bluuebunny/crossref_metadata_2025_split huggingface dataset:
Guanidinosuccinic Acid on Human Platelet Effects of Exogenous Urea, Creatinine, and Aggregation In Vitro
Authors: Davis James W. , McField James R. , Phillips Phyllis E. , Graham Barbara A. 
Published: October 2019

Abstract
Patients with severe uremia may have a bleeding tendency associated with a prolonged bleeding time and an adequate platelet count. We have tested the effects on platelet aggregation of three compounds that are found in increased concentration in the blood of patients with renal failure. The addition of urea was followed by an immediate, but transient, increase in optical density of platelet-rich plasma. This precluded the use of turbidimetric techniques for the measurement of platelet aggregation after addition of urea, until the optical density became stable. Adenosine diphosphate-, collagen-, and norepinephrine-induced platelet aggregation were shown to be inhibited 1 hr after urea was added to platelet-rich plasma to produce urea nitrogen increments of 100-300 mg/ 100 ml. Increasing concentrations of creatinine by 10 or 20 mg/100 ml did not inhibit platelet aggregation. Guanidinosuccinic acid, in a concentration in the range found in uremic plasma, also had no effect on platelet aggregation. Through inhibition of platelet aggregation, elevated blood concentrations of urea may be one of the causes of the bleeding tendency of uremic platients.
Congenital Methemoglobinemia: The Result of Age-dependent Decay of Methemoglobin Reductase
Authors: Feig Stephen A. , Nathan David G. , Gerald Park S. , Zarkowski Harold S. 
Published: October 2019

Abstract
Methemoglobin reductase activity (MHR), measured by the Hegesh assay, decreases as normal red cells age. This probably accounts for the slighlty increased concentration of methemoglobin in older red cells. Exaggeration of normal MHR age lability was demonstrated in several individuals with various molecular abnormalities of NADH-diaphorase and was associated with more striking accumulation of methemoglobin in the older red cells of those patients. Diaphorase activity, measured by the Scott assay, does not exhibit age lability in normal red cells or the cells of affected patients. While diaphorase uses either NADH or NADPH as a cofactor, methemoglobin reductase requires NADH. Methemoglobin reductase is found in hemolysates but not in membrane preparations, while approximately 1% of total red cell NADH-diaphorase activity is membrane-associated. The specific activity of NADH-diaphorase is approximately 60 times greater than that of methemoglobin reductase. Whether the two activities represent distinct enzyme proteins or differing substrate affinities of the same enzyme awaits adaptation of the Hegesh assay to enzyme electrophoresis.
Glucose-metabolizing Enzymes of the Mouse Erythrocyte: Activity Changes During Stress Erythropoiesis
Authors: Hutton John J. 
Published: October 2019

Abstract
Many features of normal and abnormal erythropoiesis have been described in the inbred mouse, but no systematic studies of enzymatic activities in mouse erythrocytes have been reported. The activities of 14 enzymes of glycolysis and the hexose monophosphate shunt have been measured in mouse erythrocytes formed under normal conditions and during hemopoietic stress induced by phenylhydrazine treatment. The responses of inbred strains A/J and C57L/J were compared. In normal cells of each strain the activity of hexokinase was lowest, that of triosephosphate isomerase the highest, and the rank order of other enzymatic activities in the mouse was similar to that reported for the human erythrocyte. All enzymatic activities increased during the reticulocytosis accompanying stress erythropoiesis, with phosphofructokinase, aldolase, phosphoglycerate mutase, and glucose 6-phosphate dehydrogenase (G6-PD) showing the greatest relative elevations. Enzymatic activities declined rapidly during the 2-wk period following the initial reticulocytosis, suggesting that large numbers of immature erythrocytes with high enzymatic activities and shortened life spans had been produced during the response to erythropoietic stress. In normal hemolysates heated at 50°C, the most labile enzymes were glucose 6-phosphate dehydrogenase, enolase, and glyceraldehyde phosphate dehydrogenase. In the presence of erythrocyte stromata, glucose 6-phosphate dehydrogenase was more thermolabile in hemolysates of strain C57L/J than in those of A/J. This difference correlates both with the markedly lower activity of G6-PD in normal erythrocytes of C57L/J mice compared to erythrocytes of A/J mice and with the more rapid decrease in G6-PD dehydrogenase activity in aging erythrocytes of C57L/J.
Endotoxin Stimulation in Patients With Lymphoma: Correlation With the Myelosuppressive Effects of Alkylating Agents
Authors: DeConti Ronald C. , Kaplan Stephen R. , Calabresi Paul 
Published: October 2019

