bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of antiserum on transplantable hematopoietic colony‐forming units during rauscher leukemia development
Authors: Okunewick J. P. , Phillips E. L. , Brozovich B. 
Published: February 2007

AbstractStudies have been carried out to determine the sensitivity of hematopoietic CFU‐S from Rauscher leukemic mice to an antiserum against the disease prepared in syngeneic mice. Test of this antiserum against Rauscher virus prior to injection showed it to be effective both in vitro and in vivo. At the same time, normal serum was shown to be without effect either against the CFU‐S or against the virus. Spleen CFU‐S were obtained from control and leukemic mice over a sequence of days following Rauscher virus injection and assayed by transplantation technique. Prior to transplantation these were incubated in vitro in either normal syngeneic serum or syngeneic antiserum. Incubation with antiserum had no effect on CFU‐S obtained from the spleens of normal mice. However, incubation in this antiserum of spleen CFU‐S from Rauscher leukemic mice resulted in a reduction of up to 50% in their colony‐forming ability. Additional tests with guinea pig complement suggested that the levels of inactivation seen are not complement limited. This antiserum‐induced reduction in colony formation was first evident in the second week after the injection of virus, coincident with the onset of splenomegaly in the leukemic mice. Thereafter, sensitivity of CFU‐S to the antiserum could be detected up to the terminal point of the leukemia (44 days).
Evaluation of survival data for chronic myelocytic leukemia
Authors: Sokal Joseph E. 
Published: February 2007

AbstractMedian survival figures are essentially worthless for evaluation of the effectiveness of therapy in different series of patients with chronic myelocytic leukemia. Such data are heavily influenced by the characteristics of the initial patient mix, which play the major role in determining mortality during the first year of treatment. The effects of differing initial proportions of poor‐risk patients are dissipated within two years, however, and the annual mortality rates thereafter reflect the influence of antileukemic therapy. Comparison of these rates, from very diverse series of patients, yielded quite consistent results and indicated superiority of effective chemotherapy over irradiation or inferior drug schedules.
Sickle cell anemia: Erythrokinetics, blood volumes, and a study of possible determinants of severity
Authors: Steinberg Martin H. , Dreiling Bernard J. 
Published: February 2007

AbstractThe variability in the clinical expression of sickle cell anemia led us to study factors which might influence the course of this disease. We examined erythrokinetics, blood volumes, and variables which influence hemoglobin function in a group of adults with sickle cell anemia of varying degrees of clinical severity. We were unable to correlate any single measurement with the clinical course; however, our patient sample was small and the data suggested areas for further study. An expansion of plasma volume was noted in all patients. This made it difficult to predict red cell mass from the hemoglobin level, which consistently underestimated its magnitude. The red cell production index and iron turnover values indicated that there is often a suboptimal erythropoietic response to anemia in sickle cell disease.
Effect of prior radiotherapy on tolerance and response to chemotherapy in non‐hodgkin's lymphoma
Authors: Bender Richard A. , Johnson Bonny L. , Norton Larry , Young Robert C. 
Published: February 2007

AbstractTwenty‐five patients who had received radiotherapy as their primary treatment for non‐Hodgkin's lymphoma subsequently relapsed; they were then treated with combination chemotherapy and their tolerance and response evaluated. Radiotherapy delivered as total body irradiation and other forms of radiotherapy delivered to > 15% of the bone marrow caused significantly lower platelet nadirs during subsequent chemotherapy when compared to patients receiving radiotherapy to ≤ 15% of their bone marrow. In spite of this thrombocytopenic effect, the eventual total doses of chemotherapy delivered were not significantly compromised. A response to chemotherapy was more likely in patients with a prolonged (> 6 months) response to radiotherapy. However, a chemotherapy response was equally likely in patients receiving involved field (IF), extended field (EF), or total nodal irradiation (TNI) as compared to those receiving total body irradiation (TBI). Chemotherapy responses (complete and partial) occurred in 75% of both radiotherapy groups with complete responses more likely in the IF, EF, or TNI group. The median durations of response were slightly longer in the IF, EF, or TNI radiotherapy group (6 months vs 5 months; p = 0.07) but were shorter than those in previously reported patients not receiving prior radiotherapy. Similarly the duration of a chemotherapy response was not affected by the histology of the tumor. However, although the survival of patients following chemotherapy was not significantly affected by the histology of the tumor there was a tendency towards a longer survival for lymphocytic histology as compared to histiocytic.
The anemia of vitamin E deficiency in swine: An experimental model of the human congenital dyserythropoietic anemias
Authors: Lynch R. E. , Hammar S. P. , Lee G. R. , Cartwright G. E. 
Published: February 2007

