scholarly journals Puerarin Attenuates Ovalbumin-Induced Lung Inflammation and Hemostatic Unbalance in Rat Asthma Model

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Feng Dong ◽  
Chengbin Wang ◽  
Jinyan Duan ◽  
Weiyi Zhang ◽  
Daijun Xiang ◽  
...  
Keyword(s):  
Lung Tissue ◽  
Factor Ix ◽  
Allergic Airway Disease ◽  
Factor Vii ◽  
Tissue Homogenate ◽  
Coagulation Disorder ◽  
Factor Xii ◽  
Thrombin Time ◽  
Factor X ◽  
Cell Counts

Aim.We aimed to investigate and evaluate the preventive activity of puerarin on the ovalbumin-induced asthma rat model.Materials and Methods.Male Wistar rats were sensitized intraperitoneally on days 0, 7, and 14 and challenged to ovalbumin intratracheally on day 21. Groups of sensitized rats were treated randomly either with placebo, puerarin, dexamethasone, or puerarin combined with dexamethasone, from days 15 to 20. Inflammatory markers, including cell counts in bronchoalveolar lavage fluid (BALF), inflammatory cytokines, histopathology, and coagulation parameters, such as coagulation tests and the activity of coagulation factors, were analyzed.Results.Puerarin significantly inhibited the recruitment of inflammatory cells in BALF and lung tissue. At the same time, the release of IL-4, IL-10, and IFN-γin serum and the expression of mRNAs in lung tissue homogenate were changed by puerarin. Administration of puerarin also effectively rectified the coagulation disorder in asthmatic rats, such as prothrombin time (PT) (P<0.01), thrombin time (TT) (P<0.05), fibrinogen (FIB) (P<0.01),the activity of factor II (FII) (P<0.01), the activity of factor V (FV) (P<0.05), the activity of factor VII (FVII) (P<0.05), the activity of factor X (FX) (P<0.05), the activity of factor VIII (FVIII) (P<0.01), the activity of factor IX (FIX) (P<0.05), and the activity of factor XII (FXII) (P<0.05).Conclusions.Our results provide a clue that puerarin was useful for the preventive of allergic airway disease in rodents.

Very Low Activated Factor VII and Reduced Factor VII Antigen in Familial Abetalipoproteinaemia

1998 ◽  
Vol 80 (08) ◽  
pp. 233-238 ◽  
Author(s):  
K. A. Mitropoulos ◽  
M. N. Nanjee ◽  
D. J. Howarth ◽  
J. C. Martin ◽  
M. P. Esnouf ◽  
...  
Keyword(s):  
Plasma Concentrations ◽  
Positive Association ◽  
Factor Ix ◽  
Factor Vii ◽  
Unesterified Fatty Acid ◽  
Factor Xii ◽  
Factor X ◽  
Factor Xi ◽  
Activated Factor Vii ◽  
Normal Mean

SummaryAbetalipoproteinaemia is a rare disorder of apolipoprotein B metabolism associated with extremely low plasma concentrations of triglyce-ride. To discover whether the general positive association between factor VII and triglyceride levels extends to this condition, 5 patients were compared with 18 controls. All patients had a triglyceride below 100 μmol/l. Plasma unesterified fatty acid concentration was normal. Although factor IX activity was only slightly reduced (mean 88% standard) and factor IX antigen was normal, mean activated factor VII in patients was strikingly reduced to 34% of that in controls, a level similar to that found in haemophilia B. The patients’ mean factor VII activity and factor VII antigen were also significantly reduced to 54% and 63% of those in controls, respectively. Mean factor XI activity and tissue factor pathway inhibitor activity were reduced in patients to 70% and 75% of control values respectively, while factor XII, factor XI antigen, factor X, prothrombin and protein C were normal.

Neonatal Polycythemia: A Disorder Associated With Hyperviscosity, Normal Coagulation Findings And Thrombocytopenia

1981 ◽  
Author(s):  
J Katz ◽  
E Rodriguez ◽  
C Madani ◽  
D Hicks ◽  
H E Branson
Keyword(s):  
Plasma Exchange ◽  
Gestational Age ◽  
Degradation Products ◽  
Factor Ix ◽  
Factor Vii ◽  
Large For Gestational Age ◽  
Factor Xii ◽  
Factor X ◽  
Platelet Counts ◽  
Before And After

