bluuebunny/crossref_metadata_2025_split huggingface dataset:
Phytohemagglutinin-induced Lymphocyte Transformation: The Relationship to Prognosis of Hodgkin’s Disease
Authors: Corder Michael P. , Young Robert C. , Brown Robert S. , DeVita Vincent T. 
Published: October 2019

Abstract
Forty-three untreated patients with Hodgkin’s disease were evaluated between 1965 and 1967 with PHA-stimulated peripheral leukocyte cultures. No correlation was found between PHA-induced lymphocyte transformation at the time of diagnosis and the clinical course of the patient’s Hodgkin’s disease. There is also no correlation between lymphocyte transformation and the histologic pattern of nodular sclerosis. Although PHA-induced lymphocyte transformation appears to be a general index of immunologic status, it has not proven of value as a prognostic sign in Hodgkin’s disease.
Granulocyte Chemotaxis in the Chediak-Higashi Syndrome of Mink
Authors: Clark Robert A. , Kimball Harry A. , Padgett George A. 
Published: October 2019

Abstract
Studies of granulocyte chemotaxis were performed in mink with the Chediak-Higashi syndrome. In vivo migration of leukocytes to an inflammatory site was reduced in the affected animals. In vitro studies documented a consistent early impairment in the chemotactic response of Chediak-Higashi mink granulocytes. Serum from Chediak-Higashi mink generated normal amounts of chemotactic factors. The cellular defect in leukocyte chemotaxis in mink is comparable to that observed in humans with the Chediak-Higashi syndrome and may contribute to the increased susceptibility to infection in this disease.
Intraerythrocytic Crystalloid Bodies in Cats
Authors: Altman Norman H. , Melby Edward C. , Squire Robert A. 
Published: October 2019

Abstract
Rectangular-shaped crystalloid bodies (C.B.) were demonstrated within the erythrocytes of intact and splenectomized cats and after incubation in hypertonic NaCl. The morphologic appearance of the C.B. is strikingly similar to that of crystals present in the erythrocytes of individuals with hemoglobin C.
PYRIDOXINE DEFICIENT DIET AND DESOXYPYRIDOXINE IN THE THERAPY OF LYMPHOSARCOMA AND ACUTE LEUKEMIA IN MAN
Authors: GELLHORN ALFRED , JONES LOGAN O. 
Published: October 2019

Abstract
Three patients with disseminated lymphosarcoma and 3 cases of acute leukemia were placed on a pyridoxine deficient diet together with desoxypyridoxine for periods of four to fourteen days. Although there was evidence of malnutrition in the form of weight loss and weakness, none of the signs of specific pyridoxine deficiency described in animals was observed in the human. There was no unequivocal evidence of depression of hemopoiesis, no significant atrophy of lymphoid tissue, no signs of demyelinization of nerves, and no abnormality of tryptophane metabolism determined by urinary xanthurenic acid excretion. The possibility that the dietary restriction of pyridoxine was too brief for the development of a deficiency syndrome was considered, but it was pointed out that the rigors of the procedure were too great to justify more protracted periods of observation.
Two patients had acute toxic manifestations following the administration of large doses of desoxypyridoxine. These were characterized by transient epileptiform convulsions. There were no sequelae and no recurrence of the symptoms when the dose of the drug was reduced.
There was no evidence that the restriction of pyridoxine in the diet together with desoxypyridoxine for periods up to two weeks had any therapeutic effect in lymphosarcoma or acute leukemia. Also, no potentiation of the cytotoxic effect of nitrogen mustard was observed in the patients with lymphosarcoma when chemotherapy was given after the completion of the pyridoxine deficient regimen. It is to be emphasized that this does not absolutely exclude the possibility that pyridoxine deficiency may adversely affect lymphosarcoma in man. The short duration of the experiment and the well known refractoriness to any form of therapy of the tumors in these patients are factors which may have militated against a satisfactory outcome of the regimen.
THE ABSENCE OF THE HETEROPHILE REACTION IN THE SPINAL FLUID IN INFECTIOUS MONONUCLEOSIS
Authors: LYONS HAROLD A. , HARRISON J. GRANT 
Published: October 2019

