bluuebunny/crossref_metadata_2025_split huggingface dataset:
Heinz Body Anemia: An Ultrastructural Study. II. Red Cell Sequestration and Destruction
Authors: RIFKIND RICHARD A. 
Published: October 2019

Abstract
This study reports electron microscope observations on the process of red cell sequestration and destruction in the spleen and liver of the phenylhydrazine-treated rabbit. Damaged red cells are recognized by virtue of their Heinz bodies, a morphologic manifestation of the oxidative injury which they have sustained. Sequestration, in the spleen, involves the selective accumulation of damaged cells within the vascular spaces of the Billroth cords. Erythrophagocytosis and the intracellular digestion of red cells follows sequestration. More severely injured cells may undergo intravascular hemolysis within the splenic red pulp. In the liver, however, no evidence for the intravascular sequestration of injured red cells is observed. Damaged cells are removed directly from the sinusoidal blood by erythrophagocytosis. The selectivity of spleen and liver for red cells subjected to different degrees of injury is discussed in terms of the observed differences in the vascular architecture of the two organs.
Erythroid Homograft Following Leukocyte Transfusion in a Patient with Acute Leukemia
Authors: SCHMIDT PAUL J. , YOKOYAMA MITSUO , MCGINNISS MARY H. , LEVIN ROBERT H. 
Published: October 2019

Abstract
The establishment of a hematopoietic graft of stem cells from a donor with chronic myelogenous leukemia in a patient with acute leukemia took place in the face of ABO red cell group incompatibility. The donor was group A and the recipient who was group O gradually increased his red cell mass to become 80 per cent group A.
There was both active and passive immunity to A present at the time of induction of the graft. The graft flourished despite persistent anti-A agglutinins and an immune response in the B agglutinin and hemolysin system.
Failure of the graft coincided with a fall in antibody levels and was followed by a second immune response which included marked elevation of 7S gamma globulin levels. Red cell incompatibility was not a barrier to this graft and failure of the graft was probably due to other immune mechanisms.
A Fetal Hemoglobin with Abnormal γ-Polypeptide Chains: Hemoglobin Warren
Authors: HUISMAN T. H. J. , DOZY A. M. , HORTON B. E. , WILSON J. B. 
Published: October 2019

Abstract
The discovery of a variant of fetal hemoglobin in the cord blood of a Negro newborn is reported. The abnormal hemoglobin, designated as Hb-Warren, was studied by different analytic procedures, such as starch gel electrophoresis, anion exchange chromatography, ultraviolet spectral absorption, immunologic reactivity with various antisera, hybridization with canine hemoglobin and the determination of the total amino acid composition. It was concluded that Hb-Warren was composed of normal α-polypeptide chains and abnormal γ-polypeptide chains.
The Sites of Hemoglobin Catabolism
Authors: KEENE WILLIS R. , JANDL JAMES H. , Files Nancye M. 
Published: October 2019

Abstract
Hemoglobin is cleared from plasma principally by the liver, moderately by the marrow, and relatively little by the spleen or other organs. Haptoglobin binding has no effect on this relative distribution, its only discernible role in hemoglobin clearance or catabolism being that of preventing the renal loss of hemoglobin.
When bone marrow is depleted of parenchymal cells, as by cytotoxic chemicals or protein deprivation, its ability to take up hemoglobin from plasma is markedly enhanced.
Brief Report: The Early Loss of Radioactivity in Cr51 Survival Curves: Destruction of Cells or Loss of the Label?
Authors: KLEINE N. , HEIMPEL H. 
Published: October 2019

Abstract
Using human erythrocytes labeled simultaneously with DFP32 and Cr51, studies of specific red cell activities within the first 24 hours after infusion of labeled cells were carried out. The results obtained suggest that the early loss of Cr51 specific red cell activity which has been observed in radiochromium survival curves is due to rapid elution of a portion of the label.
Antigenic Behavior of the S-63 Mouse Leukemia Virus
Authors: BROWN ERIC R. , GREENSPAN IRVING , SCHWARTZ STEVEN O. 
Published: October 2019

