bluuebunny/crossref_metadata_2025_split huggingface dataset:
Intravenous Iron: Evaluation of the Use of Saccharated Iron Oxide in Iron Deficiency States in Obstetrics and Gynecology
Authors: HOLLY ROY G. 
Published: October 2019

Abstract
Saccharated iron oxide has been given to 23 patients in doses of 480 to 1,430 mg. Toxic symptoms were minimal. Hematologic response was good in 21 patients. Continued bleeding accounted for the poor response in 2 persons. Saccharated iron oxide is a safe preparation for clinical use. It is easy to administer. Further clinical evaluation is warranted. Excessive amounts of intravenous iron should not be given to any individual.
Studies in Rh Sensitization
Authors: WIENER ALEXANDER S. , NAPPI RAFFAELE , GORDON EVE B. 
Published: October 2019

Abstract
The Rh antibody titer was studied during pregnancy and after delivery in 11 cases in which previously sensitized Rh-negative mothers had Rh-negative babies. In addition, 1 case was studied in which a type Rh1 mother, previously sensitized to the rh'' factor, gave birth to a type Rh1 baby. In all cases the babies were normal at birth and the baby’s serum contained univalent Rh antibodies equal in titer to those present in the maternal serum. In no case was there a rise in the antibody titer in the maternal serum either during the pregnancy or after the baby was born. Thus, it has not been possible to confirm claims concerning a "nonspecific anamnestic rise" in Rh antibody titer said to be caused by an Rh-negative baby.
Two illustrative cases are described in detail. In one of the cases described, there was no appreciable change in Rh antibody titer during the pregnancy despite the use of so-called Rh hapten; nor had there been an appreciable change in titer for as long as two and one-half years previously. The Rh antibody titer of the baby’s blood dropped about 98 per cent by the end of the sixth month, while during the same period of time the maternal antibody titer fell only approximately 35 per cent. Based on the course of the Rh antibody titer of the baby’s serum, the half-life of the antibody globulin molecule is estimated to be about thirty days.
Photosensitive or Congenital Porphyria with Hemolytic Anemia
Authors: ALDRICH ROBERT A. , HAWKINSON VIOLET , GRINSTEIN MOISES , WATSON CECIL JAMES 
Published: October 2019

Abstract
1. The clinical features, laboratory findings and special studies of a case of photosensitive (congenital) porphyria in a 4 year old girl have been presented. This case was of particular interest in view of severe hemolytic anemia with hepatosplenomegaly.
2. Copro- and uroporphyrin I were isolated from the urine and feces. The ratio of these porphyrins in the urine varied from 1:10, to 1:30 respectively, while in the feces the ratio was reversed at about 70:1. Coproporphyrin III was isolated in much smaller amount than the type I isomer, from both urine and feces. Isomer analyses of the coproporphyrins in the excreta indicated that approximately 98 per cent was type I.
3. Prior to splenectomy copro- and uroporphyrin I were isolated in crystalline form for the first time from circulating human erythrocytes. Coproporphyrin III was also isolated in lesser amount. Uroporphyrin I was crystallized from the plasma, which also contained coproporphyrin I. Microfluorospectrometry of the bone marrow revealed large amounts of porphyrin in the developing red cells. The porphyrin fluorescence spectra indicated that at least three porphyrins were present.
4. Splenectomy was followed by disappearance of uro- and coproporphyrins from the erythrocytes, and a marked decrease in plasma, urine and feces without any essential change in the type of porphyrins excreted. The metabolic defect porphyria, was still present, but now latent in character. Reduction in porphyrin excretion was apparently related to elimination of hypersplenic hemolysis and compensatory increase of erythropoiesis. Anemia and dermal photosensitivity to sunlight disappeared simultaneously with the reduction in porphyrin excretion.
5. Efforts to reproduce the skin lesions by artificial light were unsuccessful.
Photosensitive or Congenital Porphyria with Hemolytic Anemia
Authors: GRINSTEIN MOISES , ALDRICH ROBERT A. , HAWKINSON VIOLET , LOWRY PAUL , WATSON CECIL JAMES 
Published: October 2019

