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PubMedDate not supplied

[Effect of various infusion media and solutions on the kallikrein-kinin system of human plasma].

Activities of prekallikrein and Hageman factor (factor XII) were studied in some natural and artificial infusion media: polyglukine, rheoglumane, gemodes, polypher, gelatinol, saline; in solutions for parenteral nutrition--hydrolysate of casein, aminopeptide, aminokrovine, glucose solutions as well as in 10% NaCl and novocain. All the solutions studied did not affect the purified preparations of prekallikrein, but some of them activated partially purified preparations of Hageman factor. However, all these solutions, except of Ringer solution, activated Hageman factor and prekallikrein in human blood serum. Activation of prekallikrein appears to occur via the active form of Hageman factor. Among the solutions studied casein hydrolysate, 5% glucose, gelatinol and novocain exhibited the highest stimulating effect on Hageman factor and prekallikrein. Possible mechanisms of the activation are discussed.

Factor XII↗
PubMed1980

Studies on some coagulation factors (Hageman factor, plasma prekallikrein, and high molecular weight kininogen) in the normal newborn.

Normal newborn infants have a prolonged partial thromboplastin time compared to that of older infants or adults. This finding has been related to combined deficiencies of multiple clotting factors, with the exception of proaccelerin (factor V) and antihemophilic factor (factor VIII). The present study confirms the presence of decreased titers of Hageman factor (HF, factor XII), plasma prekallikrein, and high molecular weight kininogen during the neonatal period, as demonstrated in clotting assays; the degree of these relative deficiencies is usually such that only the low titer of HF appears to contribute significantly to the abnormally long PTT. Additionally, procoagulant titers of HF and plasma prekallikrein were relatively lower than the concentration of these factors determined immunologically. The mechanisms underlying this phenomenon are not known.

Antigens↗
PubMed1984

Acute effect of smoking on fibrinolysis: increase in the activity level of circulating extrinsic (tissue-type) plasminogen activator.

The acute effect of cigarette smoking on the fibrinolytic enzyme system in blood was studied. It was found imperative to have an initial 30 min rest period, after venipuncture, to obtain a stable baseline in the fibrinolytic studies. The average heart rate, in inhaling smokers, increased from 64 to a peak of 79 beats min-1, 5-10 min after commencement of smoking. A peak in fibrinolytic activity was found to occur later, at 22.5 min. Analysis of the increase in fibrinolytic activity revealed no demonstrable activation of intrinsic systems via factor XII, nor changes in plasminogen, prekallikrein and C1-inactivator. No plasmin-alpha 2-antiplasmin complexes were detectable. The increase (P less than 0.01) was found to be due to extrinsic (tissue-type) plasminogen activator, revealed as C1-inactivator-resistant plasminogen activator activity, and further identified by quenching with anti-tissue plasminogen activator IgG. Thus, smoking appears to elicit a significant increase in the level of activity of circulating extrinsic plasminogen activator.

Adult↗
PubMed1978

Plasma kallikrein activation and inhibition during typhoid fever.

As an ancillary part of a typhoid fever vaccine study, 10 healthy adult male volunteers (nonimmunized controls) were serially bled 6 days before to 30 days after ingesting 10(5)Salmonella typhi organisms. Five persons developed typhoid fever 6-10 days after challenge, while five remained well. During the febrile illness, significant changes (P < 0.05) in the following hematological parameters were measured: a rise in alpha(1)-antitrypsin antigen concentration and high molecular weight kininogen clotting activity; a progressive decrease of platelet count (to 60% of the predisease state), functional prekallikrein (55%) and kallikrein inhibitor (47%) with a nadir reached on day 5 of the fever and a subsequent overshoot during convalescence. Despite the drop in functional prekallikrein and kallikrein inhibitor, there was no change in factor XII clotting activity or antigenic concentrations of prekallikrein and the kallikrein inhibitors, C1 esterase inhibitor (C1-INH) and alpha(2)-macroglobulin. Plasma from febrile patients subjected to immunoelectrophoresis and crossed immunoelectrophoresis contained a new complex displaying antigenic characteristics of both prekallikrein and C1-INH; the alpha(2)-macroglobulin, antithrombin III, and alpha(1)-antitrypsin immunoprecipitates were unchanged. Plasma drawn from infected-well subjects showed no significant change in these components of the kinin generating system. The finding of a reduction in functional prekallikrein and kallikrein inhibitor (C1-INH) and the formation of a kallikrein C1-INH complex is consistent with prekallikrein activation in typhoid fever. The correlation of these changes with the drop in platelet count suggests that a common mechanism may be responsible.

