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Biomedical subjects

V Hofmann

Publications and source records attributed to V Hofmann.

At least 91 records · Page 5Linked to original sources
PubMed1979

[Fibrinogen metabolism and plasma fibrinopeptide A in disseminated neoplasms].

FPA immunoreactivity was elevated in 14 out of 15 patients with disseminated neoplasia. Two of the patients showed signs of DIC, two had clinically evident thrombosis and one a positive 125I-fibrinogen uptake test suggesting thrombosis. Infusion of heparin produced a prompt fall in FPA levels. FPA immunoreactivity correlated well with the turnover of intravasal 125I-fibrinogen. The results confirm that the RIA of FPA provides a specific and quantitative index of the conversion of fibrinogen into fibrin and indirectly of the thrombin action in vivo.

Disseminated Intravascular Coagulation↗
PubMed1979

[The shape of fibrin-monomer molecules in solution].

Human fibrin monomers after thrombin and reptilase proteolysis can be kept in solution at pH 4.6. Using dynamic light scattering, the hydrodynamic data of these two monomer solutions and of fibrinogen in the same buffer were compared to fibrinogen at pH 7.4. The translational diffusion coefficient DT20W of fibrinogen at pH 7.4 was 1.95 +/- 3% 10(-7).cm2.sec-1 and the rotational diffusion coefficient DR20,W 50,000 +/- 30%.sec-1. The corresponding DT and DR for the two monomer solutions and fibrinogen at pH 4.6 did not significantly deviate from the above values. It is concluded that enzymatic proteolysis of fibrinogen, triggering release of the aminoterminal fibrinopeptides A and B, does not produce a major conformational change in the resulting monomers.

Fibrin↗
PubMed1979

Fibrinogen Zurich I: impaired release of fibrinopeptide A.

Fibrinogen Zurich I is characterized by an abnormal fibrin monomer polymerization. It consists of two fractions of molecules, one with a normal aggregation and one not aggregating at all and interfering with the aggregation of the normal population. Using a radioimmunoassay for fibrinopeptide A, only approximately half of the expected fibrinopeptide A could be recovered after thrombin or Defibrase proteolysis. The defective fibrinopeptide A release could be confirmed by measurement of the N-terminal Gly/Tyr ratio. It is likely that the abnormal fibrin monomer aggregation of the abnormal fraction of fibrinogen Zurich I is due to the defective fibrinopeptide A release of this fraction.

Batroxobin↗
PubMed1979

[Angioimmunoblastic lymphadenopathy. 3 cases with polyclonal gammopathy].

Three patients with an atypical lymphoproliferative disorder disorder and polyclonal gammopathy have been reviewed retrospectively. The clinical and histological findings are compatible with the recently described entity of angioimmunoblastic lymphadenopathy. Two patients died within 6 months after the first symptoms of the disease. Circulating immuncomplexes were demonstrated in the serum of 2 patients. In one patient with a nearly fourfold increase of IgG, persistent hyponatremia was found.

Aged↗
PubMed1979

Lack of fibrin formation in exercise-induced activation of coagulation.

Strenuous physical exercise leads to a significant shortening of blood clotting in various test systems. Such short times are also characteristic of those observed in sedentary patients with thrombosis or disseminated intravascular coagulation, and of those observed in experimental animals after thrombin infusion. The patients exhibit an increase in circulating fibrinopeptide A, which is attributed to thrombin action on circulating fibrinogen, and to an increase of fibrinogen degradation products, which is thought to indicate reactive fibrinolysis. To check whether physical exercise leads to fibrinemia, 10 healthy male volunteers were subjected to strenuous exercise on a bicycle ergometer. Blood samples were taken immediately before and on completion of the exercise period. Despite a significant shortening of the activated partial thromboplastin time, the thrombin time, and the Reptilase time, no increase of fibrinopeptide A could be demonstrated and the ethanol gelation test remained consistently negative. Simultaneously, the euglobulin lysis time was significantly shortened, whereas the fibrin(ogen) degradation products did not increase. The results indicate that the shortening of the coagulation times associated with physical exercise must be explained by mechanisms other than thrombin-mediated conversion of fibrinogen to fibrin.

Adult↗
PubMed1978

[Serum ferritin in renal insufficiency, hemodialysis and kidney transplantation].

87 patients with end-stage renal failure on long-term hemodialysis, 25 not on dialysis and 37 with renal transplants have been studied. Serum ferritin was measured by immunoradiometric and radioimmuno-assay. The correlation between the two methods was excellent (p less than 0.001). In 25 patients on long-term hemodialysis a good correlation was found between serum ferritin levels and stainable iron (p less than 0.001). All patients with adequate iron stores had serum ferritin levels above 60 ng/ml, whereas only one out of 10 with decreased or absent iron stores had a higher leve (118 ng/ml). According to these criteria the iron stores were decreased in 59% of our patients on long-term hemodialysis, decreased or adequate in 14% and adequate or increased in 27%. There was no correlation between serum ferritin levels and serum iron and total iron binding capacity. The distribution pattern of the serum ferritin levels was log normal and did not significantly differ in the three groups studied, although the patients with renal transplants had nearly normal hemoglobin and creatinine levels. Elevated serum ferritin levels in patients (21%) on hemodialysis could only partly be explained by repeated transfusions or chronic infections.