AbstractThe ultrastructural and erythrokinetic characteristics of vitamin E deficiency in swine were investigated in an effort to evaluate the suitability of the swine disorder as a model of the human congenital dyserythropoietic anemias. The dominant erythrokinetic abnormality in vitamin E deficient pigs, as in the CDAs, is ineffective erythropoiesis. As in some patients with CDA, the activity of a number of erythrocyte enzymes was increased. Distinctive ultrastructual changes previously described in patients with CDA were found in normoblasts from vitamin E deficient pigs. The morphologic, erythrokinetic, biochemical and ultrastructural similarities between vitamin E deficiency in swine and the CDAs in man appear to justify the study of the animal disorder as a model of the human disease.A complete hematologic response was elicited by the administration not only of vitamin E, but also, as in the previous studies of vitamin E deficiency in monkeys, by hexahydrocoenzyme Q4. The partial hematologic response occurring after deletion of tocopherol stripped corn oil from the diet indicates that factors other than the dietary lack of vitamin E are important in the pathogenesis of this disorder.
Inhibition of bovine factor viii‐induced guinea pig platelet aggregation by simple sugars and derivatives
Authors: Kuwahara Steven S. , Malik Michael 
Published: February 2007

AbstractWorking with the hypothesis that the binding of carbohydrate groups is important in the induction of platelet aggregation by bovine factor VIII, we studied 36 different sugars and sugar derivatives for their ability to inhibit the aggregation of guinea pig platelets. Concentrations that produced 50% inhibition of the aggregation response ranged from 232 mM (galactose) to 12 mM (glucosamine and galactosamine). Using these values, we found that several factors affected the ability of sugar structures to inhibit bovine factor VIII‐induced aggregation of guinea pig platelets. In general, galactose and its derivatives were not as effective as glucose and its derivatives. Sugars possessing α‐glycosidic linkages tended to be stronger inhibitors than those having β‐linkages. Polyols were better inhibitors than their corresponding aldoses. D‐fucose (129 mM) was a weaker inhibitor than L‐fucose (66 mM), but D‐and L‐arabinitol were not significantly different. N‐acetylation of glucosamine reduced its ability to inhibit aggregation. The number of free hydroxyl groups in a molecule did not appear to be a significant determinant of its ability to inhibit aggregation.The results support the hypothesis that a binding site for carbohydrate groups exists either on the platelet membrane or on the bovine factor VIII molecule. The binding of the carbohydrate to this site is an important step in the induction of aggregation, and this binding site is relatively specific for the carbohydrate structures that it will accept.
Determination of antiplatelet antibody activity in sera cytotoxic for human lymphocytes
Authors: Colman Robert W. , Busch George J. 
Published: February 2007

AbstractPooled serum aliquots obtained from sensitized potential renal allograft recipients on chronic hemodialysis were evaluated for their lymphocytotoxicity titers against the lymphocytes and then for alloantibodies against the platelets of 7 random donors by 5 methods. Platelet donor specific lymphocytotoxicity was present in 93% of 42 combinations. Of the positive combinations, 57% had a positive test for antiplatelet activity by the 14C serotonin release assay, 16% by the platelet aggregation method, and 19% as judged by acid phosphatase availability on the platelet membrane. No serum tested released β‐glucoronidase or lactic dehydrogenase. No correlation of the height of the titer of antiplatelet activity with that for lymphocytoxicity was detected. Thus, even in sera demonstrating significant activity against donor lymphocyte antigens, detection of associated platelet antibody activity is not uniform. Thus, a positive lymphocytoxic titer does not necessarily predict detectable antiplatelet activity. Therefore, additional tests for detection of antiplatelet activity should also be considered. This study shows that of the tests evaluated, the 14C serotonin release assay is the most sensitive for detection of antiplatelet antibodies.
In vivo leukemic transformation: Cytogenetic evidence of in vivo leukemic transformation of engrafted marrow cells
Authors: Goh Kong‐Oo , Klemperer Martin R. 
Published: February 2007

