bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Use of Modified Cells to Induce an Anti‐Rh Response
Authors: Gunson H. H. , Stratton F. , Phillips P. K. 
Published: March 2008

Summary Prior to their use for the primary immunization of Rh‐negative male volunteers, group O R2 R2 cells have been coated with complement and subjected to heat treatment. Eleven out of 12 men receiving complement‐coated cells developed a serologically detectable anti‐D after a single injection, but no antibodies could be detected in the sera of six volunteers receiving heated red cells. In association with doses of untreated cells and complement‐coated cells other volunteers were given small doses of anti‐D immunoglobulin. Although seven of eight men developed anti‐D when immunoglobulin was injected at the same time as the immunizing cells, there was no apparent enhancement based on the time of appearance of the antibody after immunization. In six men, anti‐D immunoglobulin was given 1 week before the injection of R2 R2 cells. None of these men developed anti‐D.Using these cells, the frequency of the immune response appears to be higher than in other studies on the primary immunization of male volunteers. However, not all the volunteers immunized in this series produced high titres of anti‐D after successive injections of Rh positive cells and the significance of this is discussed.
Factor X in Freeze‐dried Factor‐VIII Reference Plasma
Authors: Brozović M. , Gurd L. J. , Robertson I. , Bangham D. R. 
Published: March 2008

Summary. The activity and stability of factors X and VIII were studied in three ampouled preparations of freeze‐dried pooled human plasma.Factor‐X activity in all three preparations decreased on storage. It was calculated that after 10 yr at – 20°C, between 3% and 8% of the original factor‐X activity would be lost. If stored for the same period at 4°C and 20°C the loss could be up to 54% and 90% respectively of the initial activity. If, however, factor VIII was added to restore the concentration of this factor to approximately normal level, the proportion of factor X available for activation via the intrinsic pathway remained the same irrespective of the temperature and length of storage.Factor‐VIII activity was lost more readily. It was estimated that between 20% and 30% of the activity would be lost in each of the preparations kept at ‐ 20°C in 10 years. This is in good agreement with the results of the international collaborative study carried out to establish the international standard for factor VIII.
Interference of Lysed Fibrin with Coagulation: a Quantifying Approach Using Isotopic Techniques
Authors: Regoeczi E. 
Published: March 2008

Summary. Coagulation of plasma fibrinogen in the presence of fibrin degradation products was studied in rabbits treated with ancrod (Arvin), Two techniques were employed: the first, based on trace‐labelling of plasma samples with labelled fibrinogen in vitro, was to measure the degree to which solubilized fibrin inhibited coagulation; in the second, two differently labelled fibrinogens were used, one injected intravenously and the other added in vitro, by which estimation of fibrinogen in serum relative to the amount of circulating breakdown products was attempted.The first technique is considered to provide reliable information about the extent of defective coagulation, and hence the proportion of masked fibrinogen present in serum. Because of the difficulty in obtaining resolution between fibrinogen and its breakdown products in clots, the second technique is thought to be more suitable for comparative studies rather than for measurements in absolute terms.High doses of hydrocortisone administered to rabbits for several days prior to ancrod significantly reduced the speed of the dissolution of microclots. The data obtained are consistent with the hypothesis that the hormone interfered with fibrinolysis at the plasminogen activator level.
Studies on Christmas Disease: Investigation and Treatment of a Familial Acquired Inhibitor of Factor IX
Authors: George J. N. , Miller G. M. , Breckenridge R. T. 
Published: March 2008

Summary. A family is reported in which three of four members with Christmas disease have developed an inhibitor to factor IX. Studies of this inhibitor have demonstrated that it is an IgG antibody directed against the activated form of factor IX (IXa).There was no immunologically detectable factor‐IX‐like material in the affected family member without an inhibitor. This is consistent with previous postulates that inhibitors to factor IX would only develop in patients with Christmas disease who lack the factor‐IX antigen.One member of this family who had developed an inhibitor has been successfully managed through two dental procedures after transfusion with a factor‐IX concentrate.
Nervous Regulation of Factor‐VIII Levels in Man
Authors: Mannucci P. M. , Ruggeri Z. M. , Gagnatelli Giovanna 
Published: March 2008

