Factor IX<

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Topic: Factor IX<

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Adenovirus-Mediated Expression of Human Coagulation <bb>>Factorb>bb>> IX in the Rhesus Macaque Is Associated With Dose-Limiting Toxicity -- Lozier et al. 94 (12): 3968 -- Blood

<bb>>factorb>bb>> IX (Mononine) and saw no change in the aPTT from baseline
Yao S-N, Farjo A, Roessler BJ, Davidson BL, Kurachi K: Adenovirus-mediated transfer of human <bb>>factorb>bb>> IX gene in immunodeficient and normal mice: Evidence for prolonged stability and activity of the transgene in liver.
Our studies focused on <bb>>factorb>bb>> IX expression, the immune

http://www.bloodjournal.org/cgi/content/full/94/12/3968 (5920 words)



Coagulation <bb>>Factorb>bb>> Assays

In hemophilia, <1% <bb>>factorb>bb>> VIII or IX produces severe hemophilia with spontaneous bleeding, 1% to 5% produces moderate bleeding, and >5% is considered mild hemophilia in which bleeding occurs primarily with trauma or surgery rather than spontaneously.
Factors XI and XII have the longest half-lives and therefore are often the last to be affected.
Deficiencies of <bb>>factorb>bb>>(s) VIII, IX, XI, and/or XII (intrinsic pathway)

http://www.mgh.harvard.edu/labmed/lab/coag/handbook/CO001100.htm (3048 words)



Coagulation <bb>>Factorb>bb>> Assays

<bb>>Factorb>bb>> VIII, IX, XI, and XII assays are PTT-based.
Factors XI and XII have the longest half-lives and therefore are often the last to be affected.
Deficiencies of <bb>>factorb>bb>>(s) VIII, IX, XI, and/or XII (intrinsic pathway)

http://www.mgh.harvard.edu/labmed/lab/coag/handbook/CO001100.htm (3048 words)



1.4.4 The coagulation mechanism

<bb>>Factorb>bb>> X is the first molecule of the common pathway and is activated by a complex of molecules containing activated <bb>>factorb>bb>> IX, <bb>>factorb>bb>> VIII, calcium, and phospholipid which is provided by the platelet surface, where this reaction usually takes place.
Eventually the intrinsic pathway activates <bb>>factorb>bb>> X, a process that can also be brought about by the extrinsic pathway.
<bb>>Factorb>bb>> VIII is modified by thrombin, a reaction that results in greatly enhanced <bb>>factorb>bb>> VIII activity, promoting the activation of <bb>>factorb>bb>> X. The extrinsic pathway is an alternative route for the activation of the clothing cascade.

http://nic.sav.sk/logos/books/scientific/node29.html (3048 words)



The Dynamics of Thrombin Formation -- Mann et al. 23 (1): 17 -- Arteriosclerosis, Thrombosis, and Vascular Biology

Cooperative activation of human <bb>>factorb>bb>> IX by the human extrinsic pathway of blood coagulation.
In the absence of <bb>>factorb>bb>> VIII or <bb>>factorb>bb>> IX, the intrinsic <bb>>factorb>bb>>
views regarding the tissue <bb>>factorb>bb>> pathway by which thrombin

http://atvb.ahajournals.org/cgi/content/full/23/1/17 (5742 words)



article.aspx?articleid=100096

<bb>>Factorb>bb>> X is the first molecule of the common pathway and is activated by a complex of molecules containing activated <bb>>factorb>bb>> IX, <bb>>factorb>bb>> VIII, calcium and phospholipid, which is provided by the platelet surface, where this reaction usually takes place.
The intrinsic pathway ultimately activates <bb>>factorb>bb>> X, a process which can also be brought about by the extrinsic pathway.
<bb>>Factorb>bb>> VIII is modified by thrombin, a reaction that results in greatly enhanced <bb>>factorb>bb>> VIII activity, promoting the activation of <bb>>factorb>bb>> X. The extrinsic pathway

http://www.fantalizee.com/article.aspx?articleid=100096 (5742 words)