Abstract
The present studies are an extension of earlier reports on the antibody response of mice to a leukemogenic virus (S-63). These investigations were designed to show whether a correlation exists between in vivo and in vitro determinations, and whether protective antibodies against the virus could be produced in immune-tolerant animals. Viral neutralization and protection studies in mice were compared with passive cutaneous anaphylaxis (PCA), immunodiffusion, microprecipitin, and immunofluorescent tests using similar antigens and antibodies. As shown in tables 1, 2 and 3, antibody could be demonstrated by both in vivo and in vitro methods, and these studies showed (table 2) that the antibody was protective.
The S-63 leukemia virus was isolated in 1963 from a mouse ascites cell leukemia line. That cell line had been carried in the laboratory for over 3 years. The virus has been carried in ICR mice since its isolation. Immunologic studies were carried out to determine the relation between the virus and the originating ascites cell. Studies of antibodies produced in normal rabbits against the S-63 virus were unsatisfactory for purposes of these experiments because of cross reaction with normal mouse tissue. Immune-tolerant animals have yielded valuable information:
Antibodies produced in immune-tolerant rabbits injected with the S-63 virus do not cross react against intact ascites cells from which the virus was originally isolated. Conversely, antibodies similarly produced against the ascites cells do not react against the virus antigen.
Antibodies produced in immune-tolerant rabbits against ascites cells protect mice against ascites cell-induced leukemia, but not against the disease induced by S-63 virus. Mice challenged with ascites cells and treated with antiascites cell gamma globulin are protected against the disease. The best therapeutic advantage is obtained when treatment is started either at the time of cell inoculation or in the early stages of the disease.
Antibodies which protect newborn animals from infection develop in adult ICR mice recovering from S-63 virus leukemia. These antibodies produced by convalescent mice are similar, from the standpoint of protection, to those produced in immune-tolerant rabbits.
Congenital Nonspherocytic Hemolytic Anemia, Associated with Glutathione Deficiency of the Erythrocytes
Authors: PRINS H. K. , OORT M. , LOOS J. A. , ZÜRCHER C. , BECKERS T. 
Published: October 2019

Abstract
1. A new biochemical defect of erythrocytes is described: glutathione deficiency (reduced glutathione less than 10 per cent of the amount of reduced glutathione in normal erythrocytes).
2. The defect is associated with a clinical picture of congenital nonspherocytic hemolytic anemia which is fairly well compensated.
3. The results of a family study are consistent with an autosomal recessive pattern of inheritance.
4. Labeling with Na2Cr51O4 has a damaging effect on glutathione-deficient erythrocytes. The erythrocyte life span, as estimated by a serological method (Ashby), was markedly shortened (30 days instead of 100-120 days).
5. Red cell destruction could be increased by the administration of primaquine.
6. Secondary to the glutathione deficiency, low glyoxalase activity was observed. The glutathione-reducing capacity, glycolytic activity, and the ATP level of the abnormal red cells were found to be within the normal range.
7. On incubation of the glutathione-deficient erythrocytes in vitro with glycine-C14 and glutamine-C14, no formation of labeled glutathione could be demonstrated.
Pyridoxine-Responsive Anemia Conditioned by Isonicotinic Acid Hydrazide
Authors: McCURDY PAUL R. , DONOHOE ROBERT F. 
Published: October 2019

Abstract
Three patients are described who had a pyridoxine-responsive anemia while under treatment for pulmonary tuberculosis with INH and PAS. The red cells were hypochromic and target cells were common. Two cases also had microcytosis and one had ringed sideroblasts in the bone marrow. None became hematologically normal with therapy. A somnolent reaction occurred in two of the patients following the parenteral administration of large amounts of pyridoxine, and seemed related to it. The concentration of erythrocyte glutamic oxaloacetic transaminase was less than 25 per cent of the normal mean in two of the patients at the time of relapse.
Multiple Cases of Leukemia in a Sibship
Authors: GUNZ F. W. , FITZGERALD P. H. , CROSSEN P. E. , MACKENZIE I. S. , POWLES C. P. , JENSEN G. R. 
Published: October 2019

Abstract
In a New Zealand Maori sibship of 9 (one a half-sib), 4 definite cases and 1 possible case of acute leukemia occurred in a space of 5 years. The children, 2 of whom were fraternal twins, developed symptoms at ages between 10 months and 6 years. One child had a marrow picture suspicious of leukemia nearly 2 years before the onset of symptoms.
Cytogenetic studies showed no major chromosome changes in either the parents or the 3 affected siblings examined. No linkage was found between the leukemias and any blood or serum group.
The nature of the factors causing the disease in this family is discussed.
The Activation of Proaccelerin by Bovine Thrombokinase (with Notes on the Antithrombic Activity of Phenylmethyl Sulfonylfluoride)
Authors: BRECKENRIDGE ROBERT T. , RATNOFF OSCAR D. 
Published: October 2019