Summary. Neurological procedures such as pneumoencephalography (PE), electro‐shock (ES), electrocoagulation (EC) of the ventrolateral thalamic nucleus, cerebral arteriography and myelography have been studied as experimental models in which to investigate in man the effect on plasma factor‐VIII levels of stresses applied to the CNS. A marked elevation of factor VIII followed PE and ES; the factor‐VIII levels showed some fluctuations over the period of experimental observation. The other coagulation factors were unchanged. A three‐fold increase of factor VIII was also observed after PE in a subject with mild haemophilia A. EC was followed by a significant rise of factor VIII, which was however much lower than after PE and ES. No significant change was produced by the other procedures.A number of experiments have been carried out to investigate the possibility that the observed increase might be artefactual.No evidence has been obtained that the rise measured with the bioassay results from some sort of activation or potentiation of the factor‐VIII molecule, rather than from a true molecular increase. It is suggested that the phenomenon is related to the stimulation by PE and ES of discrete neuronal structures regulating the plasma levels of factor VIII through a mechanism at present unknown.
Haemorrhagic Syndrome of Autoimmune Origin with a Specific Inhibitor against Fibrin Stabilizing Factor (Factor XIII)*
Authors: Lorand L. , Maldonado N. , Fradera J. , Atencio A. C. , Robertson B. , Urayama T. 
Published: March 2008

Summary. The biochemical defect in a patient suffering from very severe bleeding episodes was shown to be related to the presence of an inhibitor which specifically interfered only with the thrombin‐catalysed conversion of the fibrin stabilizing factor zymogen (factor XIII) into fibrinoligase, but had no effect on the transamidase activity of the latter enzyme. As such, it differed from other known inhibitors of the fibrin stabilizing factor system. Inhibition could be demonstrated against both human and bovine factor XIII.In terms of neutralizing equivalents, the patient's plasma contained about a tenfold excess of the inhibitor over the factor‐XIII content found in average normal plasma. This high potency was thought to be the reason for the patient's unresponsiveness to transfusions.Precipitation with ammonium sulphate, followed by chromatographic purification on DEAE‐cellulose, allowed recovery of the inhibitor in good yield in the ‘IgG immunoglobulin’ fraction. Since, prior to the onset of bleeding episodes at about 50 yr of age the patient received no transfusions, it could be assumed that the inhibitor was of autoimmune origin.Though the cause of the disease remains unknown, the question is raised whether previous treatment with isoniazid could be involved. Accidental modification of fibrin stabilizing factor by isoniazid could have provoked a breakdown of immunological tolerance against this component in the patient's plasma. Lorand et al (1972) have recently demonstrated the modification of proteins with isoniazid in enzymatic reactions.
Blood Clotting Activity of Reptilase and Bovine Thrombin in Vitro: A Comparative Study on Seven Different Species
Authors: Wik K. Ove , Tangen Oddvar , Mckenzie F. Neil 
Published: March 2008

Summary. The clotting activities of Reptilase and purified bovine thrombin towards platelet poor plasma from seven species and purified human and rabbit fibrinogen were studied. Bovine thrombin exhibited particularly low activity towards plasma from rat, guinea‐pig and cow compared with the other species tested. Reptilase showed a relatively larger species dependent variation in activity than thrombin, and rabbit plasma was particularly resistant to Reptilase action. This was due to a low activity of Reptilase towards rabbit fibrinogen and not to inhibition of Reptilase in rabbit plasma.The presence of 1% (w/v) dextran (70 000 mol wt) in the clotting mixtures significantly decreased both the thrombin and Reptilase clotting times in plasmas from all species.
Active and Inactive Factor VII in Dubin‐Johnson Syndrome with Factor‐VII Deficiency, Hereditary Factor‐VII Deficiency and on Coumadin Administration
Authors: Levanon M. , Rimon Sarah , Shani M. , Ramot B. , Goldberg Eugenie 
Published: March 2008

Summary. Factor VII was purified from a lyophilized powder of PTC complex (Hemoplex, Cutter Laboratories) and an antiserum was prepared in rabbits to the partially‐purified fraction. The antiserum was found to inhibit specifically factor VII of normal plasma and the activity of the purified factor‐VII preparation.Inactive factor‐VII‐like material was detected in the plasma of one out of nine patients with factor‐VII deficiency and the Dubin‐Johnson syndrome (DJS), as well as in the plasma of patients on short‐term Coumadin therapy.No inactive factor VII could be detected in the plasma of patients on prolonged Coumadin therapy or in the plasma of two patients with hereditary factor‐VII deficiency.The methodological problems are discussed.
Red‐Cell Abnormalities in HEMPAS (Hereditary Erythroblastic Multinuclearity with a Positive Acidified‐Serum Test)
Authors: Crookston J. H. , Crookston Marie C. , Rosse W. F. 
Published: March 2008

