How to Trip Rapid Review

Step 1: Select articles relevant to your search (remember the system is only optimised for single intervention studies)

Step 2: press

Step 3: review the result, and maybe amend the or if you know better! If we're unsure of the overall sentiment of the trial we will display the conclusion under the article title. We then require you to tell us what the correct sentiment is.

1,633 results for

Factor IX Deficiency

by
...
Latest & greatest
Alerts

Export results

Use check boxes to select individual results below

SmartSearch available

Trip's SmartSearch engine has discovered connected searches & results. Click to show

81. Reactions of Blood with Nonbiologic Surfaces: Ultrastructural and Clotting Studies with Normal and Coagulation Factor Deficient Bloods Full Text available with Trip Pro

test, were influenced by both the type of surface to which blood was exposed and the deficiencies of coagulation Factors I, VIII, IX, or XII. Deficiency of fibrinogen appears to enhance, minimally, activation of the coagulation sequences by test materials. However, deficiency of fibrinogen markedly reduces adhesion of platelets to foreign surfaces. Deficiency of Factor XII, but not of Factors VIII or IX, decreases platelet adhesion to nonbiologic surfaces but to a lesser extent than does deficiency (...) Reactions of Blood with Nonbiologic Surfaces: Ultrastructural and Clotting Studies with Normal and Coagulation Factor Deficient Bloods Interaction of normal and coagulation factor deficient bloods with glass, Teflon and silicone-coated glass surfaces have been studied. The morphology of the blood-surface interaction was observed by scanning electron microscopy. Activation of the intrinsic coagulation system and progression of these changes, monitored by use of the partial thromboplastin time

1972 The American journal of pathology

82. Diagnosis of haemophilia: use of an artificial factor-VIII-deficient human plasma system Full Text available with Trip Pro

Diagnosis of haemophilia: use of an artificial factor-VIII-deficient human plasma system An artificial clotting system deficient in factor VIII has been made from normal human plasma. Factors XII and XI are supplied as ;activation product'. An eluate from Al(OH)(3), which has been incubated with normal plasma, supplies factors X and IX in their ;plasma' (unactivated) form with II. Factor V is provided as the supernatant after the Al(OH)(3)- treated plasma has been precipitated at one-third (...) saturation with (NH(4))(2)SO(4). Fibrinogen is freed of factor VIII by freezing and thawing a lyophylized preparation and then added. Of these, activation product and the fibrinogen may be prepared in advance and stored frozen, and the eluate and supernatant may be made on the day of testing. A phospholipid source and CaCl(2)-solution are also required. In use, a patient's and a control plasma are first diluted in a mixture of the eluate, supernatant, and fibrinogen solution, and clotting times

1967 Journal of Clinical Pathology

83. Demonstrable Deficiency of Christmas Factor in Two Sisters Full Text available with Trip Pro

Demonstrable Deficiency of Christmas Factor in Two Sisters 13811697 1998 11 01 2018 12 02 0007-1447 1 5171 1960 Feb 13 British medical journal Br Med J Demonstrable deficiency of Christmas factor in two sisters. 479-82 COOK I A IA DOUGLAS A S AS eng Journal Article England Br Med J 0372673 0007-1447 9001-28-9 Factor IX OM Factor IX Female Hemophilia A genetics Humans Medicine Siblings HEMOPHILIA/genetics 1960 2 13 1960 2 13 0 1 1960 2 13 0 0 ppublish 13811697 PMC1967005 J Clin Pathol. 1958 May

1960 British medical journal

84. Attention Deficit Disorder

Attention Deficit Disorder Attention Deficit Disorder 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 Attention Deficit Disorder (...) Attention Deficit Disorder Aka: Attention Deficit Disorder , Attention Deficit Hyperactivity Disorder , ADHD , Attentional Disorders , Attention Deficit Disorder in Children From Related Chapters II. Epidemiology Diagnosed at one point in up to 11% of school children ages 4 to 17 years old (1-2 per classroom) At a given time 8.8% of school children have the diagnosis and 6.1% are on medication for Attention Deficit More commonly diagnosed in boys than girls (4 - 8:1) However girls are more often

