bluuebunny/crossref_metadata_2025_split huggingface dataset:
Autonomous synthesis of alpha and beta hemoglobin chains in rabbit erythroid cells
Authors: Dembure PP , Garrick MD 
Published: October 2019

Abstract
Hemoglobin beta-chain synthesis by rabbit erythroid cells was tested for dependence on availability of complementary alpha-chains. Reticulocytes and bone marrow cells were obtained from variant rabbits that have hemoglobin with isoleucine in alpha-chains but not in beta- chains. This characteristic permits the use of L-O-methylthreonine, a specific isoleucine antagonist, to inhibit selectively the synthesis of hemoglobin alpha-chains without directly affecting that of beta-chains. Study of hemoglobin synthesis by bone marrow cells presents two problems that require careful management: (A) the fragility of the globin-synthesizing apparatus and (B) the isolation of globin from the various proteins made by the mixture of nucleated cells. Disruption of synthetic activity was minimized by collecting the bone marrow in autologous plasma then removing fat and connective tissue while the cells were suspended in this medium. Purification involved gel filtration of hemoglobin and globin then CM-cellulose chromatography of globin chains. Absence of radioactive isoleucine in beta-chains demonstrated the efficacy of this scheme in removing isoleucine- containing proteins that otherwise elute with beta-chains on CM- cellulose columns. In reticulocytes, when synthesis of alpha-chains is inhibited by 30%--80%, that of beta-chains is stimulated by 20%--60%, but in marrow cells, incorporation into beta-chains stays at control level when alpha incorporation is inhibited. The data indicate that beta-chain synthesis is independent of the availability of complementary alpha-chains.
Long-term disease-free survival in acute nonlymphocytic leukemia
Authors: Peterson BA , Bloomfield CD 
Published: October 2019

Abstract
Twenty-six of 45 adults (58%) with acute nonlymphocytic leukemia who were treated with intensive induction chemotherapy over 5 yr ago entered complete remission. All patients entering remission were placed on weekly maintenance chemotherapy consisting of cytosine arabinoside and 6-thioguanine. The median duration of complete remission was 17 mo and 7 patients (27%) remained in their initial remission for 62 + to 102 + mo. All but one of the patients in complete remission over 5 yr have had treatment discontinued. Only 1 of 7 patients in remission for more than 5 yr has relapsed. Median survival is 26.5 mo, and 8 patients (31%) currently remain alive without evidence of leukemia 63--105 mo from diagnosis. It is possible to achieve long-term disease-free survival with chemotherapy alone in acute nonlymphocytic leukemia.
Effect of leukocyte antibodies on the fate in vivo of indium-111- labeled granulocytes
Authors: McCullough J , Weiblen BJ , Clay ME , Forstrom L 
Published: October 2019

Abstract
The effect of different leukocyte antibodies on the fate in vivo of granulocytes is not known. Thus, the optimum in vitro serologic tests to determine a safe and effective granulocyte transfusion or to diagnose immune destruction of granulocytes in other clinical situations have not been identified. We have studied the effect of granulocyte agglutinating (GA), granulocytotoxic (GC), and lymphocytotoxic (LC) antibodies on the intravascular recovery and half- life (t 1/2) and the extravascular localization of Indium-111- granulocytes in 50 patients. GA antibodies caused reduced granulocyte recovery and t 1/2 in three of three non-neutropenic patients (one with anti-NB1), increased sequestration of cells in the liver, and failure of granulocytes to localize at sites of infection in two of two patients (one with anti-NA1). In contrast, GC antibodies in five patients and LC antibodies in one patient did not cause reduced intravascular recovery or t 1/2 of granulocytes. In nine patients with GC and six patients with LC antibodies, incompatible granulocytes localized at known sites of infection. It appears that GA, but not GC nor LC, antibodies alter the fate in vivo of granulocytes.
Regulation of in vitro erythropoiesis by normal T cells: evidence for two T-cell subsets with opposing function
Authors: Torok-Storb B , Martin PJ , Hansen JA 
Published: October 2019