Abstract
1. Porphyrin and hemoglobin metabolism have been studied in a case of photosensitive or congenital porphyria with the aid of glycine containing N15. The case was that of a 4 year old girl who also exhibited splenomegaly and hemolytic anemia. The reticulocytes and fecal urobilinogen were markedly increased and the bone marrow was hyperplastic-normoblastic. The urine contained large amounts of uroporphyrin I and lesser amounts of coproporphyrin I, while the reverse was true in the feces. Splenectomy resulted in disappearance of anemia, together with marked reduction of porphyrin excretion.
2. In two separate periods of study a rapid incorporation of glycine N15 was observed in the hemoglobin protoporphyrin, in both coproporphyrin isomers of the urine and in the type I isomer in the feces; also in the uroporphyrin I of the urine, and in the protoporphyrin and stercobilin of the feces.
3. The N15 data obtained for the urinary and fecal coproporphyrin and the urinary uroporphyrin, clearly reveal a synthesis similar in character to that of the hemoglobin protoporphyrin. The striking decline in formation of copro- and uroporphyrin after splenectomy is believed to be correlated directly with the reduced erythropoiesis incident to removal of the excessive hemolysis.
4. In both experiments the peak concentration of N15 was earlier and greater in the copro- than in the uroporphyrin. This, together with the closely similar slopes of decrease of the N15 curves for the two substances, does not appear to support a transition of uro- to coproporphyrin in the present case. The data are more consistent with the view that coproporphyrin I is a precursor of uroporphyrin I, or that both porphyrins are synthesized independently from common precursors.
5. The amount of coproporphyrin III in the excreta was too small to permit N15 analysis except in one period early in the first experiment; here the value was approximately the same as that of the copro- I for the same period, indicating a closely related synthesis.
A Method of Measuring the Severity of a Series of Cases of Hemolytic Disease of the Newborn
Authors: MOLLISON P. L. , CUTBUSH MARIE 
Published: October 2019

Abstract
1. The hemoglobin concentration in the cord blood of infants affected with hemolytic disease is very closely related to their chance of survival. If the hemoglobin concentration is plotted against the chance of survival, a sigmoid curve is obtained. Probit analysis can be applied and the results of treatment can then be summarized in terms of the severity of the cases treated. For example, in the present series the cord hemoglobin concentration corresponding to a 50 per cent chance of survival was 8.09 Gm./100 ml.
2. Application of probit analysis makes it possible to compare results obtained in different centers, for due allowance is made for any difference in severity in the cases included in the different series.
3. In the present series, despite uniform treatment (exchange transfusion), over-all mortality fell from 37 percent in 1947 and 1948 to 3 per cent in 1950. It is shown that this can be entirely explained by a decrease in the number of severely affected infants.
4. Predictions of survival based on the cord hemoglobin concentration and cord bilirubin concentration combined are not significantly better than predictions based on cord hemoglobin concentration alone.
5. Infants with positive direct Coombs tests whose cord hemoglobin concentrations exceed 15.5 Gm./100 ml. have some risk (approximately 1 in 12) of developing kernicterus, if untreated.
A clinical trial of anti-idiotype therapy for B cell malignancy
Authors: Meeker TC , Lowder J , Maloney DG , Miller RA , Thielemans K , Warnke R , Levy R 
Published: October 2019

Abstract
Eleven patients with B lymphocytic malignancy were treated with mouse monoclonal anti-idiotype antibodies. All but one of the patients in this study had received extensive prior treatment with conventional lymphoma therapy. All antibodies were prepared against, and uniquely reactive with, the patient's own tumor. Ten patients were treated with a single antibody, but one patient received three antibodies concurrently. The treatment protocol initially used an escalating dose schedule that was intended to evaluate toxicity, pharmacokinetics and, eventually, to achieve appreciable levels of free mouse antibody in the circulation. The last two patients received substantial initial doses. Tumor sampling was performed before and during therapy to evaluate tissue penetration by antibody. None of the patients had serum paraproteins by routine clinical testing, but six had idiotype protein detectable by a sensitive immunoassay at levels greater than 1 microgram/mL, two of which were greater than 200 micrograms/mL. Plasmapheresis was capable of reducing these levels temporarily. However, the presence of serum idiotype increased the requirement for mouse antibody to achieve tumor penetration. Another obstacle to treatment was immune response to mouse Ig, which occurred in five of the 11 patients. Once an immune response had begun, further infusions of antibody were not capable of reaching the tumor or inducing tumor regression and were associated with toxicity. Our initial patient remains in an unmaintained complete remission 42 months after receiving antibody. Five of ten additional patients have had objective remissions that were also clinically significant. However, these remissions were not complete and were of relatively short duration. This therapy shows promise as an alternative modality for the treatment of B cell malignancy. Further study will be needed to determine the mechanisms of the antitumor effect and to improve the clinical results.
Inhibitors of cholera toxin-induced adenosine diphosphate ribosylation of membrane-associated proteins block stem cell differentiation
Authors: Dexter TM , Whetton AD , Heyworth CM 
Published: October 2019

