bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hemolytic Anemia with Cold Detectable IgG Antibodies
Authors: MACKENZIE MALCOLM R. , CREEVY NANCY C. 
Published: October 2019

Abstract
Erythrocytes obtained from patients who manifest autoimmune hemolytic anemia can be divided into at least three categories by the nature of their protein coats as determined by direct antiglobulin (Coombs) test: IgG alone, IgG and complement (C), C alone. IgG antibodies were detected by direct Coombs Test at 4°C but not at 37°C in patients of type 3 A.H.A. Experiments at 4, 10, 15, 20, 30 and 37°C demonstrated that the IgG antibody was not eluted from the red cells at 37°C but apparently underwent a configurational change above 10°C such that agglutination no longer occurred with the Coombs reagent. This change was reversible. The presence of cold detectable IgG antibodies provides a mechanism for C deposition on erythrocytes in some cases of A.H.A., ostensibly due to complement alone.
Fetal Effects of Coumadin Administered During Pregnancy
Authors: HIRSH J. , CADE J. F. , GALLUS A. S. 
Published: October 2019

Abstract
The safest and most practical method of administering long-term anticoagulants in pregnancy is uncertain because treatment of the mother with vitamin K antagonists may be complicated by hemorrhage in the fetus. The effects on the fetus of giving coumadin in pregnancy was evaluated in rabbits. When coumadin was given from early pregnancy until term, all of the fetuses were stillborn with widespread hemorrhages. However, the fetuses were born alive and without hemorrhage when (1) coumadin was stopped 4-5 days before delivery, at which time the level of coagulation factors had almost returned to normal and (2) when delivery was performed by cesarean section at a time when the fetal coagulation defect was severe. It is suggested that the risk of fetal hemorrhage is high only when fetuses with a severe coagulation defect are exposed to the trauma of delivery.
Combination Chemotherapy With Nitrogen Mustard, Vincristine, Procarbazine and Prednisone in Previously Treated Patients With Hodgkin’s Disease
Authors: LOWENBRAUN STANLEY , DEVITA VINCENT T. , SERPICK ARTHUR A. 
Published: October 2019

Abstract
Combination chemotherapy with four drugs—nitrogen mustard, vincristine, procarbazine and prednisone—was used in 27 previously treated patients with advanced progressive Hodgkin’s disease. Six 2-week cycles of chemotherapy were administered in the following schedule: nitrogen mustard, 6 mg./sq.M. I.V., and vincristine, 1.4 mg./sq.M. I.V., on days 1 and 8 of each cycle; procarbazine, 100 mg./sq.M. by mouth daily throughout each cycle, and prednisone, 40 mg./sq.M. orally each day of cycles 1 and 4. Each cycle was followed by a 2-week period during which no drug was given. Twenty-two patients had Stage IV disease and 17 had systemic symptoms at the time of drug administration. All patients had histories of previous therapy. Two received chemotherapy alone, 15 had radiotherapy alone and 10 had both chemotherapy and radiotherapy. Nineteen out of the 27 patients (70%) had complete responses (total regression of all lesions) to the four drug combination and five patients (19%) had partial responses (50% regression of all lesions). Fourteen out of the 19 who responded completely are still in unmaintained remission 1-24 months from therapy completion. Eighteen out of the 19 who responded completely are still surviving from 6 to 30 months after the start of combination chemotherapy. Those patients treated previously with both radiotherapy and chemotherapy did not respond as well as patients treated with prior radiotherapy alone. In general, therapy was well tolerated, with leukopenia being the major dosage-limiting toxicity. There was a progressively poorer tolerance to the drugs with increasing extent of prior radiotherapy.
Erythrocyte Glyoxalase II Deficiency With Coincidental Hereditary Elliptocytosis
Authors: VALENTINE WILLIAM N. , PAGLIA DONALD E. , NEERHOUT ROBERT C. , KONRAD PATRICIA N. 
Published: October 2019