Abstract
Estimates of the bone marrow granulocyte reserve were made in 97 patients with lymphoma utilizing the endotoxin Pyrexal. Normal granulocyte responses were observed in most patients who had not received prior myelosuppressive therapy. Patients with lymphosarcoma responded as well as those with Hodgkin’s Disease. All patients with leukopenia due to previous therapy or marrow infiltration failed to respond. In the absence of leukopenia only 47% of previously treated patients achieved normal responses. The severity of granulocytopenia produced by intravenous alkylating agent therapy was correlated with pretreatment Pyrexal responses. Patients with normal granulocyte reserves, as demonstrated by this test, tolerated subsequent chemotherapy with significantly less severe granulocytopenia (p <0.02) than patients with abnormal test responses. Nadir granulocyte values below 1000 cells/cu mm developed in 7 of 33 patients with normal Pyrexal responses and in 11 of 15 abnormal responders, despite comparable pretreatment granulocyte values.
Factor IX Deficiency and Bleeding in a Patient With Sheehan’s Syndrome
Authors: Brown Clarence H. , Kvols Larry K. , Hsu Tah-Hsiung , Levin Jack 
Published: October 2019

Abstract
Factor IX deficiency was associated with a hemorrhagic disorder in a woman who previously had experienced postpartum hypotension resulting in Sheehan’s syndrome. There was no family history of Christmas disease, and other known causes of factor IX deficiency were excluded. Plasma levels of factor IX were partially corrected by therapy with thyroid hormones and completely restored to normal by the administration of cortisone. The response of factor IX to plasma infusion resembled the response of factor VIII in patients with von Willebrand’s disease who receive plasma. Normal hemostasis and levels of factor IX have been maintained by the administration of physiologic dosages of thyroid and adrenal hormones. Blood coagulation was studied in several other patients with pituitary or thyroid dysfunction. All were normal, indicating that this patient represents an unusual example of the effects of an endocrine dysfunction on a single blood coagulation factor.
Studies on Human Erythrocyte Nucleotide Metabolism. I. Monisotopic Methodologies
Authors: Valentine William N. , Kürschner Klaus K. 
Published: October 2019

Abstract
Methods were developed to assay the activities of ribosephosphate pyrophosphokinase (RPK, PRPP synthetase, E.C. 2.7.6.1) and adenine phosphoribosyltransferase (APRT, AMP pyrophosphorylase, E.C. 2.4.2.7) in hemolysates of human erythrocytes. RPK activity was determined by measuring the production of phosphoribosyl pyrophosphate (PRPP) and the formation of adenosine mononucleotide (AMP), the two products of the reaction. The Km for adenosine triphosphate (ATP) was 0.12 mM with the PRPP method and 0.1 mM with the AMP method. The Km for ribose-5-phosphate (R-5-P) was 0.14 mM with the former method and 0.033-0.042 mM with the latter. The pH optimum with the PRPP method was between 7.6 and 8.2. The mean RPK activity of hemolysates of normal mature erythrocytes was 30.5 ± 3.78 µmoles of PRPP or 30.6 ± 3.82 µmoles of AMP produced/hr per 1010 erythrocytes at 37° C. Although RPK activity of normal mature erythrocytes did not appear to be markedly age dependent, activity was substantially increased in reticulocyte-rich blood. APRT activity was assayed by measuring the AMP produced in a system linked to the generation of oxidized nicotinamide adenine dinucleotide (NAD). The activity of normal mature erythrocytes was 3.38 ± 0.37 µmoles of AMP formed/hr per 1010 erythrocytes at 37° C. Enzyme activity was significantly elevated in reticulocyte-rich blood and in the erythrocytes of a patient with the Lesch-Nyhan syndrome. These methods obviated the need for isotopic techniques and were readily applicable to small samples of blood.
Abnormal Erythroid Maturation Following Acute Lead Toxicity in Mice
Authors: Morse Bernard S. , Germano Gerald J. , Giuliani Dennis G. 
Published: October 2019

