX deficiency after anesthesia with isoflurane. 3756695 1986 10 30 2018 11 13 0820-3946 135 6 1986 Sep 15 CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne CMAJ Acute hepatitis in a patient with mild factor IX deficiency after anesthesia with isoflurane. 645-6 Grégoire S S Smiley R K RK eng Case Reports Journal Article Canada CMAJ 9711805 0820-3946 CYS9AKD70P Isoflurane AIM IM Adult Anesthesia, General

1986 CMAJ: Canadian Medical Association Journal PubMed

1214. Phase I/II Study of Monoclonal Factor IX Concentrate for Factor IX Deficiency

Phase I/II Study of Monoclonal Factor IX Concentrate for Factor IX Deficiency Phase I/II Study of Monoclonal Factor IX Concentrate for Factor IX Deficiency - 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 (...) . Phase I/II Study of Monoclonal Factor IX Concentrate for Factor IX Deficiency 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. Read our for details. ClinicalTrials.gov Identifier: NCT00004801 Recruitment Status : Completed First Posted : February 25, 2000 Last Update Posted : June 24, 2005 Sponsor: National Center for Research Resources (NCRR) Collaborator

2000 Clinical Trials

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