Adult↗
PubMed1978

[Missing thrombinemia in the so-called hypercoagulability following physical exertion (proceedings)].

A common topic of discussion for many years has been whether stress induces hypercoagulability and/or hyperfibrinolysis. Ten healthy volunteers were subjected to strenuous physical effort on a bicycle ergometer. Blood samples were collected 10 min before and immediately after exercise. The well-known activation of blood coagulation was demonstrated by significant shortening of the activated partial thromboplastin time, thrombin and reptilase times. However, no fibrinopeptide A (FPA) was generated, nor did the ethanol gelatin test turn positive. A significant shortening of the euglobulin lysis time was indicative of fibrinolysis but no fibrin(ogen) degradation products (FDP) could be detected. These results show that the so-called hypercoagulability is not accompanied by thrombin-mediated release of fibrinopeptide A, and suggest that the activation of coagulation does not involve fibrinogen to fibrin conversion.

Adult↗
PubMed1978

[Thrombin formation in factor IX concentrates and FEIBA (factor eight inhibitor bypassing activity) (proceedings)].

Having observed a marked increase of the fibrinopeptide A (FPA) level in vivo in 5 patients after the administration of factor IX concentrates, 8 factor IX concentrates (IX-K) and one FEIBA (factor eight inhibitor bypassing activity) fraction have been studied in vitro to ascertain whether thrombin was present or could be generated. Using fibrinogen as a substrate, the release of FPA under various conditions was measured by radioimmunoassay and it was found that (1) the addition of CaCl2 to the IX-K was necessary to produce FPA release; (2) the reaction was mainly dependent on the incubation time of the concentrate and the CaCl2 and (3) the release of FPA could be inhibited by heparin. The FEIBA fraction instantly produced FPA with or without the presence of CaCl2. It is therefore questioned whether the main effect of such products is due to a "factor II bypassing activity", i.e. thrombin.

Calcium Chloride↗
PubMed1977

[Biological significance of fibrinopeptide A elevation in the blood].

In 13 patients with effusions of varying etiology, considerably higher fibrinopeptide A (FPA) immunoreactivity were found in the effusions than in the corresponding plasmas. After instillation of heparin into the effusion the FPA concentration diminished significantly but very slowly. The difference in concentration between plasma and effusion therefore represents a relative FPA accumulation in the effusion. In view of its extremely short half-life in plasma, the FPA produced in the effusions is thought not to contribute to the increased plasma FPA levels. In addition, injection of amounts of FPA into the effusion such as to produce an acute increase of the local FPA level did not lead to a significant change in the FPA level in plasma.

Breast Neoplasms↗
PubMed1977

[Fibrinogen Zürich I: defective fibrinopeptide-A release].

Fibrinogen Zurich I (FZI) is characterized by delayed fibrin monomer aggregation. It has been previously shown that the patient fibrinogen is composed of two populations of molecules, one aggregating normally and the other not aggregating at all but interfering with the aggregation of the normal population. By use of a radioimmunoassay for fibrinopeptide A (FPA), only approximately half of the expected FPA could be recovered after thrombin and Defibrase proteolysis. Even after exhaustive proteolysis with 2 thrombin units of Defibrase, no further release of FPA could be obtained. The defective FPA release was confirmed by measurement of the N-terminal Gly/Tyr ratio. It may be assumed that the abnormal aggregation of one fraction of FZI is due to the defective FPA release from this fraction.

Batroxobin↗
PubMed1977

[Proximal ureteral atresia in childhood].

A rare cause of the congenital hydronephrosis is the proximal atresia of the ureter. With the help of 6 own cases morphology, clinic and therapy of this clinical picture are discussed. The differentiation from Wilms's tumour renders differential-diagnostic difficulties. It seems that a clinical description of this picture of a disease is hitherto not yet existing.

Child↗
PubMed1976

[Conformation of the fibrinogen molecule in solution: dynamic light scattering spectroscopy].

Human fibrinogen solutions were prepared either by filtration of ultracentrifugation. The sedimentation coefficient was S20,W = 7,9 S. The translational and the rotational diffusion coefficient DT and DR and the fraction of oligomers were determined using light beating spectroscopy. DT20,W was (2.03 +/- 1%) 10(-7)-cm2-sec-1, DR120,W = 40 000 +/- 10%-sec-1. The sedimentation coefficient and DT were strongly dependent on concentration. For pH values between 6.5 and 9.0, the diffusion coefficient DT at ionic strength greater than 0.2 was constant. The diffusion coefficient as measured by nanosecond fluorescence depolarization was DR//20,W = 1.6 x 10(6) sec-1. At a fibrinogen concentration of 2 mg/ml, these hydrodynamic data are compatible with an elongated molecule of 450 A length and an axial ratio of about 1:7.

Fibrinogen↗