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Plasma Fibrinogen (plasma + fibrinogen)

Distribution by Scientific Domains

Medical Sciences	88%
Polymers and Materials Science	12%

Terms modified by Plasma Fibrinogen

plasma fibrinogen concentration

plasma fibrinogen level

Selected Abstracts

Biocompatibility of Heparin-Coated Cardiopulmonary Bypass Circuits in Coronary Patients With Left Ventricular Dysfunction Is Superior to PMEA-Coated Circuits

JOURNAL OF CARDIAC SURGERY, Issue 6 2006
Veysel Kutay M.D.
The aim of this study was to evaluate the clinical effectiveness and biocompatibility of heparin-coated and poly-2-methoxyethylacrylate (PMEA)-coated CPB circuits on coronary patients with left ventricular systolic dysfunction. Methods: Thirty-six patients who underwent elective coronary artery bypass grafting were divided into two equal groups: group H (n = 18), heparin-coated; group P (n = 18), PMEA coated. Clinical outcomes, hematologic variables, cardiac enzymes, malondialdehyde (MDA), and acute phase inflammatory response (including myeloperoxidase (MPO), catalase, hsCRP, and IL-8) were analyzed perioperatively. Results: Demographic, CPB, and clinical outcome data were similar for both groups. Plasma fibrinogen, total protein, albumin, and platelet count decreased, neutrophil count, MDA, IL-8, MPO, and catalase levels increased during CPB. During CPB, MPO and catalase values were significantly higher in group P (p = 0.02 and p = 0.01) and postoperative MDA concentration was lower in group H (p = 0.03). Platelet counts were better preserved in group H during and after CPB but neutrophil count and IL-8 level did not differ between the groups. Postoperative total protein, albumin, and fibrinogen levels were higher in group H (p < 0.05). The postoperative first day levels of troponin-I, CK-MB, and CRP increased in both groups without any significant differences between the groups. Conclusions: Heparin-coated circuit provided better suppression of perioperative inflammatory markers and exhibited more favorable effects on hematologic variables than PMEA-coated circuit. [source]

LDL-apheresis up-regulates VEGF and IGF-I in patients with ischemic limb

JOURNAL OF CLINICAL APHERESIS, Issue 3 2003
Shuzo Kobayashi
Abstract Although it is known that LDL-apheresis improves ischemic limb seen in patients with peripheral arterial occlusive disease (PAOD), the underlying mechanism(s) still remains unknown. We studied whether vascular endothelial growth factor (VEGF) and/or insulin-like growth factor-I (IGF-I) levels correlated with improvement of ischemic limbs after LDL-apheresis. Sixteen patients with PAOD (13 men, 3 women) were enrolled in our study. LDL-apheresis was performed 10 times (treated plasma 3,000 ml) for 5 weeks. Serum level of VEGF significantly increased from 262 ± 171 pg/ml to 306 ± 165 pg/ml before and after LDL-apheresis (P < 0.05). This value further increased up to 441 ± 175 pg/ml 3 months after the end of this therapy (P < 0.01, compared with the basal value and P < 0.05, compared with the value at the end of 10-times session). Increased levels of VEGF paralleled increases in the ankle-brachial pressure index (ABI). After 10-times therapy, IGF-I significantly decreased (P < 0.05), but increased over the basal value 3 months after this therapy. Plasma fibrinogen statistically decreased and remained low for 3 months. The favorable effects of LDL-apheresis may be ascribed to up-regulation of VEGF and IGF-I associated with decreased fibrinogen levels. J. Clin. Apheresis, 18:115,119, 2003. © 2003 Wiley-Liss, Inc. [source]

Elevated plasma fibrinogen ,, concentration is associated with myocardial infarction: effects of variation in fibrinogen genes and environmental factors

JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 4 2007
M. N. MANNILA
Summary., Background:, Fibrinogen ,,, a fibrinogen ,-chain variant generated via alternative mRNA processing, has been associated with susceptibility to thrombotic disease. Objective:, The present case,control study searched for potential determinants of the plasma fibrinogen ,, concentration and examined the relationship between this variant and risk of myocardial infarction (MI). Patients and methods:, The Stockholm Coronary Artery Risk Factor study, comprising 387 postinfarction patients and 387 healthy individuals, was employed. The fibrinogen gamma (FGG) 9340T > C [rs1049636], fibrinogen alpha (FGA) 2224G > A [rs2070011] and fibrinogen beta (FGB) 1038G > A [rs1800791] polymorphisms were determined. The plasma fibrinogen ,, concentration was measured by enzyme-linked immunosorbent assay. The multifactor dimensionality reduction method was used for interaction analyses on risk of MI. Results:, The FGG 9340T > C and FGA 2224G > A polymorphisms, total plasma concentrations of fibrinogen, insulin and high-density lipoprotein, and gender appeared to be independent determinants of plasma fibrinogen ,, concentration in patients, and the corresponding determinants in controls included FGG 9340T > C and FGA 2224G > A polymorphisms and plasma fibrinogen concentration. An elevated plasma fibrinogen ,, concentration proved to be an independent predictor of MI [adjusted odds ratio (OR) (95% CI): 1.24 (1.01, 1.52)]. The plasma fibrinogen ,, concentration was involved in a high-order interaction with total plasma fibrinogen and the FGG 9340T > C and FGA 2224G > A polymorphisms, associated with a further increased risk of MI [OR (95% CI): 3.22 (2.35, 4.39)]. Conclusions:, Plasma fibrinogen ,, concentration influences the risk of MI, and this relationship seems to be strengthened by the presence of an elevated total plasma fibrinogen concentration and the FGG 9340T and FGA 2224G alleles. [source]

Nighttime Vagal Cardiac Control and Plasma Fibrinogen Levels in a Population of Working Men and Women

ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 2 2009
Roland Von Känel M.D.
Background: Elevated plasma fibrinogen levels have prospectively been associated with an increased risk of coronary artery disease in different populations. Plasma fibrinogen is a measure of systemic inflammation crucially involved in atherosclerosis. The vagus nerve curtails inflammation via a cholinergic antiinflammatory pathway. We hypothesized that lower vagal control of the heart relates to higher plasma fibrinogen levels. Methods: Study participants were 559 employees (age 17,63 years; 89% men) of an airplane manufacturing plant in southern Germany. All subjects underwent medical examination, blood sampling, and 24-hour ambulatory heart rate recording while kept on their work routine. The root mean square of successive differences in RR intervals during the night period (nighttime RMSSD) was computed as the heart rate variability index of vagal function. Results: After controlling for demographic, lifestyle, and medical factors, nighttime RMSSD explained 1.7% (P = 0.001), 0.8% (P = 0.033), and 7.8% (P = 0.007), respectively, of the variance in fibrinogen levels in all subjects, men, and women. Nighttime RMSSD and fibrinogen levels were stronger correlated in women than in men. In all workers, men, and women, respectively, there was a mean ± SEM increase of 0.41 ± 0.13 mg/dL, 0.28 ± 0.13 mg/dL, and 1.16 ± 0.41 mg/dL fibrinogen for each millisecond decrease in nighttime RMSSD. Conclusions: Reduced vagal outflow to the heart correlated with elevated plasma fibrinogen levels independent of the established cardiovascular risk factors. This relationship seemed comparably stronger in women than men. Such an autonomic mechanism might contribute to the atherosclerotic process and its thrombotic complications. [source]

Decreased red blood cell aggregation subsequent to improved glycaemic control in Type 2 diabetes mellitus

DIABETIC MEDICINE, Issue 4 2003
B. Chong-Martinez
Abstract Aims Reports of rheological changes following intensification of metabolic control are limited and not concordant. The present study was designed to test the hypothesis that intensification of management of Type 2 diabetes (T2DM) with diet, exercise and insulin improves haemorheological behaviour by reducing red blood cell (RBC) aggregation. Methods Blood was sampled from 55 subjects before and following 14 ± 3 weeks of intensified management. RBC aggregation was measured in vitro for cells in plasma or in an aggregating 70 kD dextran solution. Plasma viscosity and whole blood viscosity were also measured. Results During treatment, fasting glucose fell 27%, HbA1c fell 21%, and serum triglycerides and total cholesterol fell 28% and 12%, respectively (P < 0.0001 for each). The extent and strength of RBC aggregation in plasma fell by 10,13% (P < 0.002). Similar decreases of RBC aggregation were seen for cells suspended in dextran (P < 0.002). Plasma viscosity decreased by 3% (P < 0.02) and high shear blood viscosity by 6,7% (P < 0.0001). Changes of RBC aggregation in plasma and in dextran were significantly correlated, supporting a cellular rather than a plasmatic origin for these changes. However, there were no significant correlations between RBC aggregation changes and changes of fasting glucose, HbA1c, serum triglycerides, serum cholesterol, or plasma fibrinogen. Conclusions Intensified metabolic control results in a reduction of RBC aggregation that appears to be intrinsic to RBC. Since increased RBC aggregation can impair microcirculatory flow, it is possible that haemorheological factors may contribute to the reduction of microvascular complications resulting from improved metabolic control in T2DM. [source]

