bluuebunny/crossref_metadata_2025_split huggingface dataset:
Leucocyte Alkaline Phosphatase as a Marker of Cell Maturity: a Quantitative Cytochemical and Autoradiographic Study
Authors: Williams D. M. 
Published: March 2008

Summary.A sensitive and reproducible cytochemical technique for the demonstration of leucocyte alkaline phosphatase (LAP) has been evaluated. It produces a stable reaction product which can be readily quantified microphotometrically. In the circulating neutrophil polymorphonuclear leucocytes of rats the mean LAP levels measured in this way fluctuated only slightly from day to day. A highly significant correlation was demonstrated between LAP levels of neutrophils and their age, determined by isotope labelling with tritiated thymidine and by nuclear morphology. The correlation between the age of neutrophils and the complexity of their nuclear morphology has also been confirmed. The technique provides a useful tool for the study of leucocyte kinetics in disease states.
Procoagulant Activity of Platelets in Recalcified Plasma
Authors: Vecchione Jack , Zucker Marjorie B. 
Published: March 2008

Summary.High‐spun platelet‐poor plasma (HSPPP) and platelet‐rich plasma (PRP), prepared with minimal contact activation and pH shifts, were recalcified with little dilution in the presence of phospholipid prepared from chloroform‐extracted, acetone‐dried brain tissue. The clotting times of HSPPP and PRP were the same whether or not the platelets in PRP were first incubated or aggregated with ADP or with collagen. This suggests that platelet procoagulant activity in normal recalcified plasma derives only from provision of platelet phospholipid.
T and B Cells in Myelomatosis
Authors: Jones Susan V. , McFarlane H. 
Published: March 2008

Summary.The majority of treated patients with myelomatosis had a significantly decreased number of T cells as measured by both lymphocyte stimulation to phytohaemagglutinin (PHA) and by their ability to form spontaneous rosettes with sheep red blood cells (SRBC). Seven untreated patients also had markedly depressed T cells. On the other hand, B‐cell numbers were significantly increased in the majority of the patients as judged by increased lymphocyte stimulation to pokeweed mitogen (PWM) and the markedly increased numbers of rosettes that were formed with antibody‐coated complement activated SRBC, as well as by immunofluo‐rescence cell markers to monospecific immunoglobulin antiserum.
Enzyme Abnormalities in Red Cells
Authors: Valentine William N. 
Published: March 2008

Summary.Hereditary deficiencies involving eight enzymes of the Embden‐Meyer‐hof pathway, at least five involving the hexosemonophosphate shunt, and GSH metabolism, and at least two involving nucleotide metabolism, are known to be associated with haemolytic syndromes in man. Lactate dehydrogenase deficiency is also recognized, but is not associated with haemolysis. In addition, markedly aberrant enzyme activity ratios characterize a variety of dyserythropoietic disorders, both hereditary and acquired. In some disorders, haemolysis is the sole clinical manifestation; in others, dysfunction of the nervous system, the heart, the skeletal muscle, and the leucocytes may occur. The red cell may also mirror enzymopathies having expression in non‐haematopoietic tissues without a haemolytic syndrome being present. While double heterozygosity for two separate enzymopathies or for an enzymopathy and hereditary spherocytosis or elliptocytosis is recognized in a number of cases, clinical manifestations have thus far appeared minimal or non‐existent. In a recently described haemolytic syndrome uniquely large accumulations of cytidine and uridine nucleotides have been noted secondary to a severe deficiency of a pyrimidine specific 5’nucleotidase.
Autoimmune Haemolytic Anaemia in New Zealand Black Mice
Authors: East June , Harvey Jennifer J. 
Published: March 2008

Summary.Mice of the NZB strain spontaneously develop autoimmune haemolytic anaemia and reticulum cell neoplasms, and they harbour murine leukaemia virus. This triad of autoimmunity, malignancy, and virus infection is explored in experiments designed to show how the autoimmune haemolytic disease and/or the virus are transmitted to NZB hybrids derived naturally, by ovum transplantation, and from allophenic parents. Possible cellular mechanisms for the autoimmune process are reviewed, and evidence for a genetic, hormonal, or viral aetiology of autoimmune haemolytic anaemia is discussed.
Regulation of Erythropoiesis and its Defects
Authors: Peschle C. 
Published: March 2008