AbstractA 4‐year‐old girl with acute myeloblastic leukemia was treated with 50 mg/kg cyclophosphamide daily for 4 days before being given 1.7 × 108 bone marrow cells/kg from her HL‐A identical, MLC nonreactive, cytogenetically normal brother. The patient died 92 weeks after the marrow graft. Postmortem examination showed increased myeloblasts and promyelocytes. Cytogenetic studies before transplantation showed that all sex determination metaphases had an XX pattern, and 41% of the hyperdiploid metaphases had an additional 19–20(F) chromosome. At autopsy all hyperdiploid metaphases with XY pattern and 43% of the hyperdiploid metaphases with an XX pattern had an additional F chromosome. Occasional metaphases with 47,XX,+F or 47,XY,+F were seen during the follow‐up studies. These findings indicated that an acute leukemia had developed in the XY cell line of this artifically induced sex chimeric child. This suggests that a leukemic stimulus other than that proposed to be induced by total‐body irradiation existed in this patient and transformed the engrafted cells.
Erythrocytic glutathione reductase deficiency in a hospital population in the united states
Authors: Frischer Henri 
Published: February 2007

AbstractIn the USA, erythrocytic glutathione reductase (GSSG‐R) deficiency is significantly more common, and can be considerably more pronounced in hospitalized patients (118/3198) than in outpatients (37/1639) or in apparently healthy persons (12/849). Retrospective analysis of illnesses found in 118 inpatients with erythrocytic GSSG‐R deficiency revealed a striking and previously unsuspected association of the enzyme deficiency with a variety of chemotherapeutically treated hematological or nonhematological malignancies (51/118 patients, 43.2%, or 51/170 diagnoses, 30.0%). The prevalence of erythrocytic GSSG‐R deficiency also increased in malnutrition, liver disease, and sepsis. Drugs of the nitrosourea class, particularly BCNU [1, 3‐bis(2‐chloroethyl)‐1‐nitrosourea] are causally implicated in the association of GSSG‐R deficiency with malignancies. Severe or complete GSSG‐R deficiency may handicap host response to infections.
Secondary gout in hemoglobinopathies: Report of two cases and review of the literature
Authors: Ballou Stanley , Khan Muhammad A. , Kushner Irving , Harris John W. 
Published: February 2007

AbstractAlthough patients with hemolytic hemoglobinopathies characteristically are over‐producers of urate, and hyperuricemia is frequently recognized, clinical gout has rarely been reported in such patients. Our evaluation of 2 premenopausal women with gout led to the diagnosis of previously unrecognized hemoglobinopathies (SC disease and CC disease). Investigation of these 2 patients and review of the reported cases of gout in patients with hemoglobin S or C disorders suggest that relatively minor abnormalities of renal function in these patients may lead to early development of significant hyperuricemia. With increasing lifespan of patients with hemolytic hemoglobinopathies and the likelihood of increased occurrence of renal function abnormalities, it is anticipated that gout will more frequently be responsible for joint symptoms in such patients.
Cytotoxicity of a factor from normal and abnormal human spleens for allogenic leukemia cells
Authors: Lozzio Bismarck B. , Lozzio Carmen B. , Bamberger Elena G. 
Published: February 2007

AbstractA search for an endogenous cytotoxic factor (ECF) was made by analyzing 103 spleens from normal humans and patients suffering from hematopoietic malignancies, solid tumors, inflammatory diseases, and congestive and hyperplastic splenomegalies. A highly purified ECF was obtained by a combination of gel filtration and ion‐exchange column chromatography. The factor is a low‐molecular‐weight (< 2,000) substance and is probably a peptide or peptide‐nucleotide complex. The biologic activity of the ECF was assayed on myelogenous and lymphatic leukemia cells of human origin. The spleens from normal individuals produced and/or stored the largest quantity of the ECF. The amount of ECF extractable from the pathologic spleen was drastically diminished regardless of the disease or therapeutic regimen. The ECF was significantly more cytotoxic for lymphatic than for myelogenous leukemia cells.
Acute lymphoblastic leukemia–hand mirror cell variant: A detailed cytological and ultrastructural study with an analysis of the immunologic surface markers
Authors: Stass Sanford A. , Perlin Elliot , Jaffe Elaine S. , Simon David R. , Creegan W. J. , Robinson J. J. , Holloway M. L. , Schumacher Harold R. 
Published: February 2007