Disseminated intravascular coagulation in acute leukemia: clinical and laboratory features at presentation

EUROPEAN JOURNAL OF HAEMATOLOGY, Issue 4 2006
Masamitsu Yanada
Abstract:,Background:,Although there are two major scoring systems for the clinical diagnosis of disseminated intravascular coagulation (DIC), the validity of these systems for leukemia-associated DIC remains to be confirmed. Methods:,By analyzing 125 newly diagnosed acute leukemia patients, we investigated clinical and laboratory features of leukemia-associated DIC, and determined the validity of the two established criteria. Results:,A total of 36 patients (29%) were diagnosed with DIC according to expert opinion, a method regarded as the de facto gold standard. Leukemia-associated DIC is characterized by rare manifestation of organ failure because of thrombosis and no relevance of the platelet count for the diagnosis. The results of receiver operating characteristics analysis favored fibrin degradation product (FDP) rather than D-dimer as the fibrin-related marker test. Although prothrombin time, plasma fibrinogen, and serum FDP levels were significantly different for patients with and without DIC, multivariate analysis identified FDP levels to be the only factor associated with DIC diagnosis. The cut-off level of 15 ,g/mL for FDP was found to be the most effective to differentiate DIC from non-DIC, resulting in diagnostic sensitivity and specificity of 92% and 96%, respectively. The diagnostic results for our patients produced with this FDP-based system were at least comparable with or superior to those obtained with the two currently available scoring systems. Conclusions:,Our findings suggest that an FDP-based criterion may be applicable for the diagnosis of leukemia-associated DIC. Although it appears to be simple and practicable enough for clinical use, prospective validation of this criterion is needed. [source]

Formation and Topotactical Orientation of Fibrinogen Nanofibrils on Graphite Nanostructures,

ADVANCED ENGINEERING MATERIALS, Issue 11 2009
Jörg Reichert
We studied the adsorption of human plasma fibrinogen and investigated the formation of amyloid-like fibrinogen nanofibrils and fibrinogen networks in the absence of thrombin and Ca·2+ with high resolution atomic force microscopy (AFM). We propose a possible mechanisms for the surface nanostructure mediated self assembly of fibrinogen molecules and the formation of fibrinogen nanofibrils and nanofibril networks in the absence of thrombin. [source]

Diagnosis, clinical features and molecular assessment of the dysfibrinogenaemias

HAEMOPHILIA, Issue 5 2008
M. HILL
Summary., Hereditary dysfibrinogenaemia is characterized by the presence of functionally abnormal plasma fibrinogen. Dysfibrinogenaemia is a heterogeneous disorder associated with different mutations throughout the three genes that code for the fibrinogen sub-units, affecting many different aspects of fibrinogen/fibrin activity. Dysfibrinogenaemia may be discovered during the investigation of individuals who present with bleeding or thombosis, or may be found in individuals during routine coagulation screening. More specialized coagulation tests may confirm the diagnosis of dysfibrinogenaemia but do not reliably distinguish between the different fibrinogen variants and are not usually useful in predicting bleeding or thrombotic risk. Advances in molecular diagnostics have facilitated the investigation of the molecular causes of fibrinogen disorders. Several ,hot spot' areas have been identified where mutations causing a high proportion of cases of dysfibrinogenaemia are found (A,Arg16 and ,Arg275). Molecular diagnostics have also shown that many fibrinogen variants share the same causative mutation. There is a discrepancy between the quality of the molecular and functional data available for each mutation and the clinical information on individuals and their family members. However, there are accumulating data that the ,hot spot' mutations accounting for 60,80% of cases of dysfibringenaemia are not associated with a significant bleeding or thrombosis in the absence of other risk factors. Rapid screening for these mutations may provide reassurance for patients in the presurgical setting. [source]

Effect of tourniquet pressure and intra-individual variability on plasma fibrinogen, platelet P-selectin and monocyte tissue factor