2018 FP Notebook

85. Coagulation factors

that are currently known, eg hepatitis, HIV and potential diseases, eg new variant Creutzfeld-Jacob Disease (nvCJD). Available in: 250, 500, 1000, 1500, 2000 & 3000 iu vials For use in children with Haemophilia A (Classical haemophilia/factor VIII deficiency) Recombinant Factor IX: BeneFix B-Long* Inspiration* PUP B Long* * = in clinical trials Available in: 250, 500, 1000 & 2000 iu vials For use in children with Haemophilia B (Christmas Disease/factor IX deficiency) Recombinant technology reduces exposure (...) to human blood borne infections, both those that are currently known, eg hepatitis, HIV and potential diseases, eg nvCJD Recombinant Factor VIIa Novoseven Available in: 1.2 & 5 mg vials For use in children who have developed antibodies to Factor VIII or IX, or those with severe platelet disorders, and rarely by those with intractable bleeding. It acts by bypassing the factor VIII or IX activation in the clotting cascade. Can also be used in congenital factor VII deficiency but has a very short half

2015 Publication 1593

86. Membrane carbonic anhydrase IX expression and relapse risk in resected stage I-II non-small-cell lung cancer. Full Text available with Trip Pro

Membrane carbonic anhydrase IX expression and relapse risk in resected stage I-II non-small-cell lung cancer. Adjuvant chemotherapy reduces recurrences of non-small-cell lung cancer (NSCLC). To determine which patients need adjuvant chemotherapy, we assessed factors associated with time to relapse (TTR).In 230 resected stage I-II NSCLCs, we correlated immunohistochemistry scores for factors associated with cell growth rate, growth regulation, hypoxia, cell survival, and cell death with TTR.With (...) a median follow-up of 82 months (1-158) for those alive and relapse free at last follow-up, median time to recurrence was not reached. The 2- and 5-year probabilities of maintaining freedom from recurrence were 80.7% (95% confidence interval, 75.3%, 86.4%) and 74.6% (95% confidence interval, 68.6%, 81.2%), respectively. TTR curves flattened at an apparent cure rate of 70%. In multicovariate Cox models, factors correlating with shorter TTR were membranous carbonic anhydrase IX (mCAIX) staining (any

2014 Journal of Thoracic Oncology

87. Integration-deficient Lentiviral Vectors Expressing Codon-optimized R338L Human FIX Restore Normal Hemostasis in Hemophilia B Mice Full Text available with Trip Pro

. In this article, we describe for the first time a complete correction of factor IX (FIX) deficiency in hemophilia B mice by IDLVs carrying a novel, highly potent human FIX cDNA. A 50-fold increase in human FIX cDNA potency was achieved by combining two mechanistically independent yet synergistic strategies: (i) optimization of the human FIX cDNA codon usage to increase human FIX protein production per vector genome and (ii) generation of a highly catalytic mutant human FIX protein in which the arginine (...) Integration-deficient Lentiviral Vectors Expressing Codon-optimized R338L Human FIX Restore Normal Hemostasis in Hemophilia B Mice Integration-deficient lentiviral vectors (IDLVs) have been shown to transduce a wide spectrum of target cells and organs in vitro and in vivo and to maintain long-term transgene expression in nondividing cells. However, epigenetic silencing of episomal vector genomes reduces IDLV transgene expression levels and renders these safe vectors less efficient

2014 Molecular Therapy

88. Effects and Interferences of Emicizumab, a Humanised Bispecific Antibody Mimicking Activated Factor VIII Cofactor Function, on Coagulation Assays. Full Text available with Trip Pro

Effects and Interferences of Emicizumab, a Humanised Bispecific Antibody Mimicking Activated Factor VIII Cofactor Function, on Coagulation Assays. Emicizumab bridges activated factor IX (FIX) and FX to restore the tenase function mediated by activated FVIII (FVIIIa), which is deficient in people with haemophilia A (PwHA). Unlike FVIII, emicizumab does not require activation to function; thus, in coagulation assays, the behavior of emicizumab may differ from that of FVIII. The objective