Summary. Abnormalities of the membrane of HEMPAS red cells have been demonstrated by certain serological tests and in freeze‐etch electron micrographs. There is also a marked increase in the activity of certain red‐cell enzymes.The positive acidified‐serum lysis test has proved useful in distinguishing HEMPAS from other kinds of hereditary dyserythropoietic anaemia. The greatly increased reactivity with anti‐i (although characteristic of HEMPAS) is a less specific finding, since enhancement of the i antigen is found in other dyserythropoietic anaemias, hereditary and acquired. Although the lysis of HEMPAS cells by acidified serum at first suggested that their membrane defect was similar to that present in PNH, further investigation showed that the mechanism of activation of complement is different in the two conditions. Lysis of HEMPAS cells depends on the binding of complement by a naturally‐occurring, cold antibody (“anti‐HEMPAS”) specific for an antigen present on HEMPAS cells, but not detectable on PNH or normal cells. Unlike PNH cells, HEMPAS cells are not lysed by complement in the absence of antibody.As judged by tests with anti‐I and human complement, PNH cells have a true increase in sensitivity to complement in that the binding of only a small number of complement sequences is sufficient to effect lysis. The increased lysis of HEMPAS cells by anti‐I appears to be due to the binding by antibody of many more complement sequences than are bound to PNH or normal cells. With some examples of anti‐I, an increased uptake of antibody by HEMPAS cells also contributes to their increased lysis.
Iron Absorption in Indians Studied, by Whole Body Counting: a Comparison of Iron Compounds Used in Salt Fortification
Authors: Narasinga Rao B. S. , Prasad Surendra , Apte Sharad V. 
Published: March 2008

SummaryFortification of common salt (NaCl) with iron has been suggested, for preventing iron deficiency anaemia in India. From a technological point of view three insoluble iron compounds: sodium iron pyrophosphate, ferric orthophosphate and ferric pyrophosphate have been considered suitable for this purpose. Absorption of iron from these compounds and ferrous sulphate was studied in 45 healthy male adult subjects employing 59Fe labelled salts and whole body counting. “When given alone, mean absorption of iron from ferric orthophosphate, sodium iron pryophos‐phate and ferric pyrophosphate were 8.3%, 6.3% and 0% respectively, while absorption from ferrous ascorbate was 30.6%. However, when administered with a meal of the type normally consumed in India, iron absorption from sodium iron pyrophosphate was unacceptably low, while that from ferrous sulphate was only 3.7%. It is concluded that these insoluble iron compounds are not acceptable for fortification of common salt from the point of view of availability of iron.
A Study of Storage Iron in the Placental and Foetal Tissues of the Rat
Authors: Kaufman Nathan , Wyllie John C. 
Published: March 2008

SummaryPart of the iron entering the placenta late in gestation is stored as ferri‐tin and haemosiderin; the function of placental storage iron is not known. 50–60% of foetal iron is found within storage compounds. There are relatively few studies of the foetal tissues responsible for the synthesis of storage iron‐protein.In order to investigate these aspects of iron metabolism we measured the quantity and concentration of ferritin and haemosiderin iron in the placental and foetal tissues of the rat during the latter part of gestation; the incorporation of 59Fe into these compounds was also investigated.Placental ferritin and haemosiderin iron reached peak values on day 17. A 40% decrease in the quantity of ferritin iron by day 19, without a corresponding change in placental weight, indicated mobilization of iron from placental ferritin; haemosiderin iron remained unchanged. On day 21 (parturition) both iron storage compounds again increased in quantity. The amounts of storage iron deposited in the allantoic placenta and yolk sac were similar until day 21 when the former tissue contained 75% of the total quantity. The concentration of ferritin iron was higher in the yolk sac on days 17 and 19.The major portion of foetal ferritin and haemosiderin was deposited late in gestation. The carcass and liver were the principal sites involved although small amounts were found in the spleen and gastrointestinal tract. The incorporation of 59Fe by ferritin and haemosiderin confirmed the results obtained by chemical analysis and also showed that there was a steady addition of iron to both compounds throughout the latter part of gestation.
Two Progressive Inhibitors of Factor Xa in Human Blood
Authors: Marciniak Ewa , Tsukamura Sumiko 
Published: March 2008