Abstract
Cellular interactions responsible for regulating in vitro erythropoiesis were studied using murine monoclonal antibodies recognizing antigens expressed by human mononuclear cells. Cell populations of interest were negatively selected by complement- dependent cytotoxicity and then evaluated for their effect on in vitro growth of erythroid burst-forming units (BFU-E). The data suggest that normal peripheral blood T cells contain at least two functionally distinct subpopulations with opposing regulatory effects: one that enhances burst formation had one that limits burst formation. Whether these effects are mediated by direct interactions of T cells with BFU-E or with auxillary cells remains to be determined.
Factors predicting long-term survival in diffuse mixed, histiocytic, or undifferentiated lymphoma
Authors: Fisher RI , Hubbard SM , DeVita VT , Berard CW , Wesley R , Cossman J , Young RC 
Published: October 2019

Abstract
Clinical and histopathologic material from 151 cases of diffuse mixed, diffuse histiocytic, and diffuse undifferentiated non-Burkitt's lymphomas have been reviewed to determine the factors that predict long- term survival. Median survival of all patients was 34 mo with 43% alive at 70 mo. Factors associated with a poor prognosis include: male sex, constitutional symptoms, advanced stage, bone marrow involvement, huge (greater than 10 cm) abdominal masses with gastrointestinal involvement, hepatic involvement, hemoglobin greater than 12 g/dl, or serum LDH greater than 250 U. The best prediction of a given patient's survival was defined by a set of four variables, which includes sex, symptoms, bone marrow status, and the presence or absence of a huge abdominal mass with gastrointestinal involvement. In contrast, classification of these patients according to the histopathologic categories of Rappaport of Strauchen did not define patient groups with significant differences in survival, nor did these categories correlate with the previously described clinical factors. Knowledge of the distribution of these prognostic factors in any clinical trial is needed before therapeutic results can be compared. In addition, such data may define subsets of patients for whom current therapy is inadequate and conversely those patients for whom current therapy yields excellent long-term survival.
Biochemical analysis of specific histamine HI and H2 receptors on lymphocytes
Authors: Osband ME , Cohen EB , Miller BR , Shen YJ , Cohen L , Flescher L , Brown AE , McCaffrey RP 
Published: October 2019

Abstract
It is increasingly clear that histamine mediates a variety of lymphocyte functions. Further understanding of these mechanisms requires a method for the analysis of histamine membrane receptors on the lymphocyte surface. We report now a biochemical technique for the identification and quantitation of specific histamine H1 and H2 receptors of lymphocytes. The method can be performed on small numbers of formaldehyde-fixed cells. The data this assay yields, together with that resulting from the flow cytometric analysis of histamine receptor distribution (a technique we have previously described), will be a powerful tool in the study of histamine mediation of lymphocyte function.
Monocyte-mediated antibody-dependent cell-mediated cytotoxicity: the role of the metabolic burst
Authors: Koller CA , LoBuglio AF 
Published: October 2019

Abstract
Human monocytes respond to opsonized microorganisms with a “metabolic burst” composed of an increase in oxygen consumption, an increase in hexose monophosphate shunt (HMPS) activity, and the generation of reactive oxygen species (ROS). We investigated the role of the metabolic burst in antibody-dependent cell-mediated cytotoxicity (ADCC) by human monocytes toward anti-D coated erythrocyte target cells because recent studies suggested a role for oxygen-dependent bactericidal mechanisms in ADCC. In normal monocytes, we found that ADCC was nearly halved under hypoxic conditions. Several agents known to impair activation of the burst, such as vincristine, cation chelators, and a sulfhydryl reagent, all decreased cytotoxicity if added before initiation of contact between target and effector cells. Cytotoxicity was inhibited by 2-deoxyglucose but not fluoride, suggesting a nonglycolytic role for glucose in ADCC, perhaps in the HMPS pathway. Although these data suggested a role for the metabolic burst in ADCC, scavengers of ROS did not impair cytotoxicity, and monocytes from chronic granulomatous disease (CGD) patients who had a defective metabolic burst had normal levels of ADCC. We conclude that ADCC toward anti-D coated erythrocyte target cells was the result of at least two independent but closely related cytotoxic pathways. Although one of these pathways appeared to involve the metabolic burst, the potentially cytotoxic reactive oxygen species did not appear to play a role in this system.
Lymphoblast purine pathway enzymes in B-cell acute lymphoblastic leukemia
Authors: Reaman GH , Blatt J , Poplack DG 
Published: October 2019