Adult↗
PubMed1977

Bilateral retinal vasculitis associated with clotting disorders.

We found distinct alterations of the clotting and fibrinolytic mechanisms in a 27-year-old man who suffered from typical bilateral vasculitis, clinically and fluoroangiographically manifest as obstruction of the central retinal veins. The partial thromboplastin time was slightly increased, a partial clot lysis occurred after one hour, the plasminogen level was markedly low, and alpha2-macroglobulin was decreased, as were factor XII and IgG. Kallikrein was absent. Similar changes, though not so pronounced, were also found in the patient's son and in his brother.

Adult↗
PubMed2005

Myocardial infarction and arterial thrombosis in severe (homozygous) FXII deficiency: no apparent causative relation.

Twenty-one patients (12 female and 9 male) with severe (homozygous) factor XII (FXII) deficiency and 58 (32 female and 26 male) with heterozygous FXII deficiency were observed for an average 16.2 years. No patient with homozygous FXII deficiency experienced myocardial infarction or any other arterial thrombosis. The same was true for heterozygotes. The cases of FXII deficiency and arterial thrombosis reported in the literature were evaluated. In every instance, associated risk factors were present that could justify the arterial thrombosis. Dyslipidemia, hypertension, smoking, and diabetes mellitus were the most frequent findings. The examination of the few papers that dealt with the prevalence of arterial thrombosis in patients with severe FXII deficiency showed that only 1 patient of 61 experienced myocardial infarction. In conclusion, it seems that the role of FXII deficiency in the pathogenesis of arterial thrombosis is minor.

Adolescent↗
PubMed1989

Purification and preliminary characterization of Torresea cearensis trypsin inhibitor.

An inhibitor against serine proteinases was purified from Torresea cearensis by affinity chromatography on trypsin-Sepharose. The protein is a single polypeptide of molecular weight 13,600 after reduction and has a high content of cysteine residues. Both trypsin (Ki = 0.34 nM) and chymotrypsin (Ki = 0.15 microM) are inhibited by Torresea cearensis inhibitor. Blood clotting factor XII is also inhibited (Ki = 0.24 microM), but not plasma kallikrein, tissue kallikrein or thrombin. The stoichiometry of the inhibitor-proteinase complex with trypsin is 1:1.

Fabaceae↗
PubMed2026

Deficiency of Setd2 in mesenchymal stem cells facilitates the progression of myelodysplastic syndrome to leukemia.

While previous studies have indicated that H3K36me3, which is mediated by Setd2, may regulate the cell fate of mesenchymal stem cells (MSCs) both in vitro and in vivo, the specific role of MSCs in the onset and progression of MDS remains unclear. Thus, the histone methyltransferase Setd2 is implicated in MDS-associated leukemia. This study utilized NUP98-HOXD13 (NHD13) mice with targeted deletion of Setd2 in MSCs. Here, we found that Setd2-deficient mice undergo faster leukemia transformation than control mice do, as evidenced by the abnormal differentiation of hematopoietic stem progenitor cells in the bone marrow, abnormal hematopoiesis, and increased number of blast cells. Compared with that of control mice, the morphology of NHD13 mouse MSCs with Setd2 deficiency was irregular, and the support function of hematopoietic cells was compromised. This study demonstrated that targeted deletion of Setd2 in MSCs facilitates the advancement of MDS. Furthermore, we identified increased expression of coagulation factor XII as a key leukemic transformation mediator in Setd2-deficient MSCs. Moreover, we found that SETD2 expression is significantly lower in high-risk MDS patients than in low-risk MDS patients, further suggesting that the targeted deletion of Setd2 in MSCs is associated with MDS progression. Collectively, our results suggest that Setd2 in MSCs suppresses MDS progression to leukemia through coagulation factor XII-mediated suppression of the stem cell support capacity of MSCs. Overall, this study sheds light on the pathogenesis of MDS and provides a therapeutic strategy for regulating the microenvironment in patients with MDS who cannot be cured by haematopoietic stem cell transplantation.