Thirty-two newborns with elevated capillary hematocrits >65% were studied. Twenty-two newborns required plasmaexchange transfusion. All had central (venous) hematocrits >65% and had symptoms referrable to complications associated with this syndrome. Of the 22, 15 were appropriate-for-gestational age, 5 were small-for-gestational age, and 2 were large-for-gestational age. Viscosity measurements in the 10 newborns who did not require plasma-exchanges showed increased viscosity in 2 in the slow shear rates associated with bloodflow in the smaller vessels. Coagulation data before and after plasma exchange did not show a hypercoagulable state: PT-14.2±0.7 and 12.9±1.2 secs, PTT 49.9±3.6 and 42.2±3.2 secs, factor VII 73±5 and 78±5%, factor VIII 103±10 and 94±10%, AT III levels were low 14±1.2 and 17±1.3 mg/dl, fibrin degradation products were <10μg/ml, fibrin monomer was not detected, plasminogen levels were 5±0.8 and 7±0.9mg/dl, fibrinogen levels were 203±9.8 and 200±11.8 mg%. Vitamin K dependent factors were reduced factor V 44±6 and 49±11%, factor VII 77±5 and 86±5%, factor IX 28±2 and 42±3%, factor X 35±4 and 62±6%, factor XI 55±5 and 84±9%, factor XII 47±5 and 63±5%. Statistical significant differences were found only with factors IX, X, XI and XII. Thrombocytopenia was present in 6 patients (20% incidence) and post plasma exchange the platelet counts rose significantly and in 2 patients within 3 days reached normal levels. No statistical difference in the platelet counts were noted before and after the plasma-exchange and were similar to the levels determined in 10 newborn controls. Neonatal polycythemia with thrombocytopenia may indicate a more severe disorder, with hematocrits in the 6 patients >70%. It is suggested that the mechanism of the thrombocytopenia may be aggregates of platelets that deaggregate following plasmaexchange. The complications associated with neonatal polycythemia appear related to hyperviscosity, erythrocyte and platelet “sludging” in the smaller vessels.

Regular Prophylactic Treatment with Factor IX P® in a Patient with Severe Factor X Deficiency.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 4050-4050
Author(s):  
Andrea Gerhardt ◽  
Fatima Araba ◽  
Rainer B. Zotz ◽  
Rudiger E. Scharf
Keyword(s):  
Joint Pain ◽  
Prophylactic Treatment ◽  
Factor Ix ◽  
Factor Vii ◽  
Coagulation Disorder ◽  
Factor X ◽  
Dental Surgery ◽  
Thrombotic Risk ◽  
Factor X Deficiency ◽  
Patient Reported

Abstract Background: Congenital factor X deficiency, a rare coagulation disorder with variable severity, is an inherited autosomal recessive disorder. The incidence of homozygous factor X deficiency is ~ 1 in 1 million of the general population. The gene encoding for factor X is found adjacent to that encoding for factor VII on chromosome 13q34. Bleeding sites vary according to the severity of the deficiency. Mucocutaneous soft tissue hemorrhages, including menorrhagia in women, are common. Hemarthros, exsanguinating postoperative hemorrhage, pseudotumors, and hemorrhages of the central nervous system have been reported in severely affected patients. Mildly affected patients experience easy bruising and excessive bleeding after trauma or surgery. Treatment options consist of fresh frozen plasma (FFP), prothrombin complex concentrates (PCC) containing factor X or pasteurized Factor IX P® (ZLB Behring). Disadvantage of FFP is the large infusion volume, potential viral transmission, and no standardized factor X content. These aspects, in addition to the thrombotic risk, also need to be addressed for the PCCs. Factor IX P®, which is virus inactivated, contains almost equal amounts of factor IX (1200 IU) and X (800 IU) and suits therefore well for the treatment of factor X deficiency. Case report: We report on our experience of prophylactic treatment with Factor IX P® in a 31-year-old male with severe factor X deficiency (&lt; 1%) associated with a homozygous Cys350Phe mutation in exon 8 on chromosome 13. After birth the patient experienced severe mucosal bleedings and haematomas and later on various joint bleedings with consecutive hemophilic arthropathy. Initially he received FFP on demand and later regular prophylaxis with PCC (containing 600 IU factor X) 2 to 3 times a week (~ 20–25 IU/kg/bw), age at onset of prophylaxis ~ 7 years. The patient is positive for HIV, HCV, and HBV (known since 1984). He is now on regular prophylaxis with Factor IX P® since 7 months. The prophylaxis is given 2 times a week in doses of ~ 20 IU/kg bw. The trough level after 72 hours was 12% using PCC and 20% using Factor IX P®. The patient reported on joint pain when factor X activities were below 20%. The rate of joint pain episodes is lower when using Factor IX P® two times a week as compared to PCC two to three times a week. Orthopedic and dental surgery were performed using Factor IX P® concentrate with excellent hemostatic effect, no thromboembolic complications, and no adverse drug reactions. In conclusion, prophylactic treatment with Factor IX P® in severe factor X deficient patients appears to be an effective and safe therapeutic option.