2019 Thrombosis and haemostasis

89. How to Optimize Activated Partial Thromboplastin Time (APTT) Testing: Solutions to Establishing and Verifying Normal Reference Intervals and Assessing APTT Reagents for Sensitivity to Heparin, Lupus Anticoagulant, and Clotting Factors. (Abstract)

in this pathway, most typically factors VIII, IX, and XI. The APTT is also sensitive to contact factor deficiencies, including factor XII, prekallikrein, and high-molecular-weight kininogen. The APTT may also be elevated in a variety of conditions, including liver disease, vitamin K deficiency, and disseminated intravascular coagulation. The APTT can also be used for monitoring unfractionated heparin (UFH) therapy, as well as for screening lupus anticoagulant (LA) or for assessing thrombosis risk. Which (...) How to Optimize Activated Partial Thromboplastin Time (APTT) Testing: Solutions to Establishing and Verifying Normal Reference Intervals and Assessing APTT Reagents for Sensitivity to Heparin, Lupus Anticoagulant, and Clotting Factors. The activated partial thromboplastin time (APTT) assay is a very common coagulation test, used for several reasons. The test is conventionally used for assessing the contact factor (intrinsic) pathway of blood coagulation, and thus for screening deficiencies

2019 Seminars In Thrombosis And Hemostasis

90. Vitamin K Deficiency (Overview)

with the carboxylase is not fully understood. Vitamin K is required in the synthesis of 4 clotting factors in the liver: factors II,VII, IX, and X. It is also essential in the production of protein C and S, which are anticoagulant proteins. [ ] Bone matrix proteins, specifically osteocalcin, undergo gamma carboxylation with calcium much the way coagulation factors do; this process also requires VK. Previous Next: Etiology In infants, the low transmission of vitamin K (VK) across the placenta, liver prematurity (...) Parenchymal liver disease Cystic fibrosis Inflammatory bowel disease Drugs - Antibiotics (cephalosporin), cholestyramines, warfarin, salicylates, anticonvulsants, and certain sulfa drugs) are some of the common causes of VK deficiency Massive transfusion Disseminated intravascular coagulation (DIC) - Severe Chronic kidney disease/hemodialysis [ ] The synthesis of VK-dependent factors are decreased by parenchymal liver diseases, such as cirrhosis secondary to viral hepatitis, alcohol intake, and other

2014 eMedicine.com

91. Proximal Femoral Focal Deficiency (Diagnosis)

knee arthroscopy to identify changes in cruciate ligaments and their relation to the different types of PFFD in patients with Pappas type III, IV, VII, VIII, or IX deficiency, Chomiak et al found variable changes of the cruciate ligaments in all but one patient. Although these changes were not clinically relevant in most of the patients and were not related to the Pappas classification, the authors recommended imaging of cruciate ligaments before lengthening of the extremity in order to avoid knee (...) age, whereas others will be more inclined to attempt to preserve the natural limb no matter what. Treatment must be individualized on the basis of the following factors [ ] : Limb-length discrepancy Presence of associated malformations Adequacy of musculature Proximal joint stability Previous References Oppenheim WL, Setoguchi Y, Fowler E. Overview and comparison of Syme's amputation and knee fusion with the van Nes rotationplasty procedure in proximal femoral focal deficiency. Herring JA, Birch J

2014 eMedicine Surgery

92. Vitamin K Deficiency (Diagnosis)

functions as cofactor with the carboxylase is not fully understood. Vitamin K is required in the synthesis of 4 clotting factors in the liver: factors II,VII, IX, and X. It is also essential in the production of protein C and S, which are anticoagulant proteins. [ ] Bone matrix proteins, specifically osteocalcin, undergo gamma carboxylation with calcium much the way coagulation factors do; this process also requires VK. Previous Next: Etiology In infants, the low transmission of vitamin K (VK) across (...) Infectious diarrhea Cholestatic disease Parenchymal liver disease Cystic fibrosis Inflammatory bowel disease Drugs - Antibiotics (cephalosporin), cholestyramines, warfarin, salicylates, anticonvulsants, and certain sulfa drugs) are some of the common causes of VK deficiency Massive transfusion Disseminated intravascular coagulation (DIC) - Severe Chronic kidney disease/hemodialysis [ ] The synthesis of VK-dependent factors are decreased by parenchymal liver diseases, such as cirrhosis secondary to viral