INTERNATIONAL JOURNAL OF LABORATORY HEMATOLOGY, Issue 6 2000
J. L. Ritchie
Small differences in levels of certain haemostatic components may be clinically significant. It is important therefore to eliminate potential sources of confounding variability. This study investigated the effect of removing tourniquet pressure prior to sample collection on plasma fibrinogen levels, platelet P-selectin and monocyte tissue factor expression. Blood was collected from the right arm under maintained tourniquet pressure and from the left arm following the release of pressure once the vein was sufficiently inflated for insertion of a needle. Whole blood was labelled within one hour of venepuncture to allow analysis of platelet P-selectin and monocyte tissue factor by flow cytometry. Plasma fibrinogen levels were analysed in samples stored at ,70 °C, for all individuals at the end of the study using a method based on the Clauss technique. Intra-individual variability for each of the components was assessed by collecting samples under tourniquet pressure from four individuals on the same day on three consecutive weeks. Intra-individual variations were greater than assay CVs for all three components. There were no significant differences between the two tourniquet methods of collection for fibrinogen, P-selectin or tissue factor. In conclusion, there is no reason not to use a tourniquet during collection of blood for analysis of plasma fibrinogen, platelet P-selectin or monocyte tissue factor. [source]

Improved treatment of sudden hearing loss by specific fibrinogen aphaeresis

JOURNAL OF CLINICAL APHERESIS, Issue 2 2004
Heidrun Ullrich
Abstract The etiology of sudden sensorineural hearing loss is still unclear and is thought to result from disturbances of microcirculation, infectious causes, or autoimmune disorders. So far standard therapy did not show clear improvement over spontaneous remission rate, which is assumed to be about 50% [Nakashima et al., Acta. Otolaryngol. Stockh. 514:14,16, 1994; Schuknecht and Donovan, Arch. Otorhinolaryngol. 243:1,15, 1986; Harris and Sharp, Laryngoscope 100:516,524, 1990; Mayot et al., Clin. Immunol. Immunopath. 68:41,45, 1993; Gussen, Ann. Otol. Rhinol. Laryngol. 85:94,100, 1976]. Elevated blood viscosity due to high fibrinogen levels is supposed to cause decreased cochlear blood flow and thus initiate sudden hearing loss. The specific lowering of fibrinogen immediately decreases plasma viscosity exactly to the desired extent and should lead to improved cochlear blood flow [Suckfüll et al., Acta. Otolaryngol 119:763,766, 1999; Suckfüll, Lancet 360:1811,1817, 2002; Walch et al., Laryngol. Rhino. Otol. 75:641,645, 1996; Suckfüll et al., Otol. Neurotol. 23:309,311, 2002]. In a prospective uncontrolled pilot study on 36 patients with unilateral sudden onset sensorineural hearing loss (SHL) we tried to establish that 1,3 specific fibrinogen aphaereses alone improve recovery of hearing and that it is possible to lower fibrinogen to the target of 80,100 mg/dl without important side effects. Pure tone audiometry was carried out immediately before and after each aphaeresis as well as at 2 and 4 weeks and 6 months after treatment. Sixteen patients recovered spontaneously before undergoing fibrinogen adsorption. All 20 aphaeresis patients improved during immunoadsorption; in 60% of patients auditory thresholds returned to normal after the first immunoadsorption and treatment could be discontinued, in another 20% of patients complete recovery was reached after 4 weeks. The mean plasma fibrinogen concentration of the 20 patients before the first aphaeresis session was 308.1 ± 51.5 mg/dl. Immediately after the first treatment session, the fibrinogen concentration was lowered to 100.7 ± 25.3 mg/dl (P < 0.001). The second and third sessions also showed highly significant reductions in plasma fibrinogen. No important side effects were seen. In conclusion, specific fibrinogen adsorption is a promising new treatment modality that should be tested in a prospective, randomized controlled trial in patients with sudden hearing loss. J. Clin. Apheresis 19:71,78, 2004. © 2004 Wiley-Liss, Inc. [source]

The relative kinetics of clotting and lysis provide a biochemical rationale for the correlation between elevated fibrinogen and cardiovascular disease

JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 6 2007
P. Y. KIM
Summary.,Background:,Elevated plasma fibrinogen is a well known risk factor for cardiovascular disease. The mechanistic rationale for this is not known.Objectives:,These studies were carried out to determine the fibrinogen concentration dependencies of clotting and lysis times and thereby determine whether these times rationalize the correlation between an increased risk of cardiovascular disease and elevated plasma fibrinogen.Methods:,The time courses of clot formation and lysis were measured by turbidity in systems comprising a) fibrinogen, thrombin and plasmin, or b) fibrinogen, thrombin, plasminogen and t-PA, or c) plasma, thrombin and t-PA. From the lysis times, kcat and Km values for plasmin action on fibrin were determined.Results:,The time to clot increased linearly from 2.9 to 5.6 minutes as the fibrinogen concentration increased from 1 to 9 ,M and did not increase further as the fibrinogen concentration was raised to 20 ,M. In contrast, the clot lysis time increased linearly over the input fibrinogen concentration range of 2 to 20 ,M. A similar linear trend was found in the two systems with t-PA and plasminogen. Apparent Km and kcat values for plasmin were 1.1 ± 0.6 ,M and 28 ± 2 min,1, respectively. Km values for plasmin in experiments initiated with t-PA and plasminogen were 1.6 ± 0.2 ,M in the purified system and 2.1 ± 0.9 ,M in plasma.Conclusion:,As the concentration of fibrinogen increases, especially above physiologic level, the balance between fibrinolysis and clotting shifts toward the latter, providing a rationale for the increased risk of cardiovascular disease associated with elevated fibrinogen. [source]

Elevated plasma fibrinogen ,, concentration is associated with myocardial infarction: effects of variation in fibrinogen genes and environmental factors

Long-term effects of hemostatic variables on fatal coronary heart disease: 30-year results from the first prospective Northwick Park Heart Study (NPHS-I)

JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 3 2007
B. L. DE STAVOLA
Summary. Background:,The long-term associations of established risk factors for coronary heart disease (CHD), for example cholesterol, are well known, but not for the less familiar hemostatic variables. Objectives:,To establish whether associations between hemostatic variables and CHD first identified nearly three decades ago have persisted long-term. Methods:,The first Northwick Park Heart Study (NPHS-I) recruited 2167 white men and 941 white women, average age at entry 48 years, on whom measures of factor (F) VII activity (VIIc) and plasma fibrinogen were carried out, both at entry and at follow-up approximately 6 years later. Results:,During a median follow-up of 29 years, 231 male and 36 female CHD deaths were recorded from notifications by the Office for National Statistics. VIIc at recruitment was significantly related to CHD mortality, corrected rate ratio, RR, per 1 SD increase 1.56 (95% CI 1.29, 1.88) in men and RR 1.78 (95% CI 1.17, 2.72) in women. Recruitment fibrinogen was also strongly related to CHD mortality in men, RR 1.63 (95% CI 1.33, 1.99) but not in women, RR 0.75 (95% CI 0.40, 1.43). The associations persisted after controlling for confounders and were confirmed using 6-year follow-up measurements and in analyses omitting deaths within 10 years of recruitment. Conclusions:,The hemostatic system contributes to CHD mortality, and its effect is stable over time. For VIIc, the effect was similar in men and women, while for fibrinogen it appeared to be present only in men. [source]

Dementia in subjects with atrial fibrillation: hemostatic function and the role of anticoagulation

JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 11 2004
M. Barber
Summary.,Background: Atrial fibrillation (AF) is associated with cognitive impairment and dementia, perhaps through encouraging a prothrombotic state and cardioembolism. Objectives: We wished to test the hypotheses that hemostatic function is altered in subjects with AF who develop dementia, and that long-term warfarin anticoagulation is protective against this complication. Patients and methods: Recruitment was from an observational cohort study of AF. Baseline assessment included measurement of plasma fibrinogen, fibrin D -dimer, prothrombin fragment 1+2 (F1+2), thrombin,antithrombin complexes (TAT), von Willebrand factor and tissue plasminogen activator. We assessed cognitive function after 3 years' follow-up using the 13-item modified Telephone Interview for Cognitive Status (TICSm) and the short form of the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE). Results: Of the 218 subjects assessed, 145 (66%) were prescribed warfarin. Forty-nine (22%) met TICSm/IQCODE criteria for dementia. D -dimer, F1+2 and TAT levels were higher in AF subjects with dementia compared with those without (medians 81 vs. 60 ng mL,1, P = 0.008; 0.76 vs. 0.49 nmol L,1, P = 0.006; and 1.78 vs. 1.44 µg L,1, P = 0.003, respectively). These associations became of borderline statistical significance following adjustment for age. Logistic regression showed a trend towards warfarin use being independently associated with reduced prevalence of dementia (odds ratio 0.52, P = 0.08). Conclusions: We found evidence of increased thrombin generation and fibrin turnover in subjects with AF and dementia compared with those without dementia. Long-term warfarin use may be protective against the development of dementia in subjects with AF. [source]