Activated Partial Thromboplastin Time

<bb>>Factorb>bb>> deficiencies that prolong PTT: The PTT is more sensitive to deficiencies of the intrinsic pathway (factors VIII, IX, XI, XII, prekallikrein, HMWK) than it is to deficiencies of the common pathway (fibrinogen, and factors II, V, and X).
Therefore, in these situations, an alternative assay, such as the Heparin Antifactor Xa Assay, should be used rather than the PTT to monitor heparin.
<bb>>Factorb>bb>> XII deficiencies also do not cause bleeding, but <bb>>factorb>bb>> XII deficiencies are relatively common.

http://www.mgh.harvard.edu/labmed/lab/coag/handbook/co003400.htm (5742 words)



<bb>>Factorb>bb>> IX - Wikipedia, the free encyclopedia

<bb>>Factorb>bb>> IX is inactive unless activated by <bb>>factorb>bb>> XIa (of the contact pathway) or <bb>>factorb>bb>> VIIa (of the tissue <bb>>factorb>bb>> pathway).
Over 100 mutations of <bb>>factorb>bb>> IX have been described; some cause no symptoms, but many lead to a significant bleeding disorder.
Deficiency of <bb>>factorb>bb>> IX causes Christmas disease (hemophilia <bb>>Bb>bb>>).

http://en.wikipedia.org/wiki/Factor_IX (208 words)



Clinical Trial: Cooperative Study of <bb>>Factorb>bb>> VIII Inhibitors

The rationale for <bb>>Factorb>bb>> IX was that it bypassed the defect in <bb>>Factorb>bb>> VIII caused by the inhibitor.
Because of lack of information on the natural course of patients with <bb>>Factorb>bb>> VIII inhibitors, the relative efficacy of various modes of therapy was not established.
It was intended at the very outset of the <bb>>Factorb>bb>> VIII study that therapeutic trials involving patients with inhibitors would not be a prime function, but that such studies would be monitored if necessary.

http://clinicaltrials.gov/ct/show/NCT00000582?order=8 (498 words)



Afibrinogenemia, Congenital

<bb>>Factorb>bb>> IX Deficiency is a severe genetic bleeding disorder that resembles classic Hemophilia A. <bb>>Factorb>bb>> IX is a component of the blood clotting substance thromboplastin.
Hageman <bb>>Factorb>bb>> Deficiency is a rare genetic blood disorder.
<bb>>Factorb>bb>> XIII Deficiency is a very rare inherited disorder that prevents the blood from clotting normally.

http://hw.healthdialog.com/kbase/nord/nord940.htm (498 words)



Treatment - Boston Hemophilia Center - Clinical Services - Children's Hospital Boston

Hemophilia <bb>>Bb>bb>>, caused by a deficiency of <bb>>factorb>bb>> IX, is treated with intravenous infusion of plasma-derived or synthetic recombinant <bb>>factorb>bb>> IX.
<bb>>Factorb>bb>> VIII products are made by either purification from human plasma (the liquid part of blood) or by synthetic processes.
Available as a nose spray or by intravenous infusion, this hormone increases the levels of <bb>>factorb>bb>> VIII in the blood.

http://www.childrenshospital.org/clinicalservices/Site1971/mainpageS1971P16.html (293 words)



BEAUMAN2

Injection into leg muscle was not very efficient, increasing the concentration of <bb>>factorb>bb>> IX by only 1.4 %, but it was sufficient to prevent most of the dogs' spon-taneous internal bleeding.
Doctors in Boston have injected DNA coding for a piece of the gene called vascular endo-thelial growth <bb>>factorb>bb>>, which directs blood vessel growth, into the damaged, blood-starved heart muscle of human patients who have had several bypass operations but are still doing poorly.
Researchers at the University of Pennsylvania placed DNA coding for "insulinlike growth <bb>>factorb>bb>> 1," a growth hormone, into disabled viruses and then injected them directly into the muscle of one hind leg of young, middle-aged, and elderly mice.

http://www.chilit.org/BEAUMAN2.HTM (293 words)