Abstract
Acute lead (Pb) toxicity in mice, produced by a single i.v. injection of Pb acetate, was associated with transient erythroid hypoplasia and impaired utilization of RBC 59Fe for heme synthesis. The mechanism of this Pb-induced erythroid hypoplasia was further investigated in posthypoxic plethoric mice. When Pb and erythropoietin (EP) were administered simultaneously, the resultant erythroid response was diminished relative to EP-treated controls. Twelve hours after the simultaneous EP and Pb injection, the number of early (pro) normoblasts was comparable to EP-treated controls. By 24 hr, there was a reduction of intermediate normoblasts followed by a decreased transition of these cells to late normoblasts. Excess nonheme iron was demonstrated by cytochemical technique in the cytoplasm of intermediate normoblasts in Pb-treated mice. Administration of Pb at intervals before and after EP resulted in a depressed reticulocyte response relative to EP-treated controls. The nadir of this response was observed when Pb was given 16 hr after EP. From these studies, we would suggest that the effects of Pb on erythropoiesis are best explained by the intramedullary death of intermediate normoblasts. A decrease in the conversion of early to intermediate forms, with subsequent intramedullary death of early normoblasts, may also contribute to the depression of the erythroid response. The mechanism for erythroid hypoplasia in some cases of human plumbism could be, in large measure, attributable to this process.
Thrombocytopathia Due to Abnormalities in Platelet Release Reaction—Studies on Six Unrelated Patients
Authors: Weiss Harvey J. , Rogers John 
Published: October 2019

Abstract
In Thrombocytopathia Due to Abnormalities in Platelet Release Reaction —Studies on Six Unrelated Patients, by Weiss and Rogers (Blood: No. 2, February, 187-196, 1971) page 190, the top right-hand column head in Table 2 should read "ADP release (mµM/109 platelets)."
Nature of the Defect in Congenital Factor V Deficiency: Study in a Patient With an Acquired Circulating Anticoagulant
Authors: Fratantoni Joseph C. , Hilgartner Margaret , Nachman Ralph L. 
Published: October 2019

Abstract
An 8-yr-old girl with congenital factor V deficiency and sporadic hemorrhagic episodes developed an anticoagulant to transfused factor V. This clinical complication, not previously reported, was associated with a severe bleeding episode that subsided when the anticoagulant level decreased. Anticoagulant activity was neutralized by antihuman IgG antiserum but not by anti-IgA or anti-IgM, indicating that the anticoagulant was an immunoglobulin of the IgG class. After 6 mo, anticoagulant activity was no longer detectable. At this time, neutralization studies were performed using the patient’s anticoagulant. Normal plasma and serum contained antigenic activity that neutralized the anticoagulant. Such activity was absent from the remission plasma. Thus, the genetic lesion in the case was characterized by parallel diminution of antigenically and functionally active factor V.
Hemichromes in Single Inclusion Bodies in Red Cells of Beta Thalassemia
Authors: Rachmilewitz Eliezer A. , Thorell Bo 
Published: October 2019

Abstract
Inclusion bodies in the red cells of patients with thalassemia syndromes may result from precipitation of those hemoglobin subunits that are produced in relative excess. In hemoglobin H disease, a form of α-thalassemia, the inclusions are precipitated β-subunits, while in the β-thalassemias they are α-subunits. It has been shown that the inclusions in hemoglobin H disease have the spectral characteristics of hemichrome. In the present study, microspectrophotometric examination of single inclusion bodies in ghosts prepared from the red cells of two patients with β-thalassemia major revealed the absorption spectrum of hemichrome. These results suggest that hemichrome formation is an important pathogenetic event in the production of red cell inclusions and consequent hemolysis in the thalassemias.
THE MECHANISM OF PETECHIAL HEMORRHAGE FORMATION
Authors: HUMBLE J. G. 
Published: October 2019

Abstract
1. The capillary resistance test has been studied by a special technic of capillary microscopy.
2. Seventeen cases of hemorrhagic diseases of differing etiology have been thus studied.
3. The site of capillary hemorrhage has been localized to the arteriolar end of the capillary loop.
4. Selective damage to the arteriolar-capillary junction will explain many types of hemorrhagic syndromes.
CHRONIC NEUTROPENIA: FAVORABLE RESPONSE FOLLOWING SPLENECTOMY
Authors: WEISS HARRY A. , COLLINS WILLIAM T. 
Published: October 2019