Increased plasma fibrin gel porosity in patients with Type I diabetes during continuous subcutaneous insulin infusion

JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 6 2003
G. Jörneskog
Summary.,Background:,Patients with Type 1 diabetes have a tighter plasma fibrin gel structure, to which impaired glycemic control might contribute. Improved glycemic control can be achieved with continuous subcutaneous insulin infusion (CSII). Objectives:,The aim of the present study was to investigate the effect of CSII on plasma fibrin gel properties and circulating markers of inflammatory activity in patients with Type 1 diabetes. Patients and methods:,Twenty-eight patients were investigated before and after 4,6 months' treatment with CSII. Fibrin gel structure formed in vitro from plasma samples was investigated by liquid permeation of hydrated fibrin gel networks. P-fibrinogen was analyzed by a syneresis method. Comparisons were made between patients with improved (> 0.5%) and unchanged (< 0.5%) glucosylated hemoglobin (HbA1c) during CSII. Results:,Eighteen patients showed improved and 10 patients unchanged HbA1c during CSII. P-fibrinogen, high sensitive C-reactive protein and serum amyloid A-antigen were not significantly changed, while fibrin gel permeability (Ks) and fiber mass,length ratio (µ) increased in both groups (P < 0.02). P-insulin and triglycerides decreased (P < 0.05) in both groups, while reductions of total cholesterol and intercellular adhesion molecule-1 were seen only in patients with improved HbA1c (P < 0.05). Absolute changes in Ks were inversely correlated to changes in plasma fibrinogen (r = 0.50; P < 0.01) and in LDL-cholesterol (r = 0.46; P < 0.05). Conclusions:,Treatment with CSII in patients with Type 1 diabetes is associated with increased plasma fibrin gel porosity. Slight attenuation of the inflammatory activity was also observed. The changes in fibrin gel porosity seem to be mainly mediated by changes in plasma fibrinogen and blood lipids, and are probably secondary to improved insulin sensitivity. [source]

Kinetics and residues after intraperitoneal procaine penicillin G administration in lactating dairy cows

JOURNAL OF VETERINARY PHARMACOLOGY & THERAPEUTICS, Issue 3 2009
A. L. CHICOINE
This paper describes the pharmacokinetic profile of procaine penicillin G after intraperitoneal (IP) administration in eight lactating dairy cows. Procaine pencillin G (PPG, 21 000 IU/kg) was deposited into the abdominal cavity of each cow following an incision in the right paralumbar fossa. Blood and milk samples were taken over the following 10 days, at which point the cows were euthanized. Plasma, milk, muscle, liver, and kidney penicillin concentrations were determined by HPLC, with a limit of quantification of 5 ng/mL for plasma and milk and 40 ng/g for tissue samples. A noncompartmental method was used to analyze plasma kinetics. The mean pharmacokinetic parameters (±SD) were: Cmax, 5.5 ± 2.6 ,g/mL; Tmax, 0.75 ± 0.27 h; AUC0-,, 10.8 ± 4.9 ,g·h/mL; MRT, 2.2 ± 0.9 h. All milk from treated cows contained detectable penicillin residues for a minimum of three milkings (31 h) and maximum of five milkings (52 h) after administration. Concentrations of penicillin in all muscle, liver, and kidney samples taken 10 days postadministration were below the limit of quantification. Necropsy examinations revealed foci of hemorrhage on the rumenal omentum of most cows but peritonitis was not observed. Systemic inflammation as determined by change in leukogram or plasma fibrinogen was noted in one cow. The results of this study demonstrate that IP PPG is absorbed and eliminated rapidly in lactating dairy cows. [source]

Novel fibrinogen mutation ,314Thr,Pro (fibrinogen AI duPont) associated with hepatic fibrinogen storage disease and hypofibrinogenaemia