Abstract
Activities of enzymes of the purine metabolic pathway, adenosine deaminase (ADA), purine nucleoside phosphorylase (PNP), and 5′- nucleotidase (5′-N), were investigated in the lymphoblasts of a patient with B-cell acute lymphoblastic leukemia. These lymphoblasts exhibited increased ADA activity and diminished activities of both PNP and 5′N' as compared to normal lymphocytes as well as non-T, non-B leukemia cells. This enzymatic pattern is identical to that which has been described in T-cell leukemic lymphoblasts and differs from that which has been observed in the malignant cells of undifferentiated B-cell lymphomas. These data suggest that there is biochemical heterogeneity within the spectrum of B-cell malignancies. Furthermore, inhibitors of ADA may be of use in those B-cell lymphoid neoplasms that exhibit increased ADA activity.
Loss of 111Indium as indicator of platelet injury
Authors: Joist JH , Baker RK 
Published: October 2019

Abstract
We previously demonstrated that platelets can be labeled with 111Inoxine with high labeling efficiency and that 111In is not liberated from labeled platelets during the platelet release reaction or prolonged in vitro storage. In view of these findings, we examined the potential usefulness of loss of 111In from labeled platelets as an indicator or platelet damage by comparing the loss of 111In with that of 51Cr and LDH (in some experiments also with platelet factor 3 availability) under different conditions of platelet injury. When washed human platelets labeled with either 51Cr-chromate or 111In-oxine were exposed to increasing concentrations of detergents (Triton X-100, lysolecithin), threshold, rate, and extent of loss of 111In, 51Cr and, LDH were similar. In contrast, when labeled platelets were depleted of metabolic energy by incubation in glucose-free Tyrode albumin solution or glucose-depleted plasma in the presence of antimycin A and 2-deoxy-D- glucose, loss of 51Cr (and PF3a) occurred earlier and progressed at a faster rate than that of 111In or LDH. Similar results were obtained when platelets were exposed to increasing concentrations of PlA1 antibody, causing complement-mediated immune injury. The findings indicate that with certain agents that cause rapid platelet disruption (lysis), different platelet constituents are lost at similar rates. However, under conditions of more subtle or slowly progressive platelet injury, small molecules such as adenine nucleotides (51Cr) may escape earlier and at faster rates than larger molecules such as LDH or 111In- binding platelet protein. Thus, neither 111In loss nor LDH loss appear to be suitable indicators for sublytic or prelytic platelet injury.
Intensive chemotherapy is the treatment of choice for elderly patients with acute myelogenous leukemia
Authors: Foon KA , Zighelboim J , Yale C , Gale RP 
Published: October 2019

Abstract
One-hundred and seven patients with acute myelogenous leukemia (AML) ranging in age from 15 to 82 yr who were previously untreated, received a 70 day high-dose remission induction regimen consisting of daunorubicin, cytarabine, and thioguanine (TAD). Identical complete remission rates of 65% were observed for 33 patients 60 yr of age and older and for 74 patients age 15–59 yr. Median remission duration and survival were 14 mo and 22 mo for patients 60 yr and older, and 16 mo and 22 mo for patients 15–59 yr. These differences are not significant. These data indicate that older patients respond to intensive chemotherapy in a similar manner to younger patients with this disease.
Prostacyclin and beta-adrenergic catecholamines inhibit arachidonate release and PGI2 synthesis by vascular endothelium
Authors: Adler B , Gimbrone MA Jr , Schafer AI , Handin RI 
Published: October 2019

Abstract
We have investigated the mechanism by which cyclic AMP inhibits PGI2 synthesis in cultured bovine aortic endothelial cells. Inhibition of cyclic AMP phosphodiesterase activity by 3-isobutyl-1-methylxanthine (IBMX) blocks calcium ionophore-induced PGI2 production by 62%. The addition of 3 mM dibutyryl cyclic AMP, alone with IBMX, increases the inhibition to 96%. Release o 3H-arachidonate from membrane phospholipids was inhibited 25% by dibutyryl cyclic AMP, 48% by IBMX, and 76% by isoproterenol plus IBMX. Inhibition by isoproterenol was reversed by 10 micro M propranolol. Release of 3H-arachidonate was also reduced 75% by a combination of 10 micro M PGI2 and 3 mM IBMX. We conclude that hormones like isoproterenol and PGI2 may regulate endothelial cell PGI2 biosynthesis by increasing intracellular cyclic AMP, which then inhibits release of endogenous arachidonate from membrane phospholipids.
Amphotericin-B promotes leukocyte aggregation of nylon-wool-fiber- treated polymorphonuclear leukocytes
Authors: Boxer LA , Ingraham LM , Allen J , Oseas RS , Baehner RL 
Published: October 2019