SummaryThe limited ability of human blood to inactivate human factor Xa was found to be markedly increased in human plasma and serum intensively absorbed by aluminium hydroxide. Using gel‐filtration analysis on Sephadex G‐200 it was demonstrated that the activity brought about by adsorption resides in the macro‐globulin fraction. This fraction, as obtained from nonabsorbed plasma or serum, has low antifactor‐Xa activity; it represents a progressive inhibitor of this enzyme, additional to antithrombin III. The increase of inhibitory activity due to adsorption is probably based on removal of a substance associated with macroglobulin in vivo, and on uncovering new binding sites for factor Xa. Whereas antithrombin III and the antifactor Xa of lower molecular size are probably represented by a single protease inhibitor which may be potentiated by heparin, the macroglobular anti‐factor Xa is not closely related to antithrombin activity and is unaffected by heparin.
The Role of Erythropoietin in Prenatal Erythropoiesis of Congenitally Anaemic Flexed‐tailed (f/f) Mice
Authors: Bateman A. E. , Cole R. J. , Regan T. , Tarbutt R. G. 
Published: March 2008

SummaryThe effects of the f gene on prenatal changes in liver cellularity, erythroid cell maturation, RNA, DNA, and haemoglobin synthesis, and sensitivity to erythropoietin have been investigated, f/f foetuses are smaller than f/+ but still develop a progressive deficiency in haemoglobin content/unit weight of tissue, which is 40% of normal at birth. Early f/f livers contain fewer erythroblasts, maximum numbers are reached later, and changes in relative proportions of early and late erythroblasts are retarded. Erythroid tissue and erythropoietin responsive cells persist longer in f/f than in f/+ livers. Erythropoietin induced RNA and DNA synthesis is higher in f/f than in f/+ foetal liver cell cultures. Erythropoietin causes multiphasic increments in haem synthesis in vitro. Maximum levels of synthesis by 13 day liver cells are reached later f/f but over 36 hr similar amounts are accumulated. Erythropoietin maintains the presence of early erythroid cells in both f/f and f/+ foetal liver cultures, and enhances the production of polychromatic cells.Circulating f/f foetal reticulocytes have a reduced capacity to utilize exogenous iron for haem synthesis. The deficient haemoglobin content of f/f foetuses could be caused by this abnormality and by reductions in erythroid precursor cell numbers. The reticulocyte abnormality may be a direct or indirect consequence of a failure of erythroid colonization of the foetal liver, and of the effects of secondary compensation for this failure.
Autoantibodies of U Blood Group Specificity in Autoimmune Haemolytic Anaemia
Authors: Marsh W. L. , Reid Mawon E. , Scott E. Patricia 
Published: March 2008

SummaryAutoantibody specificity in acquired haemolytic anaemia of the warm antibody type has been thought to be directed against Rh antigens or the precursors from which they arise. In many cases Rhnull red cells fail to react with these antibodies, providing apparent support for the assumption that they have Rh specificity. Rhnull red cells are also non‐reactive with anti‐U sera, and in addition have abnormal S and s antigens. We have studied 50 cases of warm antibody autoimmune haemolytic anaemia looking particularly for possible U, S or s blood group specificity of the causative antibodies. In the majority of cases the antibodies were found to be directed against antigens of the Rh complex, but in three cases multi‐specific autoantibodies were shown to have complex specificity involving the Rh and U blood groups.
Defective Erythrocyte Pyruvate Kinase with Impaired Kinetics and Reduced Optimal Activity
Authors: Paglia Donald E. , Valentine William N. , Rucknagel Donald L. , Wittenberg Julie 
Published: March 2008