Summary.A concise review of recent advances in studies of mechanisms controlling the rate of erythropoiesis, including some original results, is presented. The first and second sections are focused on erythropoietin (Ep) and the erythroid stem cell respectively. In the third one, clinical conditions caused by a defect in the regulation of erythropoiesis are discussed.
Immunopathology of Immunocytomas
Authors: Drivsholm Aage 
Published: March 2008

Summary.Immunocytomas are defined as disorders in the B‐lymphocyte series, characterized by production of an M‐component. After a basic description of the immunoglobulin molecule and the development of the cellular immune system by which it is built up, the production of M‐components is discussed in relation to possible aetiology and pathogenesis. The turn‐over of M‐components is mentioned, especially on the basis of the studies of Salmon and colleagues (Salmon, 1973) with reference to the different types of M‐components and to cellular aspects. The production of interferon and osteoclast activating factor is touched on, and a brief review is given of the most common clinical features of malignant immunocytomas. Finally, the interrelationship of the different manifestations of immunocytomas is described on the basis of the hypothesis put forward by Salmon & Seligmann (1974).
Red Cell Destruction in Vivo by Low Concentrations of IgG Anti‐A
Authors: Romano E. L. , Mollison P. L. 
Published: March 2008

Summary. Red cells coated with as little as 0.3–0.5 μg anti‐A/ml cells were found to agglutinate if mixed with plasma and rocked on a tile, whereas the minimum amount of IgG anti‐Rh required for agglutination under these conditions was about 50 μg antibody/ml cells. Complement binding by red cells coated with IgG anti‐A could be demonstrated only when the amount of antibody on the cells was at least 14 μg antibody/ml cells. Since in ABO haemolytic disease the amount of antibody on the cells is frequently less than 0.6 μg/ml cells, it seems that red cell destruction in this syndrome is not due to the activation of complement but may be due to the sequestration of agglutinated cells.A few experiments are described in which the survival in vivo of small amounts of agglutinated cells was studied. Reasons are given for considering that such experiments fail to mimic the conditions prevailing in ABO haemolytic disease.
Changes in Blood Catecholamine Levels and. Blood Coagulation and Fibrinolytic Activity in Response to Graded Exercise in Man
Authors: Hawkey C. M. , Britton B. J. , Wood W. G. , Peele M. , Irving M. H. 
Published: March 2008

Summary. Measurements of catecholamines, fibrinogen, factor VIII, thrombelastography, cuglobulin lysis time and platelet adhesiveness have been carried out on venous blood obtained from normal males exposed to exercise on a bicycle ergometer at various work loads.Significant increases in adrenaline, factor VIII and fibrinogen were found only after exercise to exhaustion at 1500 kpm min−1 whereas the euglobulin lysis time was inversely proportional to the exercise load. There was no change in platelet adhesiveness. These findings support the results of studies using adrenaline infusions or adrenergic blockade which suggest that stress‐induced increases in factor VIII are mediated via adrenergic stimulation but that activation of fibrinolysis is not dependent on adrenaline.
Methods of Evaluating the Sequestration Site of Red Cells Labelled with 5ICr: a Review of 96 Cases
Authors: Najean Y. , Cacchione R. , Dresch C. , Rain J. D. 
Published: March 2008

Summary. The technical conditions for surface counting and the methods for calculating splenic and liver sequestration after injection of51 Cr‐labelled cells were studied in 96 patients. A comparative study of different sites of positioning of the detection probes leads us to recommend the mid‐line at the third intercostal space for the precordial area, the point of maximum count‐rate obtained at each measurement for the splenic area, with the patient in right lateral decubitus position and the probe vertical, and a point situated on the midclavicular line 4 cm above the right costal margin for the liver area.A comparative study of different methods of calculation leads us to recommend the method known as ‘excess counts’, but with a correction of the gross values based on the evolution of circulating radioactivity and not of the count‐rate measured over the precordial area. Measurement of urinary excretion of radioactivity showed that only a minor part was due to the loss of the tracer from the sequestration sites, and that the level varied only slightly between subjects. Thus the loss of tracer does not interfere with the interpretation of external counting data.Much of the disagreement regarding interpretation of the results of external counting in clinical practice is due to technical problems. Standardization of techniques of measurement and interpretation of results, selecting those which this study indicates as the most reliable, would permit better exchange of information between laboratories and clearer conclusions as to the practical use of surface counting.
The von Willebrand Syndrome
Authors: Stableforth Penelope , Hughes Jane , Wilson Elaine , Dormandy Katharine M. 
Published: March 2008