Abstract
Severe pulmonary reactions have been reported in patients receiving leukocyte transfusion and amphotericin-B. To study the interaction of amphotericin-B with polymorphonuclear leukocytes (PMN), purified human PMN were incubated with 200 mg of nylon wool fiber for 60 min either in the absence or presence of 2 mM EDTA. PMN were recovered in acid citrate dextrose solution and were suspended in balanced salt solution for determination of their aggregation properties. The cells exposed to nylon wool fibers without EDTA aggregated in response to concentration as low as 1.25 micrograms/ml of amphotericin-B. Cells initially treated with EDTA, however, failed to aggregate. Serum from a patient treated with amphotericin-B aggregated PMN exposed to nylon wool fiber but not control cells, whereas serum taken before amphotericin was given without effect on the PMN treated with nylon wool fiber. Amphotericin-B at 5 micrograms/ml failed to potentiate the release of beta- glucocuronidase or lactic dehydrogenase by PMN treated by nylon wool beyond that seen with exposure to the fibers alone. Rabbit peripheral blood was similarly incubated with nylon wool fibers and the recovered PMN were infused into recipient rabbits that had received 1 mg/kg of amphotericin-B intravenously 1 hr prior to the infusion of the leukocytes. Rabbits were sacrificed 30 min after transfusion of PMN, and their lungs were excised for histologic sectioning. Those rabbits receiving a combination of amphotericin-B and 4 x 10(7) nylon-wool- fiber-treated PMN had evidence of pulmonary hemorrhage and accumulation of leukocytes in the pulmonary vasculature whereas those animals who received such cells alone had normal appearing lung tissue. In summary, amphotericin-B at concentrations achievable in vivo enhanced the aggregation of PMN damaged by incubation with nylon fiber with subsequent accumulation of the phagocytes in pulmonary tissue.
Infectious mononucleosis: sequential immunologic, cytochemical, and cytokinetic studies on single lymphoid cells in peripheral blood
Authors: Hirt A , Imbach P , Morell A , Wagner HP 
Published: October 2019

Abstract
Sequential immunologic, cytochemical, and cytokinetic studies were done on single lymphoid cells in the peripheral blood of 6 children with infectious mononucleosis (IM) and 1 child with toxoplasmosis 1–2 wk after onset of symptomatology. The absolute number of AET-SRBC rosetting (E+) cells was increased in all patients; the absolute number of cells with surface IgM (slgM+) was increased in 3 of 7 patients. On the average, 46% of all lymphoid cells were E+la+slgM-, 35% E+la-slgM-, and 5% E-la+slgM+. Of the E+la+slgM- cells, only 7% were shown to have a dot-like esterase reaction pattern. Of the E+la-slgM-cells, 17% were esterase positive. The mean labeling index of the former was 18.2%, the mean labeling index of the latter 4.4%. No proliferating slgM+ cells were observed in the 6 children with IM. The esterase reactions and the labeling indices of suppressor-cytotoxic and inducer-helper T cells were similar to those of E+la+slgM- and E+la-slgM- cells, respectively. These results suggest that the vast majority of the atypical cells in IM corresponds to activated suppressor cells, while a minority appears to be proliferating helper cells.
A rapid assay for evaluation of iron-chelating agents in rats
Authors: Pippard MJ , Johnson DK , Finch CA 
Published: October 2019

Abstract
The animal assay of potential new iron-chelating agents is at present dependent on cumbersome and imprecise iron balance studies in hypertransfused rodents. We report the development of a radioisotope assay in intact rats based on the transient labeling by ferritin 59Fe of the main source of chelatable iron within hepatocytes. The isotope was maximally available to chelators during the first 6 hr after its injection, nearly all the excretion being in the bile. The bile 59Fe/total iron ratio was independent of both the chelator and its dose. However, in iron-loaded rats, the ratio was reduced, and the isotope excretion was a less sensitive measure of intrahepatic chelation. In the proposed assay, test chelators were given to normal rats 2 hr after an intravenous injection of 59Fe-ferritin. Four hours later, the radioiron in the liver and in the gut gave a sensitive measure of the mobilization of hepatic iron to the bile. In addition, chemical iron determinations identified a small alternative source of urinary chelate with agents known to promote urine excretion in man. The assay gave a rapid and precise screen for chelators given by parenteral and oral routes.
The presence within single K-562 cells of erythropoietic and granulopoietic differentiation markers
Authors: Marie JP , Izaguirre CA , Civin CI , Mirro J , McCulloch EA 
Published: October 2019

