Fibrinogen-Fibrin-Related Antigen Pattern in Human Blood

1974 ◽  
Vol 32 (02/03) ◽  
pp. 266-276
Author(s):  
Carl D. Jacobsen ◽  
John C. Hoak ◽  
Kenneth K. WU ◽  
Glenna L. Fry
Keyword(s):  

SummaryIn serum from patients with DIC at least 3 different FR-antigenic components could be found. It was difficult to demonstrate these components in the corresponding plasma samples. It is possible that a portion of these antigens formed as a result of in vitro clotting despite the presence of proteolytic inhibitors. These results suggest that the interpretation of “increased split products in serum” may be more complex than current concepts indicate.

1973 ◽  
Vol 30 (03) ◽  
pp. 494-498 ◽  
Author(s):  
G de Gaetano ◽  
J Vermylen

SummaryThrombelastograms of both native blood and re-calcified platelet-rich plasma samples taken from subjects given a single oral dose of aspirin (1 gram) were not significantly different from the pretreatment recordings. Aspirin also did not modify the thrombelastogram when preincubated in vitro with platelet-rich plasma at concentrations inhibiting the platelet “release reaction” by collagen. Thrombelastography therefore cannot evaluate the effect of aspirin on platelet function.


2007 ◽  
Vol 232 (9) ◽  
pp. 1160-1169 ◽  
Author(s):  
Marlyn P. Langford ◽  
Thomas B. Redens ◽  
Norman R. Harris ◽  
Seungjun Lee ◽  
Sushil K. Jain ◽  
...  

The plasma levels of apoptotic DNA ladders (i.e., apoptosemia) and γ-glutamyltranspeptidase (GGT) in diabetic outpatients and rats were investigated. Apoptotic DNA ladders were detected in plasma from 26.8% of type 1 (T1) and 18.5% of type 2 (T2) diabetic children 1–20 years of age, 25.7% of hospitalized children and 35.7% of adult RA outpatients, but in only 3.5% of adult pre-op patients. Plasma from 7.7% of young streptozotocin-induced diabetic but not control rats contained apoptotic DNA ladders. Apoptosemia was detected more often in male T1 (31%) and T2 (30.8%) diabetic outpatients than in female T1 (20.8%) and T2 (15.4%) diabetic outpatients. GGT in apoptosemic plasma was significantly higher than in nonapoptosemic plasma from T1 ( P = 0.001) but not T2 diabetic children. The highest amounts of apoptotic DNA were detected most often in diabetic children ≥14 years of age. In vitro study results suggest that cell-free apoptotic DNA ladders appear prior to an increase in GGT activity in serum from human blood incubated at 37°C. The results suggest that 24.7% of plasma samples from diabetic children contained apoptotic DNA ladders, the incidence and amounts of apoptotic DNA ladders were higher in the older diabetic children, and GGT was elevated in apoptosemic T1 diabetic children ( P = 0.01). The results indicate that “silent” apoptosemia occurs in T1 and T2 diabetic children and suggest elevated GGT in diabetic children could be due to release from apoptotic cells.


2020 ◽  
Vol 3 (04) ◽  
pp. 17-29
Author(s):  
Abhijit De ◽  
S. Mojtaba Mostafavi

The toxic effect of lead (Pb) causes to anemia and iron deficiency in human body. So, the lead determination in blood/serum samples is very important.  In this study, a novel adsorbent based on sulfamethizole functionalized on nanographene oxide (C3H10N4O2S2-NGO; SM-NGO) was used for extraction of Pb(II) from human blood, serum and plasma samples in battery manufactories workers by SF-D-µ-SPE.  By procedure, 25 mg of SM-NGO mixed with 10 mL of human blood/serum or plasma samples and aspirated by 10 mL of syringe tube. After sonication of samples for 5 min, the Pb ions adsorbed based on sulfur of SM-NGO adsorbent at pH=6 and the solid phase separated by syringe coupled to Millex-FG hydrophobic PTFE membrane (0.2 µm). Then, the lead ions were back-extracted from SM-NGO/PTFE by elution phase with 0.5 mL of nitric acid solution (0.5 M). Finally, the concentrations of Pb(II) ions were determined by AT-FAAS. 


1990 ◽  
Vol 64 (03) ◽  
pp. 402-406 ◽  
Author(s):  
M D Oethinger ◽  
E Seifried

SummaryThe present in vitro study investigated dose-, time- and temperature-dependent effects of two-chain urokinase plasminogen activato(u-PA, urokinase) on normal citrated plasma. When 10 μg/ml u-PA wereadded to pooled normal plasma and incubated for 30 min at an ambient temperature (25° C), α2-antiplas-min decreased to 8% of the control value. Incubation on ice yielded a decrease to 45% of control,whereas α2-antiplasmin was fully consumed at 37° C. Fibrinogen and plasminogen fell to 46% and 39%, respectively, after a 30 min incubation at 25° C. Thrombin time prolonged to 190% of control.Various inhibitors were studied with respect to their suitability and efficacy to prevent these in vitro effects. Aprotinin exhibited a good protective effect on fibrinogen at concentrations exceeding 500 KlU/ml plasma. Its use, however, was limited due to interferences with some haemostatic assays. We could demonstrate that L-Glutamyl-L-Glycyl-L-Arginyl chloromethyl ketone (GGACK) and a specific polyclonal anti-u-PA-antibody (anti-u-PA-IgG) effectively inhibited urokinase-induced plasmin generation without interfering with haemostatic assays. The anti-u-PA-antibody afforded full protection ofα2-antiplasmin at therapeutic levels of u-PA.It is concluded that u-PA in plasma samples from patients during thrombolytic therapy may induce in vitro effects which should be prevented by the use of a suitable inhibitor such as GGACK or specific anti-u-PA-antibody.