LIVER INTERNATIONAL, Issue 10 2010
Stephen O. Brennan
Abstract Mutation in fibrinogen genes may lead to quantitative or qualitative disorders that result in bleeding, thrombosis or hepatic fibrinogen storage disease. Only three mutations in the fibrinogen , gene have been identified that cause hepatic endoplasmic reticulum storage of mutant fibrinogen. To investigate the possibility of hepatic fibrinogen storage disease in a 4-year-old male with persistently elevated serum aminotransferases and preserved synthetic function except for a prolonged INR. After informed consent, liver and blood samples were obtained. Liver sections were examined by light microscopy, anti-fibrinogen immunolabelling and electron microscopy. Purified fibrinogen was analysed by sodium dodecyl sulphate-polyacrylamide gel electrophoresis and reverse phase high performance liquid chromatography; DNA sequencing was performed using a BigDye Terminator (v. 3.1) cycle sequencing kit. Four-year-old male with persistently elevated transaminases with an INR 1.5 but otherwise normal synthetic function. Fibrinogen activity and thrombin clotting time were abnormal at 0.47 g/L and 46 s respectively. Hepatic histological examination revealed portal inflammatory infiltrates with bridging fibrosis. Clumped eosinophilic material was observed in hepatocytes that was immunoreactive to fibrinogen antisera. Ultrastructural examination showed cytoplasmic inclusions arrayed in fingerprint-like patterns. DNA sequence analysis revealed heterozygosity for a novel ,314Thr ,Pro mutation (fibrinogen AI duPont) in the fibrinogen , gene. Protein analyses showed normal patterns of A,, B, and , chains suggesting that the variant , allele was not expressed in plasma fibrinogen. We describe only the fourth mutation to be identified, ,314Thr,Pro (fibrinogen AI duPont), giving rise to hypofibrinogenaemia and hepatic fibrinogen storage disease. [source]

Correction of haemorheological disturbances in myocardial infarction by diquertin and ascorbic acid

PHYTOTHERAPY RESEARCH, Issue 1 2003
M. B. Plotnikov
Abstract In a model of the high blood viscosity syndrome, developed after myocardial infarction in rats, it was observed that a therapy of a combination of diquertin (20,mg/kg) and ascorbic acid (50,mg/kg) for a period of 6 days, resulted in an improvement of haemorheological indices. The decrease in blood viscosity was primarily due to an improved deformability of erythrocytes, and to some extent, due to a decrease in the content of plasma fibrinogen and erythrocyte aggregation. Copyright © 2003 John Wiley & Sons, Ltd. [source]

Effect of immobilization of polysaccharides on the biocompatibility of poly(butyleneadipate- co -terephthalate) films

POLYMERS FOR ADVANCED TECHNOLOGIES, Issue 8 2010
Win-Chun Jao
Abstract Aiming to improve the hydrophilicity, antibacterial activity, cytocompatibility, and hemocompatibility of poly(butyleneadipate- co -terephthalate) (PBAT) films, PBAT films were treated with ozone, grafted with chitosan (CS), and followed by covalent immobilization of either heparin (HEP) or hyaluronic acid (HA). The surface graft density of modified PBAT films was detected by X-ray photoelectron spectroscopy (XPS) and dyeing. The surface roughness of PBAT films was measured using an atomic force microscope (AFM). After immobilizing CS, PBAT films acquired antibacterial activity against Staphylococcus aureus and Escherichia coli. The adsorption of human serum albumin (HSA) and human plasma fibrinogen (HPF) on PBAT,CS,HEP and PBAT,CS,HA films was lower compared to that of native PBAT. Moreover, HEP immobilization could effectively reduce platelet adhesion and prolong the blood coagulation time, thereby improving the blood compatibility of PBAT. In addition, the growth of L929 fibroblasts was improved for HEP or HA immobilized PBAT, suggesting this surface modification was non-cytotoxic. Furthermore, PBAT,CS,HEP and PBAT,CS,HA exhibited higher cell proliferation than native PBAT. Copyright © 2009 John Wiley & Sons, Ltd. [source]

Protein adsorption and platelet adhesion of polysulfone membrane immobilized with chitosan and heparin conjugate