SummaryA unique mutant form of erythrocyte pyruvate kinase has been found associated with chronic haemolytic anaemia in a child who is apparently doubly heterozygous for the mutant isoenzyme and for pyruvate kinase deficiency of the classical quantitative type. Clinical and laboratory findings conformed closely to those typically observed in homozygous pyruvate kinase deficiency anaemia. Assayed in fresh haemolysates, the isoenzyme exhibited reduced optimal activity (c 45% of normal) and an increased Michaelis constant for phosphoenolpyruvate (four to five times greater than normal). The kinetic anomaly was only partially corrected by activation with fructose‐1,6‐disphosphate. Despite some common characteristics, this isoenzyme appears distinct from others reported in the literature and lends support to the polymorphous nature of heritable baemolytic anaemias secondary to defective pyruvate kinase.
Apparent Paradoxical Patterns of Anaerobic Glycolysis and Hexokinase Activity in the Red Blood Cells of Acutely Bled Rats, with Evidence that the Responses were in Part Hormone‐Dependent
Authors: Sabine Jean C. 
Published: March 2008

Summary. Rats were bled of c 25% of their blood volume, and anaerobic glycolysis (AG) and hexokinase activity (HxK) were assayed in the red blood cells. After 2–14 days the animals were sacrificed and AG and HxK again assayed. Four different responses were observed: (1) both parameters were elevated following blood loss in only four out of 87 intact males, as expected if increased proportions of normal young red cells are present; (2) both parameters were decreased in six animals. In the majority, two paradoxical patterns were found; (3) increased AG with decreased HxK; and (4) decreased AG with increased HxK. Response 3 was found only in immature animals, and Response 4 in animals at or beyond the minimal breeding age of 12 weeks. Results in castrated males and adult females were indistinguishable from each other and from those in immature males. In testosterone‐treated females the response was modified toward but not converted to Response 4.It is proposed that Response 3 was probably independent of sex hormones. but was converted to Response 4 when a full complement of male hormones was present. Whatever the underlying mechanism, the finding of four distinct respenses indicates that, in terms of the two parameters assayed in this investigation, there was no entity which could be termed a ‘stress reticulocyte’. There is a strong likelihood that factors not detectable by the methods used were responsible for the paradoxical findings.
Monocyte Kinetic Studies in Normal and Disease States
Authors: Meuret G. , Hoffmann G. 
Published: March 2008

Summary. Monocyte kinetics were studied in eight normal subjects and 27 patients suffering from various diseases: acute, subacute and chronic infections, malignant tumours, Boeck's sarcoid, neutropenia, and diseases associated with chronic exanthemata or splenomegaly. Autotransfusion of blood cells labelled with 3H‐diisopropylfluorophosphate in vitro was carried out and the fate of these cells in vivo was followed by autoradiographs of leucocyte concentrates prepared from venous samples.Within a few minutes the transfused monocytes equilibrated with the total blood monocyte pool (TBMP). As TBMP proved to be larger than the circulating monocyte pool (CMP), the existence of a marginal monocyte pool (MMP) was postulated. In normal subjects the CMP:MMP ratio averaged 1:3.5. Moderate deviations occurred in disease states. Monocytes left the vascular system at an exponential rate, the mean normal T4 being 8.4 hr. Slight prolongation of T4 was observed in some patients with monocytosis, the maximal values reaching 15 hr. Shortened T4 was found in one patient with acute infection (4.0 hr) and in another with gross splenomegaly (3.5 hr). The monocyte turnover rate (MTR) in normal subjects averaged 6 × 108 monocytes/hr or 7 × 106 monocytes/hr/kg. Highly significant positive correlations were evaluated between the blood monocyte count and TBMP or MTR respectively.
Effect of Alpha‐ and Beta‐blocking Drugs on the Clotting and Fibrinolytic Response to Venous Stasis in Man
Authors: Ponari O. , Civardi E. , Megha A. , Pini M. , Potì R. , Dettori A. G. 
Published: March 2008

Summary. The changes in coagulability and in fibrinolytic activity induced in local blood by venous stasis in man are not prevented by blocking of alpha‐ and beta‐adrenergic receptors.Administration of l‐propranolol and of l‐propranolol plus phentolamine in adequate doses just before the execution of a tourniquet test failed to inhibit the major changes, i.e. rise in factor‐VIII level, shortening of partial thromboplastin time (PTT) and euglobulin lysis time (ELT), hypercoagulable pattern on thromboelastogram, following venous stasis. Some other clotting tests remained unchanged in all experimental conditions.Physiopathological implications of these results are discussed, taking into account the possible role of the adrenergic system in the control of a postulated equilibrium between blood coagulation and fibrinolysis.