Abstract
Hereditary hydroxyacl-glutathione hydrolase (Glyoxalase II) deficiency was demonstrated in both homozygous and heterozygous form in kindred in which hereditary elliptocytosis was inherited independently. Homozygotes and heterozygotes for the enzyme deficiency were clearly differentiated by direct enzyme assay and a variety of indirect methods. Four homozygotes exhibited 10 per cent or less of normal activity. Leukocytes do not share the deficiency. Lactoyl-glutathione lyase (Glyoxalase I) activity was entirely normal in both leukocytes and erythrocytes, and was three times more active than Glyoxalase II. Glyoxalase II deficiency was traceable through three generations, was transmitted as an autosomal recessive trait and was not associated with discernible clinical or hematological abnormalities. It did not appear to worsen clinical manifestations of hereditary elliptocytosis where the two abnormalities coexisted.
Cellular Deformability: A Possible Determinant of the Normal Release of Maturing Erythrocytes From the Bone Marrow
Authors: LEBLOND PIERRE F. , LACELLE PAUL L. , WEED ROBERT I. 
Published: October 2019

Abstract
In vitro measurements of membrane and whole cell deformability indicate that erythroid maturation is accompanied by a progressive increase in cellular deformability. Early and intermediate normoblasts cannot be entirely deformed into a micropipette with dimensions like those of the apertures in the basement membrane which separates marrow hematopoietic cords from sinuses. Shape and nuclear rigidity are the most important determinants of rigidity in these immature cells. The marrow reticulocyte, with its distinctive clover-leaf configuration, still manifests significant intrinsic rigidity of its membrane and possibly underlying cytoplasm, which may be important to its normal retention in the bone marrow. However, further maturation is accompanied by a progressive decrease in membrane stiffness and, hence, resistance to traversing the micropipette. These results are interpreted to suggest that cellular deformability may be an important determinant of normal release of maturing erythrocytes from the bone marrow.
Analytical Review: Spontaneous Chromosomal Breakage and High Incidence of Leukemia in Inherited Disease
Authors: SCHROEDER TRAUTE M. , KURTH RENATE 
Published: October 2019

Abstract
Spontaneous chromosomal breakage has been found in six inherited diseases: ataxia telangiectasia, Bloom’s syndrome, Fanconi’s anemia, glutathione reductase deficiency, Kostmann’s agranulocytosis and pernicious anemia. These diseases are not equally well researched and the cytogenetic data are by no means uniform. However, in each disease, the incidence of leukemia is increased. Chromosomal breakage has been investigated primarily in vitro. In order to connect this phenomenon with each syndrome and with the development of malignancy, the relationship between in vitro results and in vivo events must be established. This relationship may be clarified through the use of direct chromosome preparations from the bone marrow and bone marrow smears. A few such investigations have been carried out. Any evaluation of the results must consider the complexity of the bone marrow in general, as well as in each disease and in each individual case. An understanding of in vivo events in turn would allow an evaluation of factors specific to the in vitro condition, and their ability to enhance, provoke or diminish breakage. It is our opinion that contradictory results from in vitro investigations are not yet confirmed. The kind of studies necessary for such confirmation is fairly clear and, until they have been carried out, it is premature to subgroup the various diseases. A complete understanding of these diseases is possible only when the primary metabolic defect is known. Pernicious anemia is well understood although the genetics remain to be clarified. Biochemical investigations of the other five diseases are still at a preliminary stage. However, a comparison of the cytogenetic data, the clinical picture, as well as the course of the diseases may lead to a conceptualization of the unknown metabolic defect. Although the primary causes for each disease differ they manifest themselves at the cellular level in vitro and/or in vivo as spontaneous chromosomal breakage. As a consequence of this phenomenon a change in the genetic material itself may create, by chance, primary yet unknown conditions for malignant growth. This may partially explain the correlation between spontaneous chromosomal breakage and leukemia. Methodical research in this field requires that blood cultures, bone marrow smears and direct chromosome preparations from bone marrow smears and direct chromosome preparations from bone marrow be included in the close following of the diseases. It is also imperative that the designation of types of chromosome aberrations be standardized and published in detail. This, together with continuing biochemical research will finally elucidate the primary defects involved.
Endogenous Production of 14CO: A Method for Calculation of RBC Life-span In Vivo
Authors: LANDAW STEPHEN A. , WINCHELL H. SAUL 
Published: October 2019