Summary. Five patients with an original diagnosis of von Willebrand's disease are described because their levels of factor VIII related protein, Ristocetin‐induced platelet aggregation and/or family studies differed from the main group of patients with classical von Willebrand's disease. Two had normal levels of factor VIII related protein with reduced Ristocetin aggregation when this was tested in platelet rich plasma. In one, however, this was due to a plasma defect and in the other to a platelet abnormality. After cryoprecipitate infusion all abnormal tests were corrected in both these patients. The first patient, however, failed to show a secondary rise of factor VIII whereas the second showed a secondary rise of both factor VIII and of factor VIII related protein. The other three cases, who were all very severely affected, have been separated from the main group as none of their families was segregating for classical von Willebrand's disease.It is suggested that the term von Willebrand's disease should be confined to those patients who have reduced factor VIII related protein and Ristocetin aggregation, and that von Willebrand's syndrome should be used for the various sub‐groups that are emerging.
Measurement of the Mean Cell Volume using Electronic Particle Counters
Authors: England J. M. , Down M. C. 
Published: March 2008

Under carefully controlled conditions electronic cell counters, for example the Coulter Counter, Model FN, and Channelyzcr, may be calibrated to give MCV values down to as small as 20 fl which agree with those derived from the centrifugation PCV (corrected for plasma trapping) and the red cell count.The MCV values will be too high if the instrument uses a high cell concentration, has a fixed lower threshold, no effective upper threshold and no edit facility. This may partly explain why the Coulter Counter, Model S, when standardized with 4C cell control gives higher MCV values than the Model FN linked to the Channelyzer. The difference is, on average, 2 fl with normal blood samples and 5 fl in cases of microcytic anaemia. It is suggested that standards of low MCV should be used together with those of normal MCV when calibrating the Model S.
Relation between the Inhibition of Aggregation and the Concentration of cAMP in Human and Rat Platelets
Authors: Michel Huguette , Caen J. P. , Born G. V. R. , Miller R. , DAuriac Ghislaine Angles , Meyer P. 
Published: March 2008

Summary.Adenosine inhibits the aggregation of human but not of rat platelets whereas both are inhibited by prostaglandin E1 or by the pyrimido‐pyrimidine compound RA233. In human platelets all three agents increase adenosine‐3′,5′‐cyclic monophosphate (cAMP). If the inhibition of aggregation depended on this increase, adenosine might be expected not to increase cAMP in rat platelets. Under conditions in which adenosine inhibited aggregation and increased cAMP in human platelets, adenosine caused a similar increase in cAMP in rat platelets without inhibiting their aggregation. The aggregation of rat platelets was inhibited as effectively as that of human platelets by PGE1 or RA233 at concentrations which caused greater increases in cAMP than did the highest concentrations (2.8 × 10‐4m) of adenosine it was possible to use. When the increase of cAMP in rat platelets by PGE1 was limited to that produced by adenosine, PGE1 like adenosine failed to inhibit aggregation. Therefore, the difference in the inhibitory effectiveness of adenosine on rat and human platelets was quantitative rather than qualitative and apparently depended on the inability of adenosine to increase cAMP sufficiently in rat platelets. When cAMP had been increased by adenosine, PGE1 or RA233, the addition of ADP caused cAMP to decrease rapidly in both human and rat platelets to between +22 and 18% of control values, except that the decrease in rat platelets was to +40% after RA233 had been present for 0.5 min before ADP. The increase in cAMP produced in rat platelets by adenosine at 5 × 10‐6 to 2.8 × 10‐4m for 3 min was associated with a small increase in aggregation velocity. It is suggested that the comparative ineffectiveness of adenosine as an inhibitor of platelet aggregation, particularly with rat but less so also with human platelets, is because, unlike PGE1 or RA233, adenosine has two opposing actions on aggregation; one being inhibition by activating adenylate cyclase and increasing cAMP, and the other being potentiation by uptake. This hypothesis accounts for the present results as well as for the earlier observation that dipyridamole which prevents the uptake of adenosine potentiates its inhibitory effect on the aggregation of human platelets.
A Standardized Bioassay for Platelet Factor 3 Released by Kaolin
Authors: Pérez‐Requejo J. L. 
Published: March 2008