Abstract
The spinal fluid was studied in twenty cases of infectious mononucleosis proved by clinical picture, blood studies and serological examination. It may be concluded that in acute cases of infectious mononucleosis, the heterophile antibody does not pass into the spinal fluid, but that there may be an increase in cell count, particularly lymphocytes, and in protein content, which is not necessarily proportional to the cell count elevation. These findings have no correlation with central nervous system signs or symptoms.
THE EXPERIMENTAL PRODUCTION OF MACROCYTIC ANEMIA BY OPERATIONS ON THE INTESTINAL TRACT
Authors: CAMERON D. G. , WATSON G. M. , WITTS L. J. 
Published: October 2019

Abstract
1. The literature concerning attempts to produce macrocytic anemia of the liver-deficiency type in animals by operations on the gastrointestinal tract has been reviewed. Operations on the stomach have failed consistently to produce such an anemia, but success has been achieved by operations on the small intestine with the creation of blind loops or intestinal stenosis.
2. The technic we have used to produce macrocytic anemia in the rat is described in detail. The essentials are that the blind loop should fill with peristalsis and that it should not be too low down in the small intestine.
3. Anemia does not usually develop until an interval of several weeks or months after the operation. It is then macrocytic in type and acute in course.
4. The anemia is probably dependent on stagnation in the blind loop and a change in the bacterial flora of the small intestine.
Regeneration of Marrow Tissue in Chronic Iron Deficiency in Postweanling Rats
Authors: Tavassoli Mehdi , Durocher John R. , Crosby William H. 
Published: October 2019

Abstract
The regenerative potential of chronically iron-deficient rat marrow was studied in extramedullary marrow autotransplants and intramedullary cavity after ablation. Subcutaneous implantation of normal marrow results consistently in establishment of a marrow nodule with a mean weight ratio of 30.7% of the implanted tissue. In iron deficiency, the mean weight ratio was 7.1%, and the take was 11%. After ablation of femoral marrow, the regenerative process proceeds distally from the uninjured marrow at the femoral head. The process of regeneration reached the midshaft after 11 days in iron-deficient animals but took only 5 days for normal animals. Iron repletion accelerated the process toward normal. These results are consistent with biochemical data from iron-deficient marrow (low nucleic acid content, decreased incorporation of 3H-thymidine into DNA, and decreased utilization of 59Fe and 14C-glycine for heme synthesis) and suggest that the reported hypercellularity of the marrow in iron deficiency may reflect sequestration of erythroid precursors, rather than the compensatory mechanism of increased cell proliferation.
Peripheral Cytoplasmic Characteristics of Leukocytes in Monocytic Leukemia: Relationship To Clinical Manifestations
Authors: Lichtman Marshall A. , Weed Robert I. 
Published: October 2019

Abstract
The increased prevalence of tissue infiltration in some cases of monocytic leukemia may represent an enhanced ability of monocytes for tissue entry, continued cell proliferation, an increased life span in the tissues, or a combination of these three factors. Studies in this laboratory have shown that the normal myeloblast undergoes a process of cytoplasmic maturation that adapts it for marrow egress, tissue emigration, and particle ingestion. These include a reduction in surface negative charge density, increased ability to adhere to negatively charged surfaces, increased cytoplasmic deformability, more rapid motility, and enhanced phagocytic rate. In a subject with monocytic leukemia in whom tissue infiltration was a striking feature of the clinical disease, blood monocytes were broadly distributed in regard to their peripheral cytoplasmic characteristics. One portion of the cell population had a high surface negative charge density, was weakly adherent, weakly phagocytic, and poorly deformable, akin to blast cells. A second portion of the cell population had lower surface negative charge density, was adhesive, phagocytic, and readily deformable, akin to mature blood phagocytes. In five patients with myeloblastic leukemia in whom tissue infiltration was not prominent and in whom 92% of cells were myeloblasts, the blood leukocytes had a more homogeneous distribution of surface properties, and these properties were characteristic of immaturity. The increased prevalence of tissue infiltration in some cases of monocytic leukemia may be due to the presence of cytoplasmic maturation, which normally adapts the monocyte for tissue entry.
Bone Marrow Macrophage Precursors. I. Some Functional Characteristics of the Early Cells of the Mouse Macrophage Series
Authors: Cline Martin J. , Sumner Margaret A. 
Published: October 2019