Abstract
In Endogenous Production of 14CO: A Method of Calculation of RBC Lifespan In Vivo, by Stephen A. Landaw and H. Saul Winchell (Blood 36: No. 5, November, 642-656), page 651, first paragraph, lines 10-15, the words "for example, in the normal rat … publication." should be omitted; second paragraph, line 6, "dicer" should read "differ;" Table 1, line 13, "T" should read "T."
Electrophoretic Patterns of Human Leukocyte Alkaline Phosphatase in Polycythemia Vera
Authors: BAXTER MARION F. , REINFRANK RALPH F. 
Published: October 2019

Abstract
Electrophoretic patterns of leukocyte alkaline phosphatase have been examined in seven normal and four erythrocytosis control subjects and in eight patients with polycythemia vera to determine whether changes occurred after chemotherapy. One major fast band and two narrow slow and intermediate bands of enzyme activity were found in both groups. There was no significant difference between the normal and erythrocytosis subjects. Mean values for the control group revealed that the slow band extended from the origin to 0.5 cm, the intermediate band from 0.5 to 1.0 cm, and the fast band from 1.5 to 5.0 cm, with the fast peak apex located 3.4 cm from the origin. In the eight polycythemia vera patients studied both before and after chemotherapy, there was a consistent and significant shift of the fast band from a location extending from 0.9 to 4.2 cm to a near normal position of 1.4 to 4.8 cm with a shift of the fast peak apex from 1.9 to 3.3 cm from the origin, after a remission was obtained. The slow and intermediate bands did not appear to be influenced by therapy.
Reactions of 14C-ADP and 14C-ATP With Washed Platelets From Rabbits
Authors: GUCCIONE M. A. , PACKHAM M. A. , KINLOUGH-RATHBONE R. L. , MUSTARD J. F. 
Published: October 2019

Abstract
Using suspensions of washed rabbit platelets that react to low concentrations of ADP in the same way as platelets in plasma, it has been found that the major change in added 14C-ADP is its conversion to 14C-ATP, catalyzed by nucleoside diphosphokinase at the platelet membrane. This enzyme is readily released from the platelets but the rate and extent of 14C-ADP to 14C-ATP conversion are greater in the presence of platelets than in the suspending fluid from which they have been removed. The platelets must provide the source of high-energy phosphate for the reaction, either from ATP released into the suspending fluid, or by the transfer of high-energy phosphate across the membrane. Thrombin stimulates the conversion, probably because it releases ATP from the platelets. Calcium and magnesium stimulate the conversion, whereas two of the inhibitors of ADP-induced aggregation (AMP and parachloromercuribenzenesulfonate) inhibit it. The ATPase activity of these platelets is low and it is not released into the suspending fluid. No adenylate kinase activity was demonstrable. The loss of high energy phosphate from the platelets that occurs during the conversion of 14C-ADP to 14C-ATP may be involved in the initiation of their response to ADP.
A Study of Aplastic Anemia in an Autopsy Series With Special Reference to Atomic Bomb Survivors in Hiroshima and Nagasaki
Authors: KIRSHBAUM JACK D. , MATSUO TAKESHI , SATO KAZUO , ICHIMARU MICHITO , TSUCHIMOTO TAISO , ISHIMARU TORANOSUKE 
Published: October 2019

Abstract
A study of the occurrence of aplastic anemia among atomic bomb survivors in Nagasaki and Hiroshima, Japan was made from a review of a series of 6327 autopsies from 1949 to June 1967 and the late effects of ionizing radiation were evaluated. There were 340 cases reviewed independently by a team of hematologists and pathologists. Of the 45 cases documented as aplastic anemia, 42 were definite and three were probable. Six additional cases were classified as probable. The cases were grouped into four categories depending upon the distance of the subject from the hypocenter at the time of the bomb (ATB). All patients fulfilled the requirement clinically of having pancytopenia. Bone marrow findings at autopsy from various sites revealed aplastic or hypocellular changes in 77.3%. The etiology in 42 cases was idiopathic, one case was drug-induced, one case received radiation for carcinoma of the cervix, and one case congenital in origin. No difference was noted in the exposed cases from the nonexposed. Of those who were exposed to 10 or more rad, the majority (four of five) died prior to 1955. On the basis of the data presented, there is no definite morphologic evidence that implicates ionizing radiation in the pathogenesis of aplastic anemia as a delayed complication of exposure in the A-bomb survivors.
Metabolism of Radio-iodinated Human Serum Albumin in Patients With Monoclonal Gammopathy
Authors: WELLS J. VIVIAN , FUDENBERG H. HUGH 
Published: October 2019