POLYMERS FOR ADVANCED TECHNOLOGIES, Issue 2 2003
M.-C. Yang
Abstract Polysulfone (PSF) membranes were treated with ozone to introduce peroxides, and then grafted with either acrylic acid or chitosan, followed by the immobilization of heparin. The effect of spacer arm on blood compatibility was investigated using three chitosans of different molecular weight [1170 (water soluble), 160,000, and 400,000] and similar degrees of deacetylation (75%). The hydrophilicity was evaluated by measuring the contact angle of water. Blood compatibility was evaluated using the activated partial thromboplastin time (APTT) as well as the adhesion of platelets. The protein affinity was determined by the absorption of human serum albumin (HSA) and human plasma fibrinogen (HPF). The results show that by the coupling of chitosan, the amount of heparin immobilized can be increased by four times. Water contact angle (from 78,° to 41,°) decreased with the increase of the amount of heparin immobilized, showing increased wettability. The heparinized PSF membrane showed longer APTT and decreasing platelet adhesion, compared to that of unmodified PSF membrane. The adsorption of HSA and HPF were reduced to 17 and 6%, respectively. This suggests that longer spacer binding to heparin can increase the opportunity of anti-coagulation on contacting blood. These results demonstrated that the hydrophilicity and blood compatibility of PSF membrane could be improved by chitosan and heparin conjugate. Copyright © 2003 John Wiley & Sons, Ltd. [source]

Correlation of Biochemical and Hematological Changes with Graft Failure Following Pig Heart and Kidney Transplantation in Baboons

AMERICAN JOURNAL OF TRANSPLANTATION, Issue 12 2003
Christoph Knosalla
We have explored biochemical and hematologic parameters that might indicate acute humoral xenograft rejection (AHXR) following pig organ transplantation in baboons. Baboons (n = 15) received an immunosuppressive regimen, and underwent a miniature swine or hDAF kidney (Group 1, n = 6) or heart (Group 2, n = 7) transplantation. Control baboons (Group 3, n = 2) received the immunosuppressive regimen without organ transplantation. Blood chemistry and hematologic parameters were measured daily. Baboon and porcine cytomegalovirus were monitored. In Groups 1 and 2, organ grafts survived for up to 29 days. A plasma fibrinogen of <80 mg/dL on 2 consecutive days, and a serum lactate dehydrogenase of >600 U/L and aspartate transaminase of >300 U/L, were associated with the development of AHXR in both heart and kidney grafts. In Group 1, a decrease in platelet count of >150 000/,L within 3 days, or a count of <50 000/,L, were associated with AHXR. In Group 2, a creatine phosphokinase of >500 U/L was associated with graft failure. In Group 3, no abnormalities were observed. The possibility that porcine CMV may play a role in graft injury could not be excluded. Noninvasive parameters were identified that have predictive potential for AHXR. Monitoring of these might enable therapeutic intervention to reverse rejection. [source]

Refining exposure definitions for studies of periodontal disease and systemic disease associations

COMMUNITY DENTISTRY AND ORAL EPIDEMIOLOGY, Issue 6 2008
Ryan T. Demmer
Abstract,,, Background:, Substantial variation exists in reported associations between periodontal infections and cardiovascular disease. Imprecise periodontal exposure definitions are possible contributors to this variability. We studied appropriate exposure definitions for studying associations between clinical periodontal disease (PD) and systemic disease. Methods:, Data originate from men and women aged 20,79 enrolled in the Study of Health in Pomerania (SHIP) from 1997,2001. Age and sex-adjusted correlation analysis identified PD definitions with the highest cross-sectional associations with three subclinical markers of systemic disease: plasma fibrinogen (n = 3481), serum hemoglobin A1c (HbA1c) (n = 3480), and common carotid artery intima-media thickness (c-IMT) (n = 1745, age , 45). Results:, In men and women, percent of sites with attachment loss (AL) ,6 mm and tooth loss both revealed the highest correlation with HbA1c (, = 0.11; several other definitions related similarly), while the strongest fibrinogen correlation was observed with percent of sites with pocket depth ,3 mm (, = 0.19). Findings for c-IMT among men were strongest for percent of sites with AL ,6 mm (, = 0.14; several other definitions related similarly) while among women, percent of sites with pocket depth ,5 or 6 mm had the highest observed correlation (, = 0.13). Conclusions:, A range of near optimal definitions varied according to gender and whether the systemic disease marker reflected an acute or chronic situation. Pocket depth was more strongly correlated with the acute marker fibrinogen while attachment and tooth loss tended to be more strongly correlated with the chronic markers, HbA1c, and c-IMT. These findings can be useful in designing future studies investigating the association between PD and systemic disease. [source]