Animals↗
PubMed1996

The quality of autotransfused chest-drainage blood after cardiac surgery: a study of coagulation factors.

A wide range of experience, dating back as far as 1978, has been gained with both the hard-shell cardiotomy reservoir of the heart-lung machine and the Sorensen autotransfusion system as retransfusion systems. Three remains, however, a lack of knowledge regarding the quality of retransfused blood in systems of less complex construction which are already available on the market and involve the use of a pouch (Sentinel-Seal autotransfusion system and Pleur-evac collecting system). The present study entailed the investigation of blood from the chest drainages of twenty patients after cardiac surgery by using a simple retransfusion system (Sentinel-Seal autotransfusion system). In two postoperative groups of patients with low and high blood loss from chest drainage, we determined, in addition to free plasma hemoglobin, the following: factor XII, kallikrein-like activity, thrombin-antithrombin III complex, tissue-plasminogen and d-dimers. In the collective with a low blood loss, we found remarkable cell alterations as well as highly activated and advanced coagulation and an extraordinary fibrinolytic activity. If done at all, retransfusion by the Sentinel-Seal autotransfusion system should be restricted to the first four postoperative hours in cases of high blood loss.

Antithrombin III↗
PubMed1975

Inhibition of Hageman factor, plasma thromboplastin antecedent, thrombin and other clotting factors by phenylglyoxal hydrate (38500).

Exposure of purified Hageman factor (HF, Factor XII) to phenylglyoxal hydrate (PHG), an agent reacting with arginine residues in protein, inhibited its coagulant properties upon subsequent exposure of negatively charged agents. Once HF had been exposed to kaolin or ellagic acid, however, subsequent addition of PHG was much less inhibitory. PHG had no effect upon the ability of HF to bind to negatively charged surfaces. PGH also inhibited preparations of activated PTA (Factor XI) and thrombin, and, when incubated with plasma, reduced the titer of coagulable fibrinogen, PTA Christmas factor (Factor IX), antihemophilic factor (Factor VIII), Factor VII, Stuart factor (Factor X), proaccelerin (Factor V) and prothrombin (Factor II), and to a lesser degres, HF.

Aldehydes↗
PubMed1984

Kinin activation as a predictive assay for adverse reactions to radiographic contrast medium.

The rate of conversion in vitro, of prekallikrein to kallikrein has been measured in 74 reactors to contrast medium and 70 controls. The conversion rate is significantly more rapid in reactors than controls. There was no difference in C1-esterase inhibitor and factor XII levels between reactors and controls. This retrospective investigation suggests that prekallikrein/kallikrein conversion rate may form the basis of a test for differentiating between reactors and non-reactors.

Adolescent↗
PubMed1994

Biocompatibility of a heparin-bonded membrane oxygenator (Carmeda MAXIMA) during the first 90 minutes of cardiopulmonary bypass: clinical comparison with the conventional system.

We clinically compared a heparin-bonded Carmeda MAXIMA membrane oxygenator to a nonheparin-bonded MAXIMA in 20 patients undergoing coronary artery bypass grafting or valve replacement. Reductions of fibrinogen, factor XII, and high molecular weight kininogen were greater in the MAXIMA group. Serum C3a and free hemoglobin were lower in the Carmeda group. The level of C4a, though remarkably lower than that of C3a, was higher in the Carmeda group then in the MAXIMA group. Both oxygenators performed well in terms of blood gas exchange. We conclude that the heparin-bonded Carmeda oxygenator offers superior biocompatibility during cardiopulmonary bypass.