Abstract
The continuous cell line K-562, derived from a patient with CML in blast crisis, was examined for markers of granulopoietic (My-1) and erythropoietic (spectrin) differentiation, using specific antibodies detected by indirect immunofluorescence. Both markers were seen, and in 10%--30% of cells, both were present in the same cells. In contrast, the continuous leukemic line HL-60 and KGI contained My-1 only. Controls consisted of colonies in culture containing both granulopoietic and erythropoietic cells (CFU-GEMM). In these, My-1 was seen only in granulopoietic cells and spectrin in erythropoietic cells. The suggestion is advanced that genes coding for differentiation markers are expressed abnormally in K-562.
Follow-up observations on the effect of human leukocyte interferon in non-Hodgkin's lymphoma
Authors: Louie AC , Gallagher JG , Sikora K , Levy R , Rosenberg SA , Merigan TC 
Published: October 2019

Abstract
Follow-up data for 11 patients with non-Hodgkin's lymphoma treated with partially purified human leukocyte interferon is presented. The interferon preparation used was 0.1% pure and treatment consisted of 5 x 10(6) U given intramuscularly twice daily for 60 injections. One complete, three partial, and three minimal responses were observed in five of seven evaluable patients with nodular non-Hodgkin's lymphoma. Duration of response appears to be from 6 to 12 mo. One patient achieved a second partial response on retreatment with interferon in spite of having received chemotherapy in the interval between interferon treatments. No responses were seen in three patients with rapidly progressive diffuse histiocytic lymphoma. Dose-limiting toxicity is leukopenia, which necessitated modification or cessation of treatment in three patients. Nonhematologic toxicities consisted of fever, malaise, arthralgia, and loss of appetite. In conclusion, interferon has activity against non-Hodgkin's lymphoma, and prior treatment with chemotherapy does not preclude a response to interferon.
Defective neutrophil migration in monosomy-7
Authors: Ruutu P , Ruutu T , Repo H , Vuopio P , Timonen T , Kosunen TU , de la Chapelle A 
Published: October 2019

Abstract
The migration in vitro of neutrophils from six patients with monosomy-7 or partial deletion of the long arm of chromosome 7 was studied by two methods: the Millipore filter assay and the migration under agarose assay. Four of the patients had preleukemia, one had subacute myelomonocytic leukemia, and one polycythemia vera. In four patients, chemotaxis (migration towards a higher concentration of chemoattractant) and chemokinesis (stimulated migration without a gradient) were shown to be defective by both methods. In the remaining two patients, this defect could be demonstrated only by the Millipore filter assay or by the agarose assay. Under agarose, random locomotion (no chemoattractant present) of the patients' neutrophils was less than that of the control subjects in four patients, whereas no clear difference could be shown by the Millipore filter method. This study demonstrates that the previously described defect of neutrophil migration in monosomy-7 involves not only chemotaxis but all stimulated migration and, at least in some patients, random locomotion as well. Defective migration in two patients with an apparently terminal deletion of the long arm of one chromosome 7 indicates that the distal half of 7q carries genetic material important for neutrophil locomotion.
Attachment of particle-bound IgG and complement to human neutrophils
Authors: Lawrence WD , Packman CH , Rowe JM , Lichtman MA 
Published: October 2019

Abstract
The attachment of particle-bound IgG in a nonphagocytic system stimulates formation of a microfilament-rich, organelle-poor zone in the subjacent cytoplasm of human neutrophils. The attachment site is characterized by ruffling and invagination of the neutrophil membrane. Both IgG attachment and formation of the organelle-poor zone are inhibited by the microfilament inhibitor cytochalasin-B, but not by inhibitors of microtubules, such as colchicine or vinca alkaloids. In contrast, attachment of particle-bound complement is not inhibited by cytochalasin-B in doses known to disrupt actin filaments. There is no discernable change in the subjacent cytoplasm of the neutrophil in response to complement and the membrane attachment site is smooth, without ruffling or invagination. These studies disclose that both IgG- mediated attachment to neutrophils and its sequel, peripheral cytoplasmic reorganization, are mediated by cytochalasin-sensitive structures, possibly actin. Complement-mediated attachment to neutrophils is insensitive to high doses of cytochalasin, suggesting that actin integrity is not required.