1973 ◽  
Vol 29 (03) ◽  
pp. 694-700 ◽  
Author(s):  
Paul L. Rifkin ◽  
Marjorie B. Zucker

SummaryDipyridamole (Persantin) is reported to prolong platelet survival and inhibit embolism in patients with prosthetic heart valves, but its mechanism of action is unknown. Fifty jxM dipyridamole failed to reduce the high percentage of platelets retained when heparinized human blood was passed through a glass bead column, but prolonged the inhibition of retention caused by disturbing blood in vitro. Possibly the prostheses act like disturbance. Although RA 233 was as effective as dipyridamole in inhibiting the return of retention, it was less effective in preventing the uptake of adenosine into erythrocytes, and more active in inhibiting ADP-induced aggregation and release. Thus there is no simple relation between these drug effects.


1985 ◽  
Vol 53 (01) ◽  
pp. 070-074 ◽  
Author(s):  
G Mallarkey ◽  
G M Smith

SummaryThe mechanism of collagen-induced sudden death in rabbits was studied by measuring blood pressure (BP), heart rate, ECG, the continuous platelet count and the plasma levels of thromboxane B2 (TxB2) and 6-keto prostaglandin Fia (6-keto PGF1α). Death was preceded by myocardial ischaemia and a sharp fall in BP which occurred before any fall in platelet count was observed. The calcium entry blockers (CEBs), verapamil, nifedipine and PY 108-068 protected the rabbits from sudden death without any significant effect on the decrease in the platelet count or increase in plasma TxB2 levels. 6-keto PGF1α could not be detected in any plasma samples. Indomethacin and tri-sodium citrate also protected the rabbits but significantly reduced the fall in platelet count and plasma TxB2. In vitro studies on isolated aortae indicated that verapamil non-specifically inhibited vasoconstriction induced by KC1, adrenaline and U46619 (a thromboxane agonist). It is concluded that CEBs physiologically antagonize the vasoconstricting actions of platelet-derived substances and that it is coronary vasoconstriction that is primarily the cause of death.


1963 ◽  
Vol 18 (5) ◽  
pp. 955-958 ◽  
Author(s):  
S. H. Blondheim ◽  
Gabriel Neumann ◽  
Edna Kott ◽  
Zena Ben-Ishai

The ability of human blood to acetylate p-aminobenzoic acid, determined in vitro, varied directly with the ambient temperature to which the subject was exposed before the blood was drawn. This was demonstrated by 135 determinations of the acetylating ability of the blood of 49 subjects performed over a period of 3 years, and also in acute experiments in which subjects were exposed to 6 and 37 C for up to 2 hr. Variations in the acetylating ability of blood may reflect the activity of metabolic mechanisms involved in thermal homeostasis. aromatic amines; p-aminobenzoic acid; cold; heat acclimatization; (blood) enzymes; weather; environment Submitted on September 11, 1962


Author(s):  
B Lefrère ◽  
D Wohrer ◽  
C Godefroy ◽  
M Soichot ◽  
A Mihoubi ◽  
...  

Abstract We report the case of an 11-month-old male infant with a complex congenital heart disease who was admitted in the intensive care unit following cardiorespiratory arrest at home. Toxicological urine screening reported an ethanol concentration of 0.65 g/L using an enzymatic assay, without suspicion of alcohol intake; a significant amount of ethanol concentration was found in two plasma samples using the same enzymatic assay. Plasma and urine ethanol concentrations were below the limit of quantification (LOQ) when tested using a gas chromatography method. Urine ethanol level was also below the LOQ when tested by enzymatic assay after an initial urine ultrafiltration. These results confirmed our suspicion of matrix interference due to elevated lactate and lactate dehydrogenase levels interfering in the enzymatic assay. This analytical interference, well-known in postmortem samples, extensively studied in vitro, has been rarely reported in vivo, especially in children. To the best of our knowledge, this case is only the sixth one reported in an infant’s plasma and the first initially discovered from urine. Indeed, as for ethanol, this last matrix has not been studied in the context of this artifact that may induce false-positive ethanol results while seeking a diagnosis in life-threatening or fatal situations that are potentially subject to forensic scrutiny. In parallel to a synthetic literature review, we propose a simple, informative decision tree, in order to help health professionals suspecting a false-positive result when performing an ethanol assay.


2020 ◽  
pp. 128951
Author(s):  
Nadezhda Frolova ◽  
Alena Soboleva ◽  
Viet Duc Nguyen ◽  
Ahyoung Kim ◽  
Christian Ihling ◽  
...  
Keyword(s):  

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