Abstract
Mouse bone marrow cells were cultured in vitro under conditions that allowed little granulopoiesis but permitted proliferation of mononuclear phagocytes. During 10 days’ culture, the population gradually shifted from a preponderance of undifferentiated blast cells and promonocytes to macrophages. Cells up to the A (immature) macrophage stage were capable of DNA synthesis and mitosis. B (mature) macrophages were nondividing. Blast cells were not phagocytic and lacked glass adhesiveness and demonstrable surface receptors for IgG immunoglobulin. With progressive cellular maturation, peroxidase activity disappeared after the monocyte stage. Glass adhesiveness, phagocytic ability, and surface receptors for immunoglobulins appeared to increase with cell maturation from the promonocyte through the macrophage stage of development.
Comparison of the Action of 3H-Thymidine and Hydroxyurea on Testosterone-treated Hemopoietic Stem Cells
Authors: Byron J. W. 
Published: October 2019

Abstract
The treatment of mice with a single, subcutaneous injection of either testosterone propionate or of 5β-dihydrotestosterone results in an increase in the sensitivity of spleen colony-forming cells (CFU-S) to the cytocidal action of high specific activity 3H-TdR. The effect is still present 24 hr after treatment. By 1 hr after exposure in vitro to 2.4 x 10-8M testosterone hydrogen succinate (THS), CFU-S from mouse bone marrow similarly become more sensitive to 3H-TdR. Sensitivity to the cytotoxic action of 10-3M hydroxyurea (HU) also increases. Compared with 3H-TdR sensitivity, however, there is a delay in the onset of sensitivity to HU. The lag is shortened if HU is added 1 hr after the addition of THS. The increased sensitivity of CFU-S to HU is prevented by deoxyribonucleoside, i.e., unlabeled thymidine, and the change during the first hour in 3H-TdR sensitivity is unaltered by the presence of HU. From these data, it is suggested that CFU-S from normal bone marrow contain precursors for DNA synthesis, e.g., deoxyribonucleotides. On the assumption that the action of HU is to inhibit the formation of deoxyribonucleotides from ribonucleotides, the delay in the onset of action of HU may depend on the exhaustion of such pools. It is postulated that CFU-S responding to THS are held up in a stage of the cell cycle close to the G1-S boundary.
Hereditary Defect in Platelet Function in Rats
Authors: Tschopp Thomas B. , Zucker Marjorie B. 
Published: October 2019

Abstract
Hemostatic parameters of fawn-hooded (FH) rats with an inherited hemorrhagic diathesis were compared with those of normal rats. Prothrombin time, partial thromboplastin time, plasma factor VIII, plasma fibrinogen, and platelet count and volume were normal. Bleeding time (BT) in FH rats was over 15 min vs. 1-8 min in controls, and platelet retention in glass-bead columns was reduced. Transfusion of platelet concentrates from normal rats corrected the BT of thrombocytopenic FH rats, but FH rat platelets did not shorten the BT of thrombocytopenic controls. ADP-induced aggregation, measured turbidimetrically in heparinized FH platelet-rich plasma, was normal. Connective tissue did not aggregate platelets of FH rats and released a subnormal amount of 14C-serotonin. In comparison with control platelets washed FH platelets aggregated by thrombin released virtually no ATP and ADP. Platelets, 10,11 of normal rats contained 4.49 µmoles ATP, 0.98 µmoles ADP, and 0.88 µmoles serotonin compared with only about one-half as much ATP and ADP and one-third as much serotonin in platelets of FH rats. These low values suggest the absence of the platelet, "release pool" rather than a defective release mechanism. The hemorrhagic diathesis seen in the FH rats resembles the platelet defect with storage pool deficiency observed in man.2
Morphologic Studies in a Recently Described Dyserythropoietic State
Authors: Freeman Arnold I. , Edwards John A. , Cohen Maimon , Sinks Lucius F. 
Published: October 2019

Abstract
Studies of fetal hemoglobin and bone marrow ultrastructure were performed on a patient with a recently described syndrome consisting of lymphosarcoma, short stature, defective cellular immunity, hypogammaglobulinemia, and mosaicism for a marker chromosome. Abnormalities of the erythroid cells, including multinucleated erythroblasts, nuclear bodies, megaloblasts, and frayed cytoplasm, were seen by light microscopy. Ultrastructure confirmed the findings by light microscopy and showed in greater detail nuclear malformation, loss of nuclear membrane, and loss of cytoplasmic background, as well as peculiar cytoplasmic inclusions. An increased level of fetal hemoglobin (Hb F), ranging between 12%-15%, was detected. The Hb F was discreetly distributed, occurring in a small per cent of the red blood cells. It is speculated that a clone of chromosomally abnormal erythroid precursors might be responsible for producing the erythroblasts with the structural abnormalities described and the erythrocytes with the high hemoglobin F content.
Local Production of Colony-stimulating Factor Within the Bone Marrow: Role of Nonhematopoietic Cells
Authors: Chan Soh Ha , Metcalf Donald 
Published: October 2019