Abstract
Through the kindness of Dr. J. H. Milstone we were able to perform clotting studies with purified bovine thrombokinase. Phenylmethyl sulfonylfluoride was found to inactivate bovine thrombin. Bovine thrombokinase, freed of traces of contaminating thrombin by treatment with phenylmethyl sulfonylfluoride, behaved in a manner similar to activated Stuart factor. Kinetic studies with this purified clotting factor and partially purified bovine proaccelerin supported the hypothesis that bovine proaccelerin is changed by the enzymatic action of thrombokinase to an agent which converts prothrombin to thrombin. The reaction between thrombokinase and bovine proaccelerin requires phospholipid and calcium and is blocked by soybean trypsin inhibitor. The similarities between human activated Stuart factor and bovine thrombokinase are apparent.
Sternberg-Reed Cells in the Peripheral Blood of Patients with Hodgkin’s Disease
Authors: BOURONCLE BERTHA A. , Mann Rosemary 
Published: October 2019

Abstract
Our observations of 135 patients indicate that 37 per cent of those suffering from Hodgkin’s disease exhibit abnormal cells in the leukocyte concentrates of the peripheral blood during the course of their illness. Typical Sternberg-Reed cells were found in 18.5 per cent of patients and were present only in the advanced stages of generalized Hodgkin’s disease.
The presence of Sternberg-Reed cells in the peripheral blood indicates an advanced stage of the disease but does not necessarily predict an immediately fatal outcome.
Comparative studies, searching for Sternberg-Reed cells in the splenic circulation, showed no Sternberg-Reed cells to be present in the splenic arteries of patients with Hodgkin’s disease; but numerous Sternberg-Reed cells were present in the splenic vein, particularly after mechanical squeezing of the spleen. A possible hypothesis is given to support the evidence for the circulation of Sternberg-Reed cells and an explanation for their lower incidence in the peripheral blood.
Our observations support the hematogenous metastasis of Hodgkin’s disease.
Roentgenographic Bone Changes in Chronic Iron Deficiency Anemia
Authors: AKSOY MUZAFFER , ÇAMLI NECDET , ERDEM SAKIR 
Published: October 2019

Abstract
Radiologic bone changes of the skull and long and short bones similar to those of thalassemia are described in 12 patients with chronic iron deficiency anemia. Certain differences between the roentgen findings of the present study and those of the cases reported by other investigators are discussed.
Normal Human Lymph Node Cells: An Electron Microscopic Study
Authors: BROOKS ROBERT E. , SIEGEL BENJAMIN V. 
Published: October 2019

Abstract
Lymph nodes, from 15 patients undergoing surgery for conditions not related to lymphoid tissue disease, have been examined with the electron microscope. The human lymph node cell types—including lymphocytic, reticular and plasma cells—have been described at low and medium electron microscopic magnifications, and the criteria for their identification are discussed. The characteristic features outlined for identification of these cell types provide a basis for comparison with pathologically altered lymph node cells.
Trisomy of Group C in a Myeloproliferative Disorder
Authors: WINKELSTEIN ALAN , SPARKES ROBERT S. , CRADDOCK CHARLES G. 
Published: October 2019

Abstract
A patient with an atypical myeloproliferative syndrome characterized by leukocytosis with myeloid immaturity, ineffective extramedullary erythropoiesis, overt hemolysis and low leukocyte alkaline phosphatase activity demonstrated a trisomy in the C group of bone marrow metaphase chromosomes.
Fetomaternal Passage of Leukocytes and Platelets in Erythroblastosis Fetalis
Authors: DESAI R. G. , MCCUTCHEON E. , LITTLE B. , DRISCOLL S. G. 
Published: October 2019

Abstract
Leukocytes and platelets labeled by the atabrine fluorescent technic have been demonstrated in the maternal circulation from ½ to 4 hours following intraperitoneal transfusion of the fetus in utero. The peak concentration of labeled cells was observed 2 hours after transfusion. The fetomaternal transfer of cells has been demonstrated in cases of erythroblastosis fetalis. It is not known whether this occurs in normal fetuses and the mechanism is not understood.
Promyelocytic-Myelocytic Leukemia as a Terminal Manifestation of Chronic Granulocytic Leukemia
Authors: BEN-ZEEV DAN , SCHWARTZ STEVEN O. , FRIEDMAN IRVING A. 
Published: October 2019

Abstract
1. A case of promyelocytic-myelocytic leukemia is reported as the terminal phase of chronic granulocytic leukemia. We believe that this is the first such case reported.
2. The terminal phase of this case is compared with acute promyelocytic-myelocytic leukemia; the course and laboratory data appear almost identical.
3. The nature of the abnormal granules in the promyelocytoid-myelocytoid cells and their relation to the fibrinogenopenia incite speculation.
Studies in the Pathogenesis of Autoerythrocyte Sensitization Syndrome
Authors: GROCH GEORGE S. , FINCH STUART C. , ROGOWAY WILLIAM , FISCHER DAVID S. 
Published: October 2019