2014 eMedicine.com

93. IgA and IgG Subclass Deficiencies (Treatment)

acute-onset neuropsychiatric syndrome. Pediatr Therapeut . 2012. 2:2. Murphy TK, Storch EA, Lewin AB et al. (2012). Clinical factors associated with pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections. J Pediatr . 2012. 160:314-9. Schaffer FM. Clinical assessment and management of abnormal IgA levels. Ann Allergy Asthma Immunol . 2008 Mar. 100(3):280-2. . Browning MJ. Specific polysaccharide antibody deficiency in chromosome 18p deletion syndrome (...) deficiency in children: to treat or not to treat? Case presentation and review of the literature. Pediatr Allergy Immunol . 2006 Nov. 17(7):544-50. . Garcia-Lloret M, McGhee S, Chatila TA. Immunoglobulin replacement therapy in children. Immunol Allergy Clin North Am . 2008 Nov. 28(4):833-49, ix. . . Karaca NE, Gulez N, Aksu G, Azarsiz E, Kutukculer N. Does OM-85 BV prophylaxis trigger autoimmunity in IgA deficient children?. Int Immunopharmacol . 2011 Nov. 11(11):1747-51. . Borte S, Pan-Hammarstrom Q

2014 eMedicine Pediatrics

94. IgA and IgG Subclass Deficiencies (Follow-up)

vaccine in children with recurrent infections who are unresponsive to the polysaccharide vaccine. Pediatr Infect Dis J . 1998 Aug. 17(8):685-91. . Meyts I, Bossuyt X, Proesmans M, De B. Isolated IgG3 deficiency in children: to treat or not to treat? Case presentation and review of the literature. Pediatr Allergy Immunol . 2006 Nov. 17(7):544-50. . Garcia-Lloret M, McGhee S, Chatila TA. Immunoglobulin replacement therapy in children. Immunol Allergy Clin North Am . 2008 Nov. 28(4):833-49, ix (...) IgA and IgG Subclass Deficiencies (Follow-up) IgA and IgG Subclass Deficiencies Follow-up: Further Outpatient Care, Complications, Prognosis 50% of cases) involves deficient antibody production." /> 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

2014 eMedicine Pediatrics

95. IgA and IgG Subclass Deficiencies (Overview)

immunoglobulin (Ig), or both to lacunar deficits that involve specific antibody responses to polysaccharides. The spectrum of antibody deficiency is broad, ranging from decreased total IgG levels to normal IgG levels and from primary B-cell defects to combined immunodeficiencies with antibody abnormalities associated with other immune and often nonimmune abnormalities. Although this article discusses and hypogammaglobulinemia, the emphasis is on selective Ig deficiencies, including the decreased production (...) vaccine in children with recurrent infections who are unresponsive to the polysaccharide vaccine. Pediatr Infect Dis J . 1998 Aug. 17(8):685-91. . Meyts I, Bossuyt X, Proesmans M, De B. Isolated IgG3 deficiency in children: to treat or not to treat? Case presentation and review of the literature. Pediatr Allergy Immunol . 2006 Nov. 17(7):544-50. . Garcia-Lloret M, McGhee S, Chatila TA. Immunoglobulin replacement therapy in children. Immunol Allergy Clin North Am . 2008 Nov. 28(4):833-49, ix

2014 eMedicine Pediatrics

96. Purine Nucleoside Phosphorylase Deficiency (Follow-up)

Purine Nucleoside Phosphorylase Deficiency (Follow-up) Purine Nucleoside Phosphorylase Deficiency Follow-up: Further Outpatient Care, Further Inpatient Care, Prognosis 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 (...) =aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvODg3ODIzLWZvbGxvd3Vw processing > Purine Nucleoside Phosphorylase Deficiency Follow-up Updated: Dec 11, 2018 Author: Alan P Knutsen, MD; Chief Editor: Harumi Jyonouchi, MD Share Email Print Feedback Close Sections Sections Purine Nucleoside Phosphorylase Deficiency Follow-up Further Outpatient Care See the list below: Intravenous immunoglobulin (IVIG) therapy is typically continued for 6-12 months after bone marrow transplantation. Reimmunization of the patient begins approximately 1 year after transplantation