Abstract
(mean HSA level 3.3 g/100 ml, normal with 125I-labeled human serum albumin (HSA) in five patients with monoclonal gammopathy; three with Waldenström’s macroglobulinemia (one also had a γG monoclonal protein) and one patient each with γG multiple myeloma and γG benign gammopathy. Several abnormalities in HSA metabolism occurred in different combinations in different patients and no single consistent pattern was seen. The abnormalities included hypoalbuminemia (means HSA level 3.3 g/100, normal controls 4.7 g/100 ml); hypervolemia due to an expanded plasma volume (mean plasma volume 54.4 ml/kg, normal controls 41.0 ml/kg); decreased plasma and total body albumin pools; increased plasma localization of albumin; shortened plasma T ½; reduced fractional turnover rate; and reduced albumin synthesis rate. The most marked changes were noted in two patients with Waldenström’s macroglobulinemia who required plasma-pheresis for the hyperviscosity syndrome.
Appearance of Bone Marrow Smears With Necrotic Tumor Cells
Authors: BRITTIN GEOFFREY M. , BRECHER GEORGE 
Published: October 2019

Abstract
Bone marrow smears of necrotic tumor cells stained with Romanowsky dyes frequently have a definite reddish color that contrasts so strikingly with the blue color of normal marrow that necrosis may be suspected from gross examination. The bone marrow cells appear "smudged" and are difficult to identify on microscopic examination. Commonly, only a small amount of material is obtainable by ordinary needle aspiration of bone marrow containing necrotic tumor, and all of it is used to make smears. It is therefore important to recognize that bone marrow smears with a reddish gross appearance and in which the cells appear distorted and are difficult to identify may represent necrotic tumor and not an artifact produced by poor techniques.
Lymphocyte Production and Life-span in the Bone Marrow of the Guinea Pig
Authors: ROSSE CORNELIUS 
Published: October 2019

Abstract
Guinea pigs were given 14 daily injections of 3H-thymidine to label a proportion of cells with a slow rate of turnover in addition to rapidly proliferating cells. In the bone marrow the only unlabeled cells were some reticular, endothelial, and plasma cells, damaged cells, and 14.1% of small lymphocytes. Six weeks after discontinuation of 3H-thymidine 7% of the marrow lymphocytes remained labeled. In guinea pigs injected every 4 hr with 3H-thymidine for 4 days to label all cells entering DNA synthesis, 14.4% of small lymphocytes remained unlabeled along with some reticular, endothelial, phagocytic, monocytoid, damaged, and plasma cells. The pattern of appearance of labeled lymphocytes was consistent with the kinetics of transitional cells that function as their precursors. Thus, in the bone marrow of the guinea pig the majority of lymphocytes have a short lifespan and a rapid turnover, whereas about 14% turn over more slowly and 7% have a life-span exceeding 4 wk. In this respect the kinetics of marrow lymphocyte production differs from that of the rat.
Lymphocyte Membrane Enzymes. II. Cyclic 3',5'-Adenosine Monophosphatase Located on Unstimulated Human Small Lymphocyte Nuclear Membranes
Authors: COULSON ALAN S. , KENNEDY LESLEY A. 
Published: October 2019

Abstract
This study was undertaken to localize the enzyme cyclic 3',5'-adenosine monophosphatase in unstimulated human small lymphocytes. Cyclic AMP may be of importance in mediating lymphocyte stimulation, hence localization of the enzyme that is thought to modulate its intracellular concentration, cyclic AMPase, may point to the site of action of cyclic AMP in the cell. The histochemical technique employed was that of Shanta et al.6 Cyclic AMP substrate is degraded by the phosphodiesterase, then hydrolyzed, resulting in a lead phosphate precipitate at the site of enzyme action. This is subsequently visualized as lead sulfide. The enzyme was found to be localized on the nuclear membranes, which indicates that this is the site where cyclic AMP is destroyed. It does not necessarily mean that the nuclear membrane is the site where cyclic AMP is effective; this may be at some other point in the lymphocyte stimulation pathway, including the cell membrane, and the nuclear membrane may only be the site where cyclic AMP is degraded.
Mechanisms of Recovery From Neutropenia Induced by Hemodialysis
Authors: BRUBAKER LEONARD H. , NOLPH KARL D. 
Published: October 2019