<bb>>Factorb>bb>> VIII & IX

The final report on the Registry of <bb>>Factorb>bb>> VIII and IX Concentrates was presented by Dr. C.
Barrowcliffe reported on the SSC/5 "Field Type" Collaborative Study on Concentrates, one involving F VIII, the other involving F IX, and proposed a further exercise by October 1998.
Mikaelsson summarized three studies on the characterization of recombinant <bb>>factorb>bb>> VIII with and without <bb>>Bb>bb>>-domain, and high purity plasma-derived <bb>>factorb>bb>> VIII, demonstrating equivalence of activity measured by chromogenic assay and antigen content.

http://www.med.unc.edu/isth/SSC/98minutes/FactorVIII&IX.html (1001 words)



Bleeding Disorders

A deficiency in any of these factors can lead to bleeding problems, each with its own symptoms and treatments.
For example, some people with low levels of <bb>>factorb>bb>> VII do not have bleeding problems.
<bb>>Factorb>bb>> II deficiency is confirmed if test results show a prolonged prothrombin time, prolonged partial thromoplastin time, or the level of <bb>>factorb>bb>> II is lower than normal.

http://www.accredohealth.net/hhs/bleeding_disorders/other.html (1001 words)



<bb>>Factorb>bb>> VIII Deficiencies

Other bypass agents include <bb>>Factorb>bb>> VIIa and <bb>>Factorb>bb>> IXa, which bypass the necessity for FVIII mediated activation of FIX.
Please note that this is non-specific because things like a lupus anticoagulant or treatment with heparin can also cause prolongation of the aPTT in the absence of any <bb>>factorb>bb>> inhibitors.
<bb>>Factorb>bb>> VIII is the precursor to <bb>>Factorb>bb>> VIIIa, which catalyzes the activation of <bb>>Factorb>bb>> IX to IXa.

http://medinfo.ufl.edu/year2/coag/viiidef.html (1079 words)



CATHOLIC ENCYCLOPEDIA: Pope Leo XIII

Under Leo the religious orders developed wonderfully; new orders were founded, older ones increased, and in a short time made up for the losses occasioned by the unjust spoliation they had been subjected to.
To excite Catholic students to rival non-Catholics in the study of the Scriptures, and at the same time to guide their studies, he published the "Providentissimus Deus" (1893), which won the admiration even of Protestants, and in 1902 he appointed a Biblical Commission.
Along every line of religious and educational activity they have proved no small <bb>>factorb>bb>> in the awakening and strengthening of the Christian life of the whole country.

http://www.newadvent.org/cathen/09169a.htm (1079 words)



Inhibition of Hageman <bb>>factorb>bb>>, plasma thromboplastin antecedent, thrombin and other clotting factors by phenylglyoxal hydrate (38500) -- Radnoff and Saito 148 (1): 177 -- Experimental Biology and Medicine

Inhibition of Hageman <bb>>factorb>bb>>, plasma thromboplastin antecedent, thrombin and other clotting factors by phenylglyoxal hydrate (38500) -- Radnoff and Saito 148 (1): 177 -- Experimental Biology and Medicine
Inhibition of Hageman <bb>>factorb>bb>>, plasma thromboplastin antecedent, thrombin and other clotting factors by phenylglyoxal hydrate (38500)
Christmas <bb>>factorb>bb>> (<bb>>Factorb>bb>> IX), antihemophilic <bb>>factorb>bb>> (<bb>>Factorb>bb>> VIII), <bb>>Factorb>bb>>

http://www.ebmonline.org/cgi/content/abstract/148/1/177 (1079 words)



cclement5

Cn3D presentation of thrombin, factors VII, X and IX.
CATH classification of thrombin and other coagulation factors.
BLAST and FASTA alignment of amino acid sequences for <bb>>factorb>bb>> XI and <bb>>factorb>bb>> XII.

http://www.geocities.com/cclement_us/outline7.html (1079 words)



Clotting <bb>>Factorb>bb>> Deficiencies

<bb>>Factorb>bb>> IX replacement has traditionally been with prothrombin complex concentrates (PCCs) that contain factors II, VII, and X as well as IX, and were associated with thrombotic risk.
<bb>>Factorb>bb>> X deficiency is a rare (1 per 1 million) autosomal recessive deficiency characterized by asymptomatic heterozygotes and by homozygotes with bleeding symptoms that correlate with <bb>>factorb>bb>> activity.
<bb>>Factorb>bb>> VII deficiency is a rare (1 per 500,000) autosomal recessive deficiency that exhibits little correlation between the bleeding risk and the <bb>>factorb>bb>> activity.