Summary.The test for platelet factor 3 described by Hardisty & Hutton (1975) has been modified to conform to the usual design for a parallel‐line bioassay. Manchester Comparative Thromboplastin has been used as assay Standard, allowing an arbitrary unit of activity to be adopted. However, experiments suggested that the platelet activity measured was different from tissue factor activity. Platelets are tested as platelet‐rich plasma diluted in a standardized mixture of plasma and fibrinogen, so that differences between the clotting factors of the test samples are eliminated, as verified by experiments on haemophiliacs and patients on anticoagulant treatment. Sonication and repeated freezing and thawing of platelet‐rich plasma showed that approximately 15% of the PF3 is released by kaolin. In vivo, a single dose of 600 mg of aspirin reduced the PF3‐release to half the previous value in 2 h; initial values were regained in 5–8 days.
In Vivo Behaviour of Homologous Urea‐Soluble 131I‐Fibrin and 125I‐Fibrinogen in Rabbits: the Effect of Fibrinolysis Inhibition
Authors: Müller‐Berghaus G. , Mahn I. , Köveker G. , Maul F.‐D. 
Published: March 2008

Summary.The in vivo behaviour of urea‐soluble fibrin monomer (FM) was compared with that of fibrinogen in rabbits. Purified rabbit 125I‐fibrinogen was injected into 36 unanaesthetized rabbits. Three days later the rabbits received either purified rabbit 131I‐FM 1 mg/kg body weight, which corresponds to c 1% of the circulating plasma fibrinogen pool or 131I‐fibrinogen, or buffered urea only. The distribution volume of FM was 43.4±6.9 ml/kg and of fibrinogen 43.5±7.7 ml/kg (mean±SD). The elimination curve of urea‐soluble FM as represented by the clottable 131I‐radioactivity, plotted on a semi‐logarithmic paper, consisted of an initial steep decay within the first 6 h and a slow flattening of the slope 6 to 24 h after injection of FM. Although a terminal single‐exponential slope, as observed in fibrinogen elimination, could not be computed for the 24 h following FM injection the mean half‐life time of the last segment of the clottable‐radioactivity curve, between 12 h and 24 h, was 12 h. Within 24 h a mean of 83.5% of the injected FM were removed from the circulating blood. The elimination characteristics of fibrinogen were not influenced by the injected FM. Control experiments showed that buffered 3.0 M urea, the solvent of FM, does not influence distribution volume and elimination of 125I‐fibrinogen. The distribution of 131I as well as 125I‐radioactivities in organs representing FM and fibrinogen respectively did not differ from each other. Elevated levels of 131I‐radioactivity, however, were found in the urine after FM injection suggesting an accelerated elimination of FM in comparison to fibrinogen. Fibrinolysis inhibition with high doses of aprotinin did not significantly reduce the urinary excretion of 131I‐radioactivity representing breakdown of FM. Furthermore, inhibition of the fibrinolytic system had no influence on the elimination characteristics of either fibrinogen or FM. In order to explain the results obtained in this study the following theory is proposed. Intravenously injected FM forms complexes with fibrinogen and fibrinolytic degradation products. The complexes continuously increase in size until they dissociate into fibrin oligomers and carrier proteins. The oligomers are eliminated whereas the carrier proteins recycle.
Evidence for Rapid Loss of Newly Synthesized Haemoglobin S Molecules in Sickle Cell Anaemia and Sickle Cell Trait
Authors: Desimone J. , Adams J. G. , Shaeffer J. 
Published: March 2008

The present study indicates that newly completed haemoglobin S molecules rather than free βS‐chains are preferentially bound to the reticulocyte stroma of individuals with sickle cell trait and sickle cell anaemia. Reticulocytes from individuals with HbAA, AS and SS were incubated with [3H]leucine from 1.25 min to 120 min. Unlike the stroma‐free haemolysates, the stroma of all individuals contained an excess of labelled β‐chains relative to α‐chains after short incubation times. In haemoglobin AA and AS individuals, the stromal βA radioactivity was 1–2% of the total cellular βA radioactivity. In haemoglobin AS and SS individuals, the stromal βS radioactivity was 3–5% and 10–20% of the total cellular βS radioactivity, respectively. All of the stroma β‐chain radioactivity was associated with completed haemoglobin molecules. Because of the unlabelled free α‐chain pool found in reticulocytes, after short incubation times newly completed haemoglobin molecules have predominantly labelled β‐chains and unlabelled α‐chains. These findings suggest that part of the discrepancy between the stroma and stroma‐free haemolysate α/β radioactivities seen in HbAS and HbSS individuals may result from normal labelling kinetics.A pulse chase experiment performed on an individual with HbSS revealed that completed HbS molecules, in addition to being associated with the stroma, were lost from the cell.
A Circadian Variation of Melphalan (L‐Phenylalanine Nitrogen Mustard) Toxicity to Murine Bone Marrow: Relevance to Cancer Treatment Protocols
Authors: Simpson H. W. , Stoney P. J. 
Published: March 2008