Abstract
Local production of the granulocyte and macrophage regulator, colony-stimulating factor (CSF), within the mouse bone marrow cavity was assessed by determining the capacity of marrow cells or the bone shaft to release or produce active material in liquid cultures. Assays for colony-stimulating activity were performed in agar cultures of mouse bone marrow cells. Following flushing of femoral marrow cells, with or without trypsinization, less than 5% of total marrow cells remained in the bones. However, media conditioned by such bones from adult mice had eight to 20 times the total colony-stimulating activity of media conditioned by the entire extruded marrow cell population. The difference was more marked in femurs from neonatal mice. This activity of both bone and marrow cells was radioresistant. During regeneration following wholebody irradiation, marrow cell activity remained constant, but a significant rise in the capacity of shaft-related cells to conditioned medium occurred simultaneously with the onset of regeneration of granulocytic and monocytic progenitor cells. Local production of CSF by nonhematopoietic cells in the marrow appears to be a significant factor in regulating granulopoiesis and monocyte formation.
Inhibition of the Generalized Shwartzman Reaction by Hypofibrinogenemia
Authors: Bell William R. , Miller Robert E. , Levin Jack 
Published: October 2019

Abstract
The effect of hypofibrinogenemia on production of the generalized Shwartzman reaction (GSR) by the administration of Thorotrast (3 ml/kg) and Escherichia coli endotoxin (50 µg) to rabbits was determined. Severe hypofibrinogenemia (fibrinogen less than 15 mg/ 100 ml) was produced by Arvin, a proteolytic coagulant from the venom of the Malayan pit viper, Agkistrodon rhodostoma. Development of the GSR was inhibited significantly only when hypofibrinogenemia was produced 30 hr before the preparatory injection of Thorotrast and maintained for the duration of the experiment. Severe hypofibrinogenemia of 2-20-hr duration before administration of endotoxin did not block the production of the GSR. Elevated levels of fibrinogen degradation products were demonstrated in the serum of all animals that received Arvin. The concentration of fibrinogen degradation products decreased markedly prior to death only in those animals that developed the GSR. The GSA was not observed in rabbits that received only Thorotrast and Arvin, although these animals had the highest levels of fibrinogen degradation products. The data suggest an essential role for fibrinogen or fibrinogen degradation products and endotoxin in the production of the GSR.
Intravascular Coagulation in Acute Leukemia: Clinical and Subclinical Abnormalities
Authors: Gralnick Harvey R. , Marchesi Sally , Givelber Harry 
Published: October 2019

Abstract
Fifteen patients with acute leukemia were found to have evidence of a generalized hemostatic disorder. These patients could be divided into three groups. The first group consisted of three patients with increased fibrinogen catabolism without clinical or laboratory evidence of intravascular coagulation. The second group of five patients had laboratory evidence of intravascular coagulation without clinically evident bleeding or thrombosis. The third group of seven patients developed symptomatic intravascular coagulation characterized by bleeding, renal failure, and poor response to platelet transfusions. Laboratory evidence for intravascular coagulation in these patients included falling plasma fibrinogen and factor V levels and elevated serum levels of fibrinogen degradation products. Heparin therapy resulted in clinical improvement in all seven patients. Rising plasma fibrinogen and factor V levels correlated with a beneficial clinical response to heparin. Increased fibrinogen catabolism, asymptomatic intravascular coagulation, and symptomatic intravascular coagulation form part of a spectrum of generalized hemostatic disorders in acute leukemia.
Mucopolysaccharide Sulfation in Normal and Leukemic Leukocytes
Authors: Lau Peter , Gottlieb Arlan J. , Williams William J. 
Published: October 2019