Abstract
The case of a patient with chronic neutropenia without splenomegaly, but responding favorably to splenectomy is reported. The surgical procedure appeared to be indicated by the following: (1) exclusion of the extrinsic causes of neutropenia; (2) failure of response to the agents commonly employed to stimulate granulopoiesis; (3) demonstration of granulopoiesis in the sternal marrow; (4) increase in the circulating neutrophils following the parenteral administration of epinephrine; (5) the presence of coexisting diabetes with the potential hazard of infection.
The implication of the spleen as the main factor in the causation of the neutropenia in this case seems well established, although the specific mechanism is not apparent. There was no evidence of abnormal phagocytosis in the microscopic examination of the spleen.
PREPARATION OF STABILIZED SOLUTIONS OF HEMOGLOBIN
Authors: PENNELL ROBERT B. , SMITH WILLIAM ELLIOTT 
Published: October 2019

Abstract
It is possible to prepare self-stabilizing solutions of hemoglobin from human erythrocytes by the use of dextrose, nicotinic acid amide and ammonia during the preparation and in the final solutions themselves. Co++, Mn++ and Mg++ ions, nile blue and hexose diphosphate contribute to the speed of stabilization of these solutions. Stabilization is obtained by the faculty of the solutions, presumably by enzymic action, to convert the hemoglobin to the reduced form and to maintain it in this form. The hemoglobin solutions described are suitable for intravenous administration.
THE BLOOD AND BONE MARROW IN PATIENTS WITH CIRRHOSIS OF THE LIVER
Authors: BERMAN LAWRENCE , AXELROD ARNOLD R. , HORAN THOMAS N. , JACOBSON SAMUEL D. , SHARP ELWOOD A. , VONDERHEIDE ELMORE C. 
Published: October 2019

Abstract
The peripheral blood and bone marrow findings in patients with cirrhosis of the liver have been analyzed on the basis of a review of the literature and the authors’ study of 25 patients with diagnoses verified by biopsy of the liver.
The principal blood findings are macrocytic or normocytic anemia with normal or elevated mean corpuscular hemoglobin values, lymphopenia and thrombocytopenia in the majority of cases.
Anemia may be independent of bleeding, and the severity of anemia or macrocytosis does not appear to be related to the severity of the liver lesion.
The consistent change in the bone marrow is extension of the marrow organ so that active hematopoiesis is found in the shafts of the long bones.
Regardless of the presence or absence of bleeding or anemia, the marrow of the sternum is of normal or increased cellularity, with normal or increased erythrocytogenesis and megakaryocytogenesis in most cases.
Hypocellularity of the marrow is an unusual finding, even in patients with advanced liver lesions.
Macronormoblastic erythropoiesis is seen in patients with macrocytic anemia, but megaloblastic erythropoiesis dces not result from cirrhosis of the liver.
The presence of peripheral cytopenias (anemia and thrombocytopenia) in spite of normal or increased formation of erythroblasts and megakaryocytes in the marrow is suggestive of hypersplenism in patients with hepatic cirrhosis.
In patients with chronic hemorrhage the blood and bone marrow pictures are those of iron deficiency anemia, although other changes such as lymphopenia and thrombocytopenia tend to persist.
The combined peripheral blood and sternal marrow examination is often of value in establishing the diagnosis of cirrhosis of the liver.
BONE MARROW REGENERATION IN EXPERIMENTAL BENZENE INTOXICATION
Authors: STEINBERG BERNHARD 
Published: October 2019

Abstract
Benzene intoxication was induced in a number of rabbits in order to study the factors which regulate production of leukocytes. One or more of the marrows of long bones was completely extirpated. After varying intervals, the animals were killed. The regenerated marrow was studied. Comparisons were made with regeneration in normal animals and with the intact marrow of animals treated with benzene. The appearance of regenerated and intact marrow was correlated with the degree of benzene intoxication.
In normal animals, regeneration of extirpated marrow proceeded in a more or less sequential order. At first there was formation of sheets of primitive reticular cells and bone trabeculae, followed by fat cells and then by myeloid tissue. In severe benzene intoxication, the extirpated marrow regenerated only to the point of formation of primitive reticular cells. Further regeneration was halted at the point of formation of fat cells. Myeloid activity appeared to be predicated upon the presence of fat cells. At least, one part of the mechanism by which benzene induces aplasia of bone marrow is probably the inhibition of cell division and maturation past the level of the primitive reticular cell.
THE PARALLEL EFFECTS OF MAGNESIUM ON THE COMPLEMENTARY AND COAGULATIVE ACTIVITIES OF BLOOD SERUM
Authors: MALTANER FRANK , DE ALMEIDA JOSÉ O. 
Published: October 2019