Abstract
Two potent inhibitors of mono-adenosine diphosphate (ADP) ribosylation have recently been described and characterized, named p- methoxylbenzylaminodecamethylene guanidine sulfate (MBAMG) and benzylaminododecylguanine hydrochloride (BADGH). We have used these agents to investigate the role of ADP ribosylation in hematopoiesis using long-term marrow cultures. The addition of MBAMG (10(-6) mol/L) or BADGH (5 X 10(-4) mol/L) led to both an inhibition of mature cell production and the development of colony-stimulating factor (CSF-1)- responsive GM-CFC, but had no effect upon spleen colony-forming units (CFU-S) or on progenitor cells which respond to the multilineage stimulating factor present in WEHI-3B cell-conditioned medium. These data indicate that these inhibitors of mono-ADP ribosylation can block the commitment and/or differentiation of stem cells and infers that ADP ribosylation may be of some importance in the hematopoietic process.
Influence of Dimethylaminoazobenzene on Leukocyte Production in the Rat
Authors: DINNING JAMES S. , PAYNE LOU DEWEES , DAY PAUL L. 
Published: October 2019

Abstract
1. Supplementation with p-dimethylaminoazobenzene plus vitamin B12 prevented leukopemia in rats fed a methionine-deficient basal diet. p-Dimethylaminoazobenzene was ineffective in this regard in the absence of supplementary vitamins B12.
2. Possible relationships of this observation to the theory of p-dimethylaminoazobenzene carcinogenesis are discussed.
Genetic Aspects of Sickle Cell Anemia and Microdrepanocytic Disease
Authors: SILVESTRONI E. , BIANCO I. 
Published: October 2019

Abstract
1. A brief review is presented of the genetic theories of sickle cell anemia and the sickle cell trait.
2. The genetic data on 2 families of asymptomatic individuals with the sickle cell trait and of 3 families of patients with sickle cell anemia are reported. These data confirm the heterozygous-homozygous theory of Neel.
3. The possibility is considered that many of the cases of sickle cell anemia described in the white race are actually examples of "microdrepanocytic disease."
4. Microdrepanocytic disease is a new syndrome, first described by the authors from Italy. It has some of the characteristics of both sickle cell anemia and Mediterranean anemia. On the basis of studies in 11 families, the presence of the sickle cell trait in one parent and of microcythemia (Mediterranean anemia trait) in the other, results in microdrepanocytic disease in some of the offspring. Hematologic studies in these patients indicate the simultaneous presence of both sickle cell and microcythemic genes.
5. Genetic studies of these families suggests that the genes for microcythemia and for sicklemia are located on different chromosomes and are inherited independently of each other. On the other hand, their simultaneous presence leads to a disease of a moderate degree of severity having many of the features of sickle cell anemia.
Hemorrhagic Disease in an Infant Due to Deficiency of a Previously Undescribed Clotting Factor
Authors: SCHULMAN IRVING , SMITH CARL H. 
Published: October 2019

Abstract
1. A case of hemorrhagic disease in an infant due to deficiency of a previously undescribed plasma coagulation factor has been presented.
2. The patient demonstrated all presently accepted criteria for a diagnosis of hemophilia, but the deficient factor was demonstrably different in the two conditions.
3. The deficient factor was found in both normal and hemophilic plasmas.
4. The plasma factor deficient in the patient appeared essential for the formation of active thromboplastin.
5. Localization of the deficient factor was carried out by means of plasma fractionation.
6. The possible relationship of the patient to other cases of nonfamilial hemophilia was suggested.
Recombinant granulocyte-macrophage colony-stimulating factor after autologous bone marrow transplantation for relapsed non-Hodgkin's lymphoma: blood and bone marrow progenitor growth studies. A phase II Eastern Cooperative Oncology Group Trial
Authors: Lazarus HM , Andersen J , Chen MG , Variakojis D , Mansour EG , Oette D , Arce CA , Oken MM , Gerson SL 
Published: October 2019