Abstract
Profound, transient neutropenia is observed early in hemodialysis. The present studies were performed during 11 twin-coil dialyses in eight patients with chronic renal failure to determine if the rapid recovery reflects remobilization of sequestered neutrophils and/or if marrow reserves are utilized. In five studies, in vitro cell tagging with diisopropylfluorophosphate-32P (DF 32P) and reinfusion were performed 4-6 hr before routine hemodialysis. In all 11 studies a marked decrease of the absolute neutrophil count occurred within 15 min of starting blood return from the coil. In nine studies carried on over a sufficient period of time, a rebound of the neutrophil count to levels significantly higher than the highest control counts occurred by 1½-3½ hr after starting dialysis. In the radioactive studies during the rebound phase, most or all of the expected number of labeled neutrophils returned to the circulation, but simultaneously in all cases a large number of extra unlabeled neutrophils appeared in circulation. Since there are two sources for additional circulating neutrophils—the marginated pool and the marrow reserves—and since the marginated pool under the study conditions would be expected to have the same specific radioactivity as the circulating pool, the data are consistent with the hypothesis that there was an immediate marrow response to neutropenia.
Reversal of Resistance to Methotrexate in L1210 Murine Leukemia by Uracil
Authors: WALLERSTEIN HARRY , SLATER LEWIS M. , ENG BEN , CALMAN NEIL 
Published: October 2019

Abstract
BDF1 mice bearing L1210 leukemia, when treated with a regimen of uracil and methotrexate, show an increase in survival time greater than when treated with methotrexate alone. The uracil and methotrexate regimen also delays the development of methotrexate resistance as L1210 leukemia is transferred with therapy through multiple generations of mice. When uracil is applied to multiple generations of mice bearing tumor resistant to methotrexate, there is a return to sensitivity to methotrexate. It is also noted that uracil blocks the responsiveness of L1210 leukemia to 6-mercaptopurine.
The responsiveness of these tumor lines to the addition of uracil in their regimens was monitored by in vitro tritiated thymidine incorporation into DNA and by dihydrofolate reductase activities. These data, when integrated with survival time data, suggest that in part, the reported results are mediated by a uracil-induced reduction in the availability of dihydrofolate reductase and phosphoribosylpyrophosphate.
Inhibition of Fibrin Monomer Polymerization by Lambda Myeloma Globulins
Authors: Coleman Morton , Vigliano Edward M. , Weksler Marc E. , Nachman Ralph L. 
Published: October 2019

Abstract
Blood obtained from seven patients with lambda type myeloma proteins showed evidence of gelatinous bulky clots, impaired clot retraction, and circulating anticoagulant activity associated with interference of fibrin monomer polymerization. Five patients had γG1 and two had γA1 myeloma proteins. The pathologic plasmas and isolated myeloma proteins had anticoagulant activity that prolonged both thrombin and reptilase times, that was not absorbed by BaSO4 or neutralized by protamine sulfate, and that resisted heating to 56°C for 10 min. Addition of excess calcium partially corrected the anticoagulant effect. The anticoagulant activity of the isolated whole myeloma proteins, the enzymatic fragments, and polypeptide chains was measured by a thrombin time assay and a spectophotometric system with fibrin monomer. Low concentrations of the isolated IgGL proteins inhibited fibrin polymerization. The IgAL proteins did not demonstrate this activity at low concentrations but were active at concentrations comparable to in vivo levels. F(ab')2 and Fab fragments produced from the IgG proteins by enzymatic digestion possessed full inhibitory activity of the native intact proteins. Fc fragments and isolated polypeptide chains did not display significant anticoagulant activity. The results suggest that the Fab sites of certain lambda myeloma proteins may bind to fibrin during clotting and fibrin polymerization.
Migration of Cells From Shielded to Irradiated Marrow
Authors: Maloney Mary A. , Patt Harvey M. 
Published: October 2019

Abstract
Studies were made with CBA T6T6 chimeras to evaluate the contribution of migrating cells to the recovery of x-irradiated marrow. It was observed that cell migration from a shielded limb is essentially entirely responsible for the 30-day recovery of marrow irradiated with 1000 rad. Thus, these findings provide a direct demonstration of the generally accepted inference of stem cell migration from unirradiated to irradiated sites.