http://www.clevelandclinicmeded.com/diseasemanagement/hematology/clotting/clotting.htm (2553 words)



Abstract number: OC847

Among patients with high levels of <bb>>factorb>bb>> II, IX or XI, the RR of recurrence was 0.6 (95% CI 0.2-2.1), 1.1 (95% CI 0.4-2.8) and 1.3 (95% CI 0.5-3.5) after adjustment for age, sex, duration of anticoagulation, presence of <bb>>factorb>bb>> II G20210A or <bb>>factorb>bb>> V Leiden, and <bb>>factorb>bb>> VIII levels.
The relative risk (RR) of recurrent VTE was 0.9 (95% CI 0.8-1.2), 1.0 (95% CI 0.9-1.2) and 1.1 (95% CI 0.9-1.2) for each increase of 10 IU/dL in the plasma levels of <bb>>factorb>bb>> II, IX or XI, respectively.
percentile of the study population, respectively, compared to 40 of 348 (12%), 40 of 348 (12%) and 47 of 398 (12%) patients with lower <bb>>factorb>bb>> II, IX or XI levels.

http://www.schattauer.de/abstracts/absOC847.html (2553 words)



abstract.asp?id=7949

Elevated levels of coagulation <bb>>factorb>bb>> VIII (F VIII:C), <bb>>factorb>bb>> IX (F IX:C) and <bb>>factorb>bb>> XI (F XI:C) are risk factors for venous thrombosis, but their role in arterial thrombosis is less clear.
We investigated whether elevated levels of coagulation <bb>>factorb>bb>> VIII, IX and XI are risk factors for myocardial infarction (MI) in young women.
We conclude that high vWF:ag levels, non-O blood group, high F VIII:C and F IX:C levels are associated with an increased risk of MI in women.

http://www.blackwellpublishers.co.uk/isth2003/abstract.asp?id=7949 (2553 words)



Coagulation <bb>>Factorb>bb>> IX

Coagulation <bb>>Factorb>bb>> IX is an important protein in the process of hemostasis and normal blood clotting.
Coagulation <bb>>Factorb>bb>> IX This webpage was created as an assignment for an undergraduate course at Davidson College.
One of the earliest mutated forms of Coagulation <bb>>Factorb>bb>> IX was found to be a single-base mutation (from G to A) at nucleotide 6 in the 5' UT region, later termed the Leyden-specific region.

http://www.bio.davidson.edu/Courses/Molbio/MolStudents/spring2003/WoodC/coag.html (1166 words)



NHF HANDI Hemophilia <bb>>Bb>bb>> Leyden Fact Sheet

Hemophilia <bb>>Bb>bb>> Leyden is a form of inherited <bb>>factorb>bb>> IX deficiency characterized by a gradual increase in <bb>>factorb>bb>> IX levels that begins at puberty.
The type of hemophilia <bb>>Bb>bb>> Leyden at presentation correlates with the specific mutation in the <bb>>factorb>bb>> IX gene.
Recovery from hemophilia <bb>>Bb>bb>> leyden: an androgen-responsive element in the <bb>>factorb>bb>> IX promoter.

http://www.hemophilia.org/resources/hemob.htm (925 words)



Neonatal or hepatocyte growth <bb>>factorb>bb>>-potentiated adult gene therapy with a retroviral vector results in therapeutic levels of canine <bb>>factorb>bb>> IX for hemophilia <bb>>Bb>bb>> -- Xu et al. 101 (10): 3924 -- Blood

Neonatal or hepatocyte growth <bb>>factorb>bb>>-potentiated adult gene therapy with a retroviral vector results in therapeutic levels of canine <bb>>factorb>bb>> IX for hemophilia <bb>>Bb>bb>>
Neonatal or hepatocyte growth <bb>>factorb>bb>>-potentiated adult gene therapy with a retroviral vector results in therapeutic levels of canine <bb>>factorb>bb>> IX for hemophilia <bb>>Bb>bb>> -- Xu et al.
Continuous intravenous infusion of deleted form of hepatocyte growth <bb>>factorb>bb>> attenuates hepatic ischemia-reperfusion injury in rats.

http://www.bloodjournal.org/cgi/content/full/101/10/3924 (7788 words)



What is Hemophilia?