Abstract
Sixteen patients with relapsed non-Hodgkin's lymphoma underwent autologous bone marrow transplantation and infusion of recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF). Treatment consisted of involved-field radiotherapy, cyclophosphamide 60 mg/kg/d intravenously (IV) for 2 days, and fractionated total body irradiation (1,200 cGy). Autologous bone marrow was thawed and infused IV, followed 3 hours later by the first infusion of IV rhGM-CSF 11 micrograms/kg/d over 4 hours. Infusions of rhGM-CSF were continued daily until either both neutrophil count exceeded 1,500/microL and platelet count exceeded 50,000/microL, or until 30 days after marrow re- infusion. Toxicities encountered were mild and included fever, chills, hypertension, alopecia, rash, diarrhea, stomatitis, myalgias, and synovial (knee) effusions. Neutrophil recovery greater than 500/microL occurred a median of 14 days (range, 9 to 30 days) after marrow infusion, significantly earlier than in a comparable group of historic controls who recovered counts at a median time of 20 days (range, 12 to 51 days) (P = .00002). Median time to self-sustaining platelet counts greater than 20,000/microL was 23.5 days (range, 12 to 100 days), comparable with the historic group (P = .38). One bacteremia (central venous catheter exit site infection with Staphylococcus epidermidis) and one local infection (Giardia lamblia in stool) occurred. Patients received a median of 11.4 (range, 4.4 to 20.2) x 10(4) colony-forming unit granulocyte-macrophage (CFU-GM) progenitors per kg. Stem cell progenitors CFU-GM, CFU-granulocyte, erythroid, monocyte, megakaryocyte (CFU-GEMM), and burst-forming unit-erythroid (BFU-E) were detected in the bone marrow as early as 7 days after marrow re-infusion, and increased in proportion to peripheral blood counts, but by 30 to 60 days still remained much lower than before transplant. Neutrophils transiently decreased in 13 of 16 patients (median decrease, 42%) within 24 to 72 hours of discontinuing rhGM-CSF infusions. These data suggest that rhGM-CSF therapy enhances neutrophil recovery by forcing stem cells to produce mature elements at an enhanced rate but may not affect marrow stem cell and early progenitor population sizes.
Molecular basis for antithrombin III type I deficiency: three novel mutations located in exon IV
Authors: Vidaud D , Emmerich J , Sirieix ME , Sie P , Alhenc-Gelas M , Aiach M 
Published: October 2019

Abstract
Antithrombin III (AT III) type I deficiencies are characterized by a 50% decrease of both immunoreactive and functional protein and carry a high risk of thrombotic complication. We have studied the molecular basis for such deficiencies by asymmetric polymerase chain reaction amplification and direct sequencing of the seven exons and of the intron-exon junction of the AT III gene. Three different mutations were observed in the exon IV: a 4-bp deletion, a 2-bp deletion, and a nucleotide insertion. Each of these mutations results in a frameshift introducing premature stop codons at positions 313, 309, and 232, respectively. These results were confirmed by dot-blot analysis with allele-specific oligonucleotide probes. Furthermore, no mutation was observed in the other six exons. The comparison of the type of mutations observed by our group in six cases of type I deficiencies and in 16 cases of type II heparin binding site variants deficiencies suggests that the former are caused by heterogeneous molecular abnormalities while the latter are caused by recurrent missense mutations.
Characterization of prostaglandin and thromboxane receptors expressed on a megakaryoblastic leukemia cell line, MEG-01s
Authors: Watanabe T , Yatomi Y , Sunaga S , Miki I , Ishii A , Nakao A , Higashihara M , Seyama Y , Ogura M , Saito H 
Published: October 2019