Biocompatible Materials↗
PubMed1988

A patient with an interstitial deletion of the short arm of chromosome 6.

The clinical history and subsequent progress of a child with an interstitial deletion in the short arm of chromosome 6 is described. This abnormality coupled with a reduced Hageman factor (Factor XII) led to an earlier publication which suggested that this gene was localized to the breakpoint region involved. A review of similar phenotypes from the literature is presented.

Child, Preschool↗
PubMed1976

Von Willebrand disease San Diego, a new variant.

A reduced level of factor XII has been observed in 9 of 39 patients with von Willebrand's disease. This apparent common variant of von Willebrand's disease has not previously been described, and its significance is not known.

Adult↗
PubMed2002

Changes of selected morphotic parameters and blood plasma proteins in blood of divers after a single short-time operational heliox exposure.

In the Polish Navy, deep-water dives, performed for the needs of the maritime industry, are conducted using our own national technology and trimix as a breathing medium. In this paper are presented the results obtained during a short-time deep-water diving test using the principles of US Navy technology, combined with the use of diving equipment type AF-2 and heliox-type breathing mixture in the open circuit. In the performed examinations changes in clinical parameters were assessed viz.: blood morphology, hematocrit level, concentration of C3c, C4, IgG, IgA, IgM, CRP, concentration of fibrinogen and factor XII level, obtained 30 minutes prior to commencement, immediately after completion, and 24 hours after termination of the exposure. The results thus generated were subjected to a preliminary analysis by the description of trends observed. It was revealed that the diving technology employed did not generate substantial changes in the examined parameters of blood in divers, and the increase of neutrophils, blood platelets and fibrinogen concentration in the blood plasma immediately after diving is of temporary character, being a typical reaction observed during diving.

Adult↗
PubMed2003

Perioperative use of the Thrombelastograph in patients with inherited bleeding disorders.

There are few reports of the use of Thrombelastgraph (TEG) in patients with isolated or inherited bleeding disorders. Three surgical patients are presented with von Willebrand's disease, factor XII deficiency, and hemophilia A with dysfibrinogenemia in which the abnormalities detected by the TEG were similar to the expected coagulation abnormalities based on preoperative laboratory studies. This initial report suggests that this potential application of the TEG be further investigated.

Adenoidectomy↗
PubMed1977

Hageman factor substrates. Human plasma prekallikrein: mechanism of activation by Hageman factor and participation in hageman factor-dependent fibrinolysis.

Two molecular forms of prekallikrein can be isolated from pooled normal human plasma. Their approximate molecular weights by sodium dodecyl sulfate-gel electrophoresis are 88,000 and 85,000. The two bands observed are shown to represent prekallikrein by functional, immunochemical, and structural criteria. Both forms are cleaved by activated Hageman factor, they appear to share antigenic determinants, they are not interconvertible upon incubation with activated Hageman factor or kallikrein, and the ratio of kinin-generating, and plasminogen-activating activities of the preparations are independent of the relative proportion of each band. Activated Factor XII converts prekallikrein to kallikrein by limited proteolysis and two disulfide-linked chains designated kallikrein heavy chain (Mr = 52,000) and kallikrein light chains (Mr = 36,000 or 33,000) are formed. The active site is associated with the light chains as assessed by incorporation of [3H]diisopropyl fluorophosphate. No dissociable fragments were observed in the absence of reducing agents. However, kallikrein could digest prekallikrein to diminish its molecular weight by 10,000. In addition, two factors capable of activating plasminogen to plasmin have been isolated; one is identified as kallikrein. The second principle fractionates with Factor XI and is demonstrable in normal and prekallikrein-deficient plasma.

Enzyme Activation↗