Generation Of Coagulation Factors By The Isolated Rat Liver Perfused With A Synthetic Blood Substitute

1981 ◽  
Author(s):  
C A Owen ◽  
E J W Bowie
Keyword(s):  
Factor Viii ◽  
Rat Liver ◽  
Blood Substitute ◽  
Factor Ix ◽  
Factor Vii ◽  
Clotting Factor ◽  
Isolated Perfused Rat Liver ◽  
Factor Xii ◽  
Factor V ◽  
Factor X

Measuring the release of small amounts of a clotting factor from an isolated perfused rat liver is difficult if the perfusate already contains some of the factor. Further, platelet-containing perfusates generate a coagulant activity that may invalidate clotting assays.We have successfully employed a completely synthetic blood substitute for rat liver perfusions. The perfusate is “Fluosol-43” generously furnished by Alpha Therapeutic Corporation. The oxygen-carrying perfluorochemical is FC-43 (perfluorotributylamine) and the substitute for albumin is hydroxyethyl starch. Using the Brauer perfusion technique, we found that rat livers in 5 hours released an average of 2.3% of the normal plasma concentration of prothrombin, 8.4% factor V, 16.2% factor VII, 7.0% factor IX, 3.7% factor X, 28.3% factor XI and 12.3% factor XII. Antithrombin III and plasminogen were also generated.Only minute amounts of factor VIII were released unless serum, cryoprecipitate or cryoprecipitate-free plasma was added; then the yield was 8.8% on average. The more “venom factor” (platelet aggregability with Bothrops alternata venom) added to the synthetic perfusate, the more factor VIII was released.

scholarly journals Activation of human factor VII in the initiation of tissue factor- dependent coagulation

Blood ◽  
1986 ◽  
Vol 68 (3) ◽  
pp. 685-691 ◽  
Author(s):  
LV Rao ◽  
SI Rapaport ◽  
SP Bajaj
Keyword(s):  
Tissue Factor ◽  
Factor Ix ◽  
Factor Vii ◽  
Activate Factor ◽  
Factor Xii ◽  
Factor X ◽  
Clotting Time ◽  
Activated Factor Vii ◽  
Peptide Release ◽  
Minimal Generation

Abstract We have used activation peptide release assays to compare factor VII and activated factor VII (VIIa) activation of factor X, normal factor IX (IXN), and a variant factor IX (IXBmLE), which, after activation, is unable to back-activate factor VII. In purified systems, factor VII and VIIa each rapidly activated factor X, but after a one minute lag for factor VII. VIIa also readily activated both IXN and IXBmLE. Factor VII initially failed to activate substantial amounts of either IXN or IXBmLE; on further incubation factor VII activated IXN but not IXBmLE. Activation of IXN began when approximately 10% of factor VII had been converted to VIIa, as measured by 125I-factor VII radioactivity profiles. Adding factor VII to VIIa slowed its activation of IXBmLE. However, in the presence of factor X, factor VII alone rapidly activated IXBmLE. Unlike purified systems, 1 nmol/L VIIa added to factor VII-deficient plasma failed to activate factor IX. Increasing factor VII to 10 nmol/L (plasma concentration) either as native VII or VIIa yielded similar activation curves for factor IX and similar activation curves for factor X. Adding 5% VIIa to factor X-deficient plasma and to factor XII-deficient plasma substantially shortened the dilute tissue factor clotting time of only the former. These data support the hypothesis that factor VII/tissue factor complex initiates tissue factor-dependent clotting through a minimal generation of Xa. This Xa then rapidly back-activates a small amount of factor VII, following which the rates of activation of both factors IX and X increase dramatically.

scholarly journals Activation of human factor VII in the initiation of tissue factor- dependent coagulation

Blood ◽  
1986 ◽  
Vol 68 (3) ◽  
pp. 685-691 ◽  
Author(s):  
LV Rao ◽  
SI Rapaport ◽  
SP Bajaj
Keyword(s):  
Tissue Factor ◽  
Factor Ix ◽  
Factor Vii ◽  
Activate Factor ◽  
Factor Xii ◽  
Factor X ◽  
Clotting Time ◽  
Activated Factor Vii ◽  
Peptide Release ◽  
Minimal Generation