Abstract
1. Two of three female patients with the autoerythrocyte syndrome were tested for sensitivity to various components of the erythrocyte membrane. One was consistently sensitive to purified phosphatidyl serine.
2. It is suggested that in at least one patient with autoerythrocyte purpura the phosphatidyl serine of the red cell membrane may play a role in the pathogenesis of the purpuric lesions.
3. It is likely that a broad spectrum of autosensitivity-type purpuric disorders exists in women with complex emotional problems. The threshold of reactivity may be modified by the psyche.
Ribonucleic Acid Biosynthesis in Human Leukocytes
Authors: CLINE MARTIN J. 
Published: October 2019

Abstract
Phagocytosis has profound effects on several aspects of the RNA metabolism of human leukocytes. The major changes induced by particle ingestion appear to be (1) an increased uptake of pyrimidine precursors from the suspending medium, (2) a contraction in the size of the nucleotide pool, (3) an accelerated rate of destruction of preexisting RNA, and (4) an increased rate of RNA synthesis. Sucrose density gradient analysis of the newly synthesized RNA suggests that several classes of RNA are involved in this process. The increased turnover rate of the nucleotide pool and of the cellular RNA of the leukocyte is proportional, within limits, to the total load of ingested particles.
Interaction of Influenza Virus with Blood Platelets
Authors: TERADA HIDEO , BALDINI MARIO , EBBE SHIRLEY , MADOFF MORTON A. 
Published: October 2019

Abstract
The interaction of human blood platelets with influenza virus (PR-8) was studied in vitro and in vivo.
It was found that "live" influenza virus was rapidly adsorbed onto human blood platelets at 4 C. and completely eluted at 37 C. "Dead" virus was adsorbed at 4 C. but not eluted at 37 C. unless the platelets were treated with RDE (receptor destroying enzyme). Adorption of virus also occurred at tem peratures above 4 C. (from 20 to 37 C.). However, while adsorption was maintained throughout incubation at 4 C., slow elution occurred after 30 to 90 minutes incubation at 26 to 37 C. Storage of the platelets for lengthy intervals at 4 C. or coating of the platelets with macromolecules did not interfere with virus adsorption. After one cycle of adsorption-elution, blood platelets could not adsorb virus again. Treatment with RDE greatly reduced virus adsorption. During the process of virus adsorption, prominent platelet clumping occurred. During elution, clumping remained unchanged, and gross alterations in morphology of the platelets were observed. In the process of virus adsorption-elution, large numbers of platelets were lysed.
Comparative experiments were performed simultaneously with human red blood cells (RBC) and identical results were obtained as with blood platelets. However, the extent of adsorption of live virus was equal for platelets and RBC only when the relationship between platelet number and RBC number in the preparations used was 6:1. This suggested a direct proportion between the surface area of both platelet and RBC and the number of available virus receptors.
Virus suspensions infused into rabbits produced a sharp and sustained drop of the platelet count. Survival of radioactively labeled platelets treated with virus prior to infusion was markedly shortened with live virus and was only slightly reduced with dead virus.
It is suggested from these experiments that blood platelets, as other blood cells, may serve as carriers of viruses in the circulation and that in this process the platelets are damaged and partially destroyed.
The Effect of Ellagic Acid on the Thrombin-Induced Hemorrhagic Syndrome in the Rat
Authors: CLIFFTON E. E. , GIROLAMI A. , AGOSTINO D. 
Published: October 2019

Abstract
The intraperitoneal administration of thrombin increased the bleeding due to the amputation of the tail in the rat (average blood loss 4.6 ml.). The intravenous administration of ellagic acid in thrombin-injected rats reduced the average blood loss to 0.6 ml. This value was slightly more than the average blood loss noted in animals given only ellagic acid (0.2 ml.). Both these figures were much less than the average blood loss observed in control animals (3.2 ml.).
Jordans’ Anomaly in White Blood Cells
Authors: ROZENSZAJN L. , KLAJMAN A. , YAFFE D. , EFRATI P. 
Published: October 2019