<bb>>Factorb>bb>> IX deficiency hemophilia, because <bb>>Factorb>bb>> 9 (written <bb>>Factorb>bb>> IX) is the blood protein which is lacking and whose absence slows down the normal clotting process.
<bb>>Factorb>bb>> VIII deficiency hemophilia, because it is the lack of the <bb>>Factorb>bb>> 8 (written <bb>>Factorb>bb>> VIII) protein in the blood that causes the clotting problem.
As hemophilia is an hereditary disorder, people are affected at birth.

http://www.hemophilia.ca/en/2.1.1.php (468 words)



Hemophilia: Bleeding and Clotting Disorders: Merck Manual Home Edition

Recombinant forms of both <bb>>factorb>bb>> VIII and IX are available; the dose, frequency, and duration of therapy are determined by the site and severity of the bleeding problem.
Hemophilia <bb>>Bb>bb>> is a deficiency in clotting <bb>>factorb>bb>> IX.
As a result, <bb>>factorb>bb>> replacement therapy becomes less effective.

http://www.merck.com/mmhe/ag/print/sec14/ch173/ch173f.html (602 words)



Hemophilia <bb>>Bb>bb>> Description and Treatment

This is done by a process called "<bb>>factorb>bb>> replacement therapy." People with this type of hemophilia must inject replacement <bb>>factorb>bb>> IX directly into their blood, a process called "infusion."
About 15% of people with hemophilia have hemophilia <bb>>Bb>bb>>. People with hemophilia <bb>>Bb>bb>> need to increase the level of <bb>>factorb>bb>> IX in their blood.
Hemophilia <bb>>Bb>bb>> is a deficiency of <bb>>factorb>bb>> IX.

http://www.zlbbehring.ca/ab/n25240/PFDiseaseCatProd3.htm (108 words)



Hemophilia Village References

Use of recombinant <bb>>factorb>bb>> IX in subjects with haemophilia <bb>>Bb>bb>> undergoing surgery.
Human recombinant <bb>>factorb>bb>> IX: safety and efficacy studies in hemophilia <bb>>Bb>bb>> patients previously treated with plasma-derived <bb>>factorb>bb>> IX concentrates.
Orthopaedic surgery in persons with haemophilia A. Thromb Haemost.

http://www.hemophiliavillage.com/hcp_refrences.asp (108 words)



eMedicine - <bb>>Factorb>bb>> VII : Article Excerpt by: Jeyanthi Ramanarayanan, MD

<bb>>Factorb>bb>> VIIa bound to tissue <bb>>factorb>bb>> in the presence of calcium and phospholipids facilitates the conversion of <bb>>factorb>bb>> IX to factors IXa and X to <bb>>factorb>bb>> Xa.
Tissue <bb>>factorb>bb>> is an intrinsic membrane glycoprotein that is normally not exposed on the surface of intact blood vessels.
In 1951, Alexander and colleagues identified <bb>>factorb>bb>> VII as the key initiator of coagulation when they reported the first case of <bb>>factorb>bb>> VII deficiency in a child and called it serum prothrombin conversion accelerator deficiency.

http://www.emedicine.com/med/byname/factor-vii.htm (671 words)



Morrissey Lab

Activation of <bb>>factorb>bb>> VII during alimentary lipaemia occurs in healthy adults and patients with congenital <bb>>factorb>bb>> XII or <bb>>factorb>bb>> XI deficiency, but not in patients with <bb>>factorb>bb>> IX deficiency.
<bb>>Factorb>bb>> VIIa/tissue <bb>>factorb>bb>> generates a form of <bb>>factorb>bb>> V with unchanged specific activity, resistance to activation by thrombin and increased sensitivity to activated protein C. Biochemistry 38:1829-1837, 1999.
The influence exerted by a restricted phospholipid microenvironment on the expression of tissue <bb>>factorb>bb>> activity at the cell plasma membrane surface.

http://tf7.org/pubsthree.htm (1512 words)

Topic: <b>Factor</b> <b>IX<

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