2014 eMedicine Pediatrics

97. Purine Nucleoside Phosphorylase Deficiency (Overview)

Purine Nucleoside Phosphorylase Deficiency (Overview) Purine Nucleoside Phosphorylase Deficiency: 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 (...) =aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvODg3ODIzLW92ZXJ2aWV3 processing > Purine Nucleoside Phosphorylase Deficiency Updated: Dec 11, 2018 Author: Alan P Knutsen, MD; Chief Editor: Harumi Jyonouchi, MD Share Email Print Feedback Close Sections Sections Purine Nucleoside Phosphorylase Deficiency Overview Practice Essentials Purine nueoside phosphorylase (PNP) deficiency causes a form of severe combined immunodeficiency (SCID) characterized by profound T cell deficiency, failure to thrive (FTT), recurrent deep seeded infection, developmental delay

2014 eMedicine Pediatrics

98. Purine Nucleoside Phosphorylase Deficiency (Diagnosis)

Purine Nucleoside Phosphorylase Deficiency (Diagnosis) Purine Nucleoside Phosphorylase Deficiency: 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 (...) =aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvODg3ODIzLW92ZXJ2aWV3 processing > Purine Nucleoside Phosphorylase Deficiency Updated: Dec 11, 2018 Author: Alan P Knutsen, MD; Chief Editor: Harumi Jyonouchi, MD Share Email Print Feedback Close Sections Sections Purine Nucleoside Phosphorylase Deficiency Overview Practice Essentials Purine nueoside phosphorylase (PNP) deficiency causes a form of severe combined immunodeficiency (SCID) characterized by profound T cell deficiency, failure to thrive (FTT), recurrent deep seeded infection, developmental delay

2014 eMedicine Pediatrics

99. Glucuronyl Transferase Deficiency (Overview)

Glucuronyl Transferase Deficiency (Overview) Unconjugated Hyperbilirubinemia: 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=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvMTc4ODQxLW92ZXJ2aWV3 processing (...) % is derived from the hepatic turnover of heme proteins, such as myoglobin, cytochromes, and catalase. A small portion of daily bilirubin is derived from the destruction of young or developing erythroid cells. Bilirubin is poorly soluble in water at physiologic pH because of internal hydrogen bonding that engages all polar groups and gives the molecule an involuted structure. The fully hydrogen-bonded structure of bilirubin is designated bilirubin IX-alpha-ZZ. The intramolecular hydrogen bonding shields

2014 eMedicine Pediatrics

100. Antithrombin III Deficiency (Treatment)

of vitamin K–dependent procoagulant factors (II, VII, IX, X) is reduced adequately for anticoagulation. The duration of warfarin therapy in children with acquired or heterozygous congenital antithrombin III deficiency experiencing their first clot is controversial, but therapy is generally continued for at least 3-6 months before cessation of anticoagulation. If the underlying triggering event cannot be removed, indefinite anticoagulation should be considered. Antithrombin III–deficient patients (...) . Previous References Gaman AM, Gaman GD. Deficiency Of Antithrombin III (AT III) - Case Report and Review of the Literature. Curr Health Sci J . 2014 Apr-Jun. 40 (2):141-3. . . Yilmaz S, Gunaydin S. Inherited risk factors in low-risk venous thromboembolism in patients under 45 years. Interact Cardiovasc Thorac Surg . 2015 Jan. 20 (1):21-3. . Beauchamp NJ, Pike RN, Daly M, et al. Antithrombins Wibble and Wobble (T85M/K): archetypal conformational diseases with in vivo latent-transition, thrombosis

2014 eMedicine Pediatrics

To help you find the content you need quickly, you can filter your results via the categories on the right-hand side >>>>