We have used activation peptide release assays to compare factor VII and activated factor VII (VIIa) activation of factor X, normal factor IX (IXN), and a variant factor IX (IXBmLE), which, after activation, is unable to back-activate factor VII. In purified systems, factor VII and VIIa each rapidly activated factor X, but after a one minute lag for factor VII. VIIa also readily activated both IXN and IXBmLE. Factor VII initially failed to activate substantial amounts of either IXN or IXBmLE; on further incubation factor VII activated IXN but not IXBmLE. Activation of IXN began when approximately 10% of factor VII had been converted to VIIa, as measured by 125I-factor VII radioactivity profiles. Adding factor VII to VIIa slowed its activation of IXBmLE. However, in the presence of factor X, factor VII alone rapidly activated IXBmLE. Unlike purified systems, 1 nmol/L VIIa added to factor VII-deficient plasma failed to activate factor IX. Increasing factor VII to 10 nmol/L (plasma concentration) either as native VII or VIIa yielded similar activation curves for factor IX and similar activation curves for factor X. Adding 5% VIIa to factor X-deficient plasma and to factor XII-deficient plasma substantially shortened the dilute tissue factor clotting time of only the former. These data support the hypothesis that factor VII/tissue factor complex initiates tissue factor-dependent clotting through a minimal generation of Xa. This Xa then rapidly back-activates a small amount of factor VII, following which the rates of activation of both factors IX and X increase dramatically.

scholarly journals Mathematical Models for the Prediction of Coagulation Activity in Patients with Paroxysmal Atrial Fibrillation

2020 ◽  
Vol 3 (2) ◽  
pp. 1-6
Keyword(s):  
Atrial Fibrillation ◽  
Linear Regression ◽  
Paroxysmal Atrial Fibrillation ◽  
Linear Regression Analysis ◽  
Factor Ix ◽  
Factor Vii ◽  
Factor Xii ◽  
Factor X ◽  
Coagulation Activity ◽  
Coagulation Parameters

Our previous studies showed activation of coagulation in the early hours of the clinical manifestation of paroxysmal atrial fibrillation (PAF). Plasma coagulation activity of factor II, factor V, factor VII, factor VIII, factor IX, factor X, factor XI, factor XII, vWF, tissue factor levels, FVIII, vWF, prothrombin fragment 1+2(F1 + 2) and fibrinopeptide A (FPA) were significantly increased as early as the first twenty-four hours of the disease. The results suggest that there is a correlation between the studied parameters and development of the disease. Aim: To search for a statistical model that predicts coagulation activity in PAF patients. Materials and methods: Coagulation parameters were examined in 51 PAF patients (26 males, 25 females; mean age 59.84 ±1.60 years, onset of PAF episode < 24h prior to hospitalization). Controls included 52 individuals (26 males, 26 females; mean age 59.50 ± 1.46 years) with no prior anamnestic or ECG AF data, corresponding to patients in sex, age, BMI and comorbidities. A linear regression model was used to predict coagulation activity in PAF. Regression models showed good correlation between the duration of arrhythmia and six of the fourteen coagulation parameters studied: F1+2 (r = 0.83, p <0.001), FPA (r = 0.84, p <0.001), FVIII levels (r = 0.85, p <0.001) as well as activity of FII (r = 0.83, p <0.001), FVIII (r = 0.83, p <0.001) and FXII (r = 0.78, p <0.001). Changes in F1+2 plasma levels were most sensitive to PAF duration, where the contribution of duration to the values of the indicator is the greatest (b = 15.31). Conclusion: Linear regression analysis allowed us to create models with a high correlation coefficient for predicting the values of F1+2, FPA, FVIII levels, as well as activity of FII, FVIII and FXII in PAF patients. These models could allow for quantification of the procoagulatory process and thrombotic potential of the disease.