Abstract
Persistent vacuoles were seen in the protoplasm of granulocytes, monocytes and occasional lymphocytes of 2 sisters suffering from ichthyosis. In the bone marrow these vacuoles were found in the cytoplasm of promyelocytes, myelocytes, metamyelocytes and rarely in plasma cells. They were not observed in blasts or in red cells and thrombocytes and their precursors.
With the help of cytochemical staining technics and fluorescence microscopy studies, it was determined that the vacuoles contained lipids. A similar abnormality of leukocytes was described previously by Jordans in 2 brothers suffering from muscular dystrophy.
Ichthyosis was transmitted in this family in an autosomal recessive way.
Tabular and Ultrastructural Studies of Agranulocytes of the Thoracic Duct of Calves
Authors: WEBER ALVIN F. , JOEL DARREL , Smith Joyce , Frommes Stephen 
Published: October 2019

Abstract
1. Ultrastructural studies were made of 400 agranulocytes, each from the thoracic duct effluent of 12 normal Holstein calves of both sexes.
2. Tabular electron microscopic evaluation of the agranulocytes present demonstrated that 89 per cent were lymphocytes, 4.8 per cent plasmacytes, 1.3 per cent reticular lymphocytes, 4 per cent proplasmacytes, and 0.7 per cent mitotic forms of the various cell types enumerated.
3. Mitochondrial tabular studies demonstrated that profile numbers (6.2-8.2) and profile sizes (0.15-0.25 µ2) were similar among cell sections of the five designated cell groups in the calf and the lymphocyte of the human. Monocyte mitochondrial profiles of the human were highly significantly smaller (0.05 µ2) than those of other cells studied. These studies provided added proof that monocytes probably are not present in the thoracic effluent of the calf.
4. Nuclear bodies were found to be present only in lymphocytes. They were present on the average in 12 per cent of thin sections of cells in this class. In contrast to nuclear bodies of other nonblood cells,20 in lymphocytes they were not associated with the nucleolus, were smaller in overall diameter, and often contained practically no electron opaque central portion.
Mechanism of the Hereditary Anemia of Slm Mutant Mice
Authors: KALES A. N. , FRIED W. , GURNEY C. W. 
Published: October 2019

Abstract
The anemia of mutant homozygote C57BL/6SlmSlm mice is due to a gastrointestinal bleeding defect and to an erythropoietic defect. The anemic animals lose approximately 3.5 per cent of their blood volume into the gastrointestinal tract daily. The cause of this blood loss has not been established. The anemic animals also have an erythropoietic defect which renders them unable to respond normally to erythropoietin or to hypoxia. Although the homozygotes appear refractory to erythropoietin in moderately large single doses, they do respond if sufficiently large doses are given repeatedly.
The erythropoietic defect detected in the homozygote is also evident in the heterozygote. However, the defect remains latent in the heterozygote, for although this animal is subnormally responsive to erythropoietin and to hypoxia, it is not anemic.
Stilbestrol-Induced Porphyria: Increase in Hepatic δ-Aminolevulinic Acid Synthetase
Authors: LEVERE RICHARD D. 
Published: October 2019

Abstract
An increase in hepatic δ-aminolevulinic acid synthetase is demonstrated in a patient with cutaneous porphyria induced by stilbestrol. A genetically determined increase in this rate-limiting enzyme appears to be the basic abnormality in all of the hepatic porphyrias.
Ribonucleic Acid Biosynthesis in Human Leukocytes: The Fate of Rapidly Labeled RNA in Normal and Abnormal Leukocytes
Authors: CLINE MARTIN J. 
Published: October 2019

Abstract
Ribonucleic acid (RNA) was isolated from a variety of human leukocyte populations exposed to tritiated uridine in vitro. Several species of RNA were extractable from leukocytes in a phenol-water system. With mild conditions of extraction a pH 7.6 fraction was obtained, which contained 60 to 75 per cent of total cellular RNA. After removal of this RNA component reextraction at elevated temperature and pH yielded a pH 9 fraction which contained 25 to 40 per cent of total cellular RNA. The pH 7.6 fraction contained 28 and 18 S ribosomal RNA and 4 S RNA. The pH 9 RNA fraction was heterogeneously distributed in a sucrose density gradient. The 28 and 18 S components were slowly labeled by H3-uridine and were relatively stable. The 4 S component was rapidly labeled and was unstable. The pH 9 RNA fraction contained most of the rapidly labeled RNA, which was either of high molecular weight or heterogeneous as to molecular size.
The pattern of incorporation of H3-uridine into the various components of RNA was similar in normal and neoplastic granulocytes and lymphocytes.
Rapidly labeled leukocyte RNA had the following characteristics: (1) its synthesis was actinomycin sensitive; (2) it was unstable, having a half-life in the range of 16 to 225 minutes; and (3) it was in part a precursor of ribosomal RNA.
The sensitivity of granulocyte protein synthesis to inhibition of RNA synthesis suggests that granulocytes have both stable and unstable templates.