Abstract
Magnesium chloride enhances the coagulation and complement activities of blood serum in parallel degree. These enhancing effects are inhibited by inactivated serum or by disodium phosphate.
Distortion in the results of complement-fixation tests occurs with the addition of ionized magnesium salts to the system. This is due to the antagonistic effect of the inactivated test serum. In the quantitatively standardized test, however, where the titer is expressed as the ratio of the reaction of serum and antigen to that of serum alone, the findings are the same with or without added magnesium salts.
A FACTOR IN SERUM WHICH ACCELERATES THE CONVERSION OF PROTHROMBIN TO THROMBIN
Authors: ALEXANDER BENJAMIN , DE VRIES ANDRE , GOLDSTEIN ROBERT , ADDELSON EUNICE , PROMISEL ELAINE 
Published: October 2019

Abstract
1. The evolution of a factor in serum which accelerates prothrombin conversion to thrombin has been studied in normal subjects.
2. Mechanical agitation of fresh blood or the addition of thromboplastin supplements increases the amount of SPCA evolved and decreases the amount of prothrombin activity remaining in the serum.
3. Retarding coagulation by large doses of heparin or by handling the blood with siliconized apparatus decreases SPCA evolution and increases residual serum prothrombin activity.
4. Hypoprothrombinemic blood resulting from dicumarol administration evolves subnormal amounts of SPCA during its coagulation.
THE EFFECT OF VARIOUS ANTICOAGULANTS ON THE SPECIFIC GRAVITY OF BLOOD AND OF PLASMA, AND ON THE HEMATOCRIT
Authors: MCLAIN PAUL L. , RUHE C. H. WILLIAM , PASTORIUS GEORGE J. 
Published: October 2019

Abstract
The effects of several commonly employed anticoagulant procedures on the specific gravity of blood and of plasma, and on the relative red cell volume, were studied in freshly drawn samples of arterial blood from rabbits. Measurements on treated blood, or its fluid component, were compared with corresponding results on portions of the same samples without treatment and prior to coagulation.
Satisfactory preservation of the specific gravity of whole blood was obtained by defibrination or by the use of ammonium-potassium oxalate mixture.
Satisfactory preservation of the specific gravity of plasma was obtained by defibrination or by the use of heparin solution.
The relative volume of red cells was essentially unaltered by the use of dry heparin, oxalate mixture, 1.6 per cent solution of potassium oxalate, or by defibrination.
Dry potassium oxalate and sodium citrate caused marked changes, increasing the specific gravity of blood and of plasma, and shrinking the red cells.
Dry heparin caused significant increases in the specific gravity of blood and of plasma.
Ammonium-potassium oxalate mixture increased the specific gravity of plasma markedly and consistently.
THE USE OF EXCHANGE TRANSFUSION FOR THE TREATMENT OF SEVERE ERYTHROBLASTOSIS DUE TO A-B SENSITIZATION, WITH OBSERVATIONS ON THE PATHOGENESIS OF THE DISEASE
Authors: WIENER A. S. , WEXLER I. B. , HURST J. G. 
Published: October 2019

Abstract
Two unusual cases of severe erythroblastosis due to A and B sensitization have been presented. When injections of A and B group substances failed to arrest the disease, exchange transfusions were carried out, using 900 to 1,000 cc. of fresh group O blood. In each case the response was prompt and dramatic, although the convalescence in one was prolonged by an intercurrent diarrhea. Both infants have made complete recoveries and have developed normally both physically and mentally.
Observations have been presented regarding the pathogenesis of erythroblastosis and icterus precox due to A-B sensitization. The following conclusions seem to be warranted on the basis of the evidence presented:
1. The greatest majority of cases of jaundice and anemia of the newborn that cannot be explained on the basis of Rh incompatibility are caused by incompatibility of the major blood groups.
2. High maternal alpha and beta antibody titers per se are not necessarily correlated with disease in the infant.
3. Univalent alpha and beta antibodies present in the maternal serum traverse the placenta and are the cause of the disease in the infant. Bivalent antibodies are held back by the intact placenta and play no or hardly any role in the causation of the disease. Univalent alpha and beta antibodies are demonstrable in the sera of a large proportion of "normal" individuals.
4. A-B sensitization in pregnancy occurs mainly when the infant belongs to the secretor type.
5. A theory is suggested that the quality of the alpha and beta antibodies, namely, whether they are homospecific or heterospecific, may affect the severity of the manifestations in the infant.
Technics of titrating alpha and beta and Rh antibodies are described and discussed. A table has been prepared which converts antibody titers into concentrations of immune globulin in the serum, and demonstrates the impossibility of certain extravagantly high titers claimed in the literature.