Abstract
Mucopolysaccharide sulfation was demonstrated in leukemic granulocytic precursors in short-term suspension culture by incorporation of 35SO4 into a compound identified chromatographically as chondroitin sulfate. The gel filtration pattern of sulfated mucopolysaccharide obtained from leukemic leukocytes was qualitatively similar to that found with normal granulocytic precursors. Sulfation of mucopolysaccharide was about 50% of the normal level in cells from chronic granulocytic leukemia, and approximately 15% of the normal level in cells from acute granulocytic leukemia or chronic granulocytic leukemia in blastic crisis. Lymphocytes from acute and chronic lymphocytic leukemia showed only traces of sulfate incorporation. Leukocyte mucopolysaccharide sulfation was studied in cultured cells from patients with acute leukemia to determine whether this reaction could aid in distinguishing acute granulocytic leukemia from acute lymphocytic leukemia. Significant levels of sulfation were obtained in cells from all leukemias judged to be acute granulocytic, while virtually no incorporation was found in cells from acute lymphocytic leukemia when a 24-hr incubation period was employed. In studies employing a 3-hr incubation, agreement as to the cell of origin of the leukemia and the degree of sulfation in the intracellular fraction was obtained in 16 of 18 determinations performed on 16 patients with acute leukemia. It is proposed that determination of 35SO4 incorporation in the intracellular fraction may help to differentiate acute granulocytic and acute lymphocytic leukemia.
Hypothesis: Engrafted Human Bone Marrow and Blood Cells in Culture
Authors: von Heyden Hans W. , Moore George E. 
Published: October 2019

Abstract
Lymphoblasts appearing in immunosuppressed patients after bone marrow transfusion are compared to those that can be established in vitro as permanent lymphoid cell lines. It is suggested that Epstein-Barr virus (EBV) could be responsible for the recurrent "lymphoblastic leukemia" in these patients and that the transplanted cells may be a clone of nonmalignant cells that has become capable of growing without normal restraints. It is important that in future patients the transplanted cells be characterized as to morphology, chromosome constitution, relative clonability and transplantability, the presence of EBV, T or B cell-like traits, and their growth potential in immunosuppressed heterologous hosts. The antibody titer to EBV should be measured before and after leukocyte transfusion.
Glycogen Metabolism in the Normal Red Blood Cell
Authors: Moses Shimon W. , Bashan Nava , Gutman Alisa 
Published: October 2019

Abstract
Evidence for active glycogen metabolism in normal mature red blood cells (RBC) is presented. Initial rates of 14C-U-glucose incorporation into erythrocyte glycogen were found to be independent of substrate concentration over a range of 3.3-16.6 mM. Incorporation of label into glycogen was initially linear but reached a plateau after a variable period of time that was inversely related to RBC concentration in the medium. The major part of the incorporated radioactivity resided in the outer branches of the glycogen molecule. The optimum pH for 14C-U-glucose incorporation into glycogen was pH 7.6. Replacing the radioactive glucose employed for incorporation after 1 hr of incubation with nonlabeled glucose resulted in a gradual loss of radioactivity from erythrocyte glycogen. In normal cells, glycogen synthesis and breakdown do not result in any significant accumulation of glycogen, whereas in erythrocytes with enzyme defects affecting glycogen breakdown, substantial deposition of glycogen may be observed.
Artificially Induced Thyroid Suppression in Sickle Cell Disease
Authors: Seward Charles W. , Eaton John W. , Chaplin Hugh 
Published: October 2019

Abstract
Depression of thyroid function in patients with hemoglobin SS disease might be expected to: (1) reduce tissue oxygen consumption, (2) decrease erythrocyte 2, 3-diphosphoglycerate, (3) decrease p50, (4) increase the average level of erythrocyte oxygenation, and (5) increase in vivo red cell survival with associated improvement in anemia and possibly in musculoskeletal symptoms. Accordingly, 150-200 mg of 6-n-propylthiouracil were administered three times a day for 143 days to a 21-yr-old male with hemoglobin SS disease. Thyrosuppression was indicated by typical symptoms and appropriate changes in physical and biochemical parameters. Detailed hematologic follow-up, including multiple measurements of red cell mass, 51Cr erythrocyte survival, red cell 2,3-diphosphoglycerate, and p50, showed no change. Furthermore, musculoskeletal symptoms continued in the pattern characteristic of the euthyroid state. A possible explanation for the lack of any change in clinical status may be that decreased cardiac output, with attendant prolonged circulation time and increased tissue oxygen demand per red cell per unit time, offset the absolute decrease in tissue oxygen consumption. The study provided an opportunity to make detailed clinical observations of sickle cell disease in association with thyroid suppression. The results suggest that thyrosuppression within the limits of symptomatic and physiologic tolerance has no therapeutic application in the clinical management of hemoglobin SS disease.