Abstract
MEG-01s, an established human megakaryoblastic leukemia cell line, exhibited specific high-affinity binding sites for [3H]iloprost, a stable prostaglandin (PG) I2 analogue, for [3H]SQ-29548, a stable thromboxane (TX) A2 antagonist and, for [3H]PGE2/PGE1, but not for [3H]PGD2. In the MEG-01s cells, iloprost/PGI2, or PGE1 stimulated cAMP production with ED50 values practically identical to the IC50 values for the [3H] iloprost binding. STA2 and U46619, TXA2/PGH2 agonists, PGE2/PGE1, iloprost/PGI2, and thrombin elevated the intracellular concentrations of Ca2+ ([Ca2+]i), as determined by Fura-2 fluorescence signals. Elevation of [Ca2+]i by PGE2/PGE1 and iloprost, but not that by TX-agonists or thrombin, was totally dependent on the presence of extracellular Ca2+. This effect by PGE2/PGE1 was partially inhibited by prior treatment of the cells with islet-activating protein (IAP), while that by TX-agonists or by PGI2/iloprost was not affected. We tentatively conclude from these results that: (1) MEG-01s cells express (a) PGI2/PGE1 receptor(s) coupled to adenylate cyclase and Ca2+ influx, a TXA2/PGH2 receptor coupled to the phosphatidylinositol-turnover-Ca2+ system, and the PGE2/PGE1 receptor coupled to Ca2+ influx; (2) the receptors for TXA2/PGH2 and iloprost and those for PGE2/PGE1 and thrombin are coupled to IAP-insensitive and IAP-sensitive GTP-binding proteins, respectively, and function in a different manner to elevate [Ca2+]i. Thus, the MEG-01s cell line is a pertinent model for studying eicosanoid receptor-mediated signal transduction in platelet/megakaryocyte systems.
Cytokine regulation of colony-stimulating factor (CSF) production in cultured human synovial fibroblasts. II. Similarities and differences in the control of interleukin-1 induction of granulocyte-macrophage CSF and granulocyte-CSF production
Authors: Hamilton JA , Piccoli DS , Cebon J , Layton JE , Rathanaswani P , McColl SR , Leizer T 
Published: October 2019

Abstract
Synovial fibroblasts are likely to be a significant source of granulocyte-macrophage colony-stimulating factor (GM-CSF) and granulocyte-CSF (G-CSF), which could be crucial to the pathogenesis of rheumatoid arthritis. Using specific enzyme-linked immunosorbent assays (ELISAs) and Northern analysis, GM-CSF and G-CSF expression were followed in human synovial fibroblast-like cells in response to a number of agents, either alone or in the presence of an optimal stimulatory concentration of interleukin-1 (IL-1). For both CSFs, interferon-gamma (100 U/mL) did not increase their levels but dramatically suppressed the stimulatory action of IL-1, while basic fibroblast growth factor (10(-8) mol/L), although nonstimulatory by itself, potentiated IL-1 action. The glucocorticoid, dexamethasone (10(- 7) mol/L), inhibited IL-1-stimulated CSF production. However, evidence was obtained for noncoordinated CSF regulation. Cyclooxygenase inhibitors potentiated the action of IL-1 on GM-CSF synthesis but suppressed G-CSF synthesis, suggesting that endogenous cyclooxygenase products can have opposite effects in modulating the levels of each CSF. Also, the lymphokine, IL-4 (250 pmol/L), slightly inhibited GM-CSF formation in the presence of IL-1 but elevated the G-CSF levels in these cultures without having an effect by itself. Transforming growth factor beta (less than or equal to 20 ng/mL) did not modulate levels of either CSF. Mesenchymal cell production of both GM-CSF and G-CSF is generally viewed as being under coordinate control; our findings suggest that their synthesis in IL-1-stimulated human synoviocytes can be modulated by a number of agents, in some cases with divergent actions depending on which CSF is examined.
Disturbed platelet aggregation to collagen associated with an antibody against an 85- to 90-Kd platelet glycoprotein in a patient with prolonged bleeding time
Authors: Deckmyn H , Van Houtte E , Vermylen J 
Published: October 2019

Abstract
We studied a 5-year-old girl presenting with a markedly prolonged bleeding time. Her platelets were refractory to collagen stimulation, but the response to other agonists was normal. There were no coagulation abnormalities as measured by standard tests. Two- dimensional electrophoresis showed no abnormalities of the patient's platelet membrane glycoproteins. When the patient's plasma or purified plasma IgG was mixed with normal platelets, collagen-induced platelet aggregation was blocked. Western blotting showed the presence of an antibody in the patient's plasma directed against a protein of molecular weight 85 to 90 Kd under both reducing and nonreducing conditions. This protein comigrated with glycoprotein (GP) IV immunoprecipitated by OKM5 from 125I-labeled platelets. Immunoprecipitation of 125I-labeled normal platelet glycoproteins with the patient's IgGs also yielded an 85- to 90-Kd protein that migrated on the diagonal following nonreduced/reduced two-dimensional sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). Despite similarities in electrophoretic behavior, the antigen was not demonstrated to be GPIV, since purified GPIV was not recognized by the antibody.