Gel Filtration Properties of Factors II, VII, IX, IXa, and X

1972 ◽  
Vol 28 (02) ◽  
pp. 317-324 ◽  
Author(s):  
Bjarne Østerud ◽  
Sandra Schiffman
Keyword(s):  
Gel Filtration ◽  
Apparent Size ◽  
Factor Ix ◽  
Tris Buffer ◽  
Factor Vii ◽  
Factor Xii ◽  
Factor X ◽  
Clotting Factors ◽  
Filtration Properties ◽  
Plasma Factors

SummaryThe following gel filtration properties of the vitamin ढ dependent clotting factors have been established :1. The elution patterns of factors II, VII, IX, and X in 0.5 M NaCl are the same in factor XII deficient native plasma, anticoagulated plasma, and BaSO4 eluates.2. In 0.01 M Tris buffer pH 7.3 or 0.5 M NaCl, plasma factors II, IX, and X elute together; factor VII élûtes later as a smaller molecule. All 4 plasma activities elute as larger molecules in 0.01 M Tris buffer and smaller ones in 0.5 M NaCl.3. In 0.01 M Tris - 0.005 M EDTA peak factor II activity elutes first, followed by factor IX, factor X, and then factor VII.4. Activation decreases the apparent size of factor IX.

The Activation of Human Factor X in Sodium Citrate: the Role of Factor VII

1976 ◽  
Vol 36 (01) ◽  
pp. 104-114 ◽  
Author(s):  
D. L Aronson ◽  
A. J Mustafa
Keyword(s):  
Sodium Citrate ◽  
Human Factor ◽  
Deae Cellulose ◽  
Factor Ix ◽  
Factor Vii ◽  
Factor X

SummaryHuman factor X was purified by several different procedures yielding products which had varying amounts of factor VII and factor IX. Treatment with CHC13 during the fractionation of the factor X removed 95% of the factor VII and factor IX activity and the resulting factor X activated more slowly when incubated in 25% sodium citrate. Removal of residual factor VII by DEAE cellulose chromatography yielded a factor X which activated still more slowly and less completely. When the factor VII, removed by chromatography, was added to the chromatographed factor X, the ability to be activated in 25% sodium citrate was restored. Confirmatory evidence for the role of factor VII in this reaction was the inhibition of the conversion of the factor X by both DFP and SBTI.

HAEMOSTATIC CHANGES INDUCED BY TWO LOW DOSE TRIPHASIC ORAL CONTRACEPTIVES

1987 ◽  
Author(s):  
S J Machin ◽  
I J Mackie ◽  
K Walshe ◽  
M D Gillmer
Keyword(s):  
Oral Contraceptives ◽  
Protein C ◽  
Low Dose ◽  
Factor Vii ◽  
Cycle Period ◽  
Factor Xii ◽  
Factor X ◽  
Combined Oral Contraceptives ◽  
First Time ◽  
Protein C Activity

The haemostatic system was investigated in 26 women taking cyclically administered triphasic combined oral contraceptives for the first time during their first six cycles. Fourteen women received Logynon (mean dose 32.4μg ethinyloestradiol, 92pg progestagen) and 12 received SHD 415G (Schering) which contains a mean dosage of 32.4μg ethinyloestradiol and 78pg gestodene, a recently developed progesterone. The Logynon group showed a significant increase (p<0.005) in fibrinogen (pre-mean 284.4 g/1; after 1 cycle 347.3 g/1, after 6 cycles 318.6 g/1) , factor VII (65.8 u/1 to 73.9 u/1 to 83.2 u/1), factor XII (1.74 u/1 to 2.41 u/1, to 2.25 u/1), plasminogen (100.9 u/1 to 135.1 u/1 to 126.3 u/1); decrease in ATIII (115.9 u/1 to 103.1 u/1 to 93.4 u/1) but no significant change in factor X (98.4 u/1 to 108.9 u/1 to 102.4) or protein C (0.85 u/1 to 0.88 u/1 to 0.94 u/1) activity. The SHD 415G group showed similar changes with an increase in fibrinogen (247.9 g/1 to 330.8 g/1 to 373 .1 g/1), factor VII (63.1 u/1 to 73.1 u/1 to 90.3 u/1, factor X (98.3 u/1 to 112.0 u/1 to 124.4 u/1), factor XII (1.46 u/1, to 1.93 u/1, to 2.03 u/1), plasminogen (110.8 u/1 to 125.4 u/1 to 136.7 u/1); decrease in ATIII (113.1 u/1 to 96.3 u/1 to 89.7 u/1), but no change in protein C (0.84 u/1 to - 0.78 u/1 to 0.85 u/1) activity. These changes were apparent after the first cycle of therapy and the differences were maintained over the six cycle period. There was no increase in protein C activity despite changes in the other vitamin K dependent proteins factors VII and X. Both low oestrogen dose triphasic pills caused similar prothrombotic changes which were not modified by the new progesterone, gestodene.

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