The toxicity of Melphalan to murine bone marrow was assessed by automated Coulter counts of femoral marrow nucleated cells. A significant dose‐response slope (P0.001) was shown and also a significant variation along the 24 h scale. With food available ad libitum and light from 06.00 to 18.00 hours, the minimum marrow depression occurred around 16.00 hours. Extrapolating these findings to human chemotherapy it would appear that prescription of the drug during the early part of the activity span (usually breakfast) will minimize marrow depression. This differs from a human study in which Melphalan was given at ‘bedtime’as an adjuvant to mastectomy in breast carcinoma and in which there was leucopenia at some stage of treatment in all 103 patients.It is recommended that in future cancer therapy protocols test for circadian variability of white cell depression by varying treatment times systematically along the 24 h scale.
Haematological Changes Associated with the McLeod Phenotype of the Kell Blood Group System
Authors: Wimer B. M. , Marsh W. L. , Taswell H. F. , Galey W. R. 
Published: March 2008

The McLeod phenotype is inherited as an X‐linked characteristic. The red cells have weak antigenicity in the Kell blood group and lack Kx, a precursorlike substance that appears to be necessary for proper biosynthesis of Kell antigens. Kx antigen is also required for establishment of normal cell morphology. Absence of Kx antigen causes a membrane abnormality, in which the most prominent feature is acanthocytosis, and a compensated haemolytic state.The X‐linked gene that determines normal Kx production is called X1 k. Inheritance of a variant allele at the Xk locus is responsible for lack of Kx synthesis and the McLeod phenotype. The Xk locus is inactivated by the Lyon effect, and female carriers of the variant gene exhibit blood group mosaicism in the Kell system and have a dual red cell population of acanthocytes and discocytes.
Differentiation Linked Expression of p28,33 (Ia‐like) Structures on Human Leukaemic Cells
Authors: Janossy George , Goldstone Antony H. , Capellaro David , Greaves Melvyn F. , Kulenkampff Jörg , Pippard Martin , Welsh Ken 
Published: March 2008

Summary. A differentiation linked expression of ‘Ia‐like’ (B cell associated) structures was detected by heterologous antisera against p28,33 antigen on human leukaemic cells in immunofluorescence test. A double fluorochrome immunofluorescence test was used to distinguish Ia+ (p28,33, +) leukaemic cells from B lymphocytes. Leukaemic cells with varying intensities of anti‐p28,33 staining were separated using the Fluorescence Activated Cell Sorter. The results indicate that p28,33 is very strongly expressed on undifferentiated blast cells from Philadelphia chromosome (Ph1) positive ‘lymphoid’ blast crisis and non‐T,non‐B acute lymphoid leukaemia. In Ph1 positive myeloid blast crisis and in acute myeloid leukaemia the p28,33 antigen was only moderately strongly expressed on myeloblasts and virtually absent on promyelocytes. The p28,33 antigen was also absent on the relatively more mature cells during the chronic phase of chronic myeloid leukaemia. Non‐leukaemic samples such as bone marrow samples from fetus, and from patients with severe megaloblastic anaemia or myeloid hyperplasia (due to hypersplenism in Felty syndrome) were also found to contain p28,33 positive (and membrane immunoglobulin negative) immature blast cells.On the basis of these observations the hypothesis is proposed that ‘Ia‐like’ antigens on leukaemic cells reflect the origin of these leukaemias from haemopoietic stem cells which are themselves Ia positive. The corollary of this view is that ‘Ia‐like’ membrane structures may play an important role not only in immunological responses of B cell, but also in the regulation of early haemopoietic cell differentiation.