AbstractAcute lymphoblastic leukemia was observed in a 22‐year‐old white female patient and was manifested by normal platelet counts, 50–60% hand mirror cells (HMC) in the bone marrow, and prolonged survival without treatment. The characteristic neoplastic cell had a nucleus within the “mirror” portion and a cytoplasmic uropod forming the “handle” portion. The presence of acid phosphatase and B‐glucuronidase activity suggested that the cell was a T cell lymphoblast. However, extensive immunologic surface marker studies indicated the cells were non‐T, non‐B. Terminal transferase activity further supported the lymphoid nature of the cell. The hand mirror cells were considered a real phenomenon since they were demonstrated on phase contrast microscopy, scanning electron microscopy, and transmission electron microscopy. The cells did not grow in tissue culture and cytogenetics revealed a normal female karyotype. From the above observations, the HMC is a lymphoblast with morphological, cytochemical, and immunological features which may differentiate it from the usual cell in acute lymphoblastic leukemia. Therefore, cases involving increased numbers of hand mirror cells in the bone marrow and acute lymphoblastic leukemia require further investigation to elucidate the full importance of this cell. This study represents the first attempt to investigate this cell in detail.
Sequential pure red cell and megakaryocyte aplasia associated with chronic liver disease and ulcerative colitis
Authors: Fox Richard M. , Firkin Frank C. 
Published: February 2007

AbstractThe clinical course of a patient with chronic hepatitis and previous ulcerative colitis who subsequently developed pure red cell aplasia (PRCA) is described. The PRCA remitted initially with corticosteroid therapy. A subsequent relapse responded to cyclophosphamide therapy following splenectomy. This was followed by a fatal third episode of red cell aplasia associated with megakarocyte aplasia.
Abnormalities of the peripheral blood as a presenting feature of immunodeficiency
Authors: Blanchette Victor S. , Hallett Jospeh J. , Hemphill J. Michael , Winkelstein Jerry A. , Zinkham William H. 
Published: February 2007

AbstractThe predisposition of immunodeficient patients to the development of peripheral blood abnormalities is well documented. Less often recognized is the presence of immune defects in patients who initially present with “idiopathic” forms of thrombocytopenic purpura or autoimmune hemolytic anemia in the absence of symptomatology indicative of an immunodeficiency. In this report we describe two children, each of whom had intermittent and at times severe hemolysis and thrombocytopenia secondary to formation of autoantibodies. Although the initial clinical impression was the presence of an “idiopathic” form of platelet or red cell destructive phenomenon, subsequent observations demonstrated abnormalities of the immune system which affected both B and T lymphocytes. In one of the patients there was a marked deficiency of IgA with a moderate but progressive decrease in IgM and IgG. The other patient had a moderate decrease in IgA and a failure to sensitize to dinitrochlorobenzene. Both exhibited dysmorphic features, including small stature, abnormal dentition, hyperelasticity of the skin, and hyperextensibility of the joints. Neither had significant problems with bacterial, fungal, or viral infections. These observations highlight the importance of evaluating the immune system in children with “idiopathic” forms of hemolytic anemia or thrombocytopenia. Demonstration of these abnormalities can have important therapeutic implications and may also provide information regarding the etiology of the blood abnormalities.
Granulocytic colonies on macrophage‐coated membranes
Authors: Turner A. R. , Pfrimmer W. J. , Torok‐Storb B. J. , Boggs D. R. 
Published: February 2007

AbstractA macrophage cell coating covering a cellulose acetate disk was an effective microenvironment for the production of peroxidase‐positive hematopoietic colonies. These developed after intraperitoneal injection of marrow cells with a linear cell relationship of dose to colonies formed. One colony formed for every 2,000 nucleated marrow cells injected. Observation of colony formation daily showed a steady increase in number and size until seven days after cell inoculation. X‐irradiation (400 rads) eliminated intrinsic colony formation in BALB/c mice. Irradiation of the donor of the ip marrow cells resulted in a Do of 95 rads. Treatment of the marrow donor with cytosine arabino‐side had a suppressive effect on colony formation as did treatment of the host animal after receipt of the ip marrow. These results indicate that the precursor of the granulocytic colonies seen in the macrophage layers are more similar to committed granulocytic precursors than to the pluripotential stem cell.
Platelet satellitism—An ultrastructural study
Authors: Skinnider L. F. , Musclow C. E. , Kahn W. 
Published: February 2007

AbstractUltrastructural studies by scanning and transmission electron microscopy were carried out on one of four cases of platelet satellitism. Adherence to the neutrophils was mainly by focal contact between small surface projections of the platelets and neutrophils. Phagocytosis was not seen with the neutrophils but was evident in the monocytes. The degree of satellitism noted increased with the time the blood anticoagulated with EDTA was left at room temperature. Mixing experiments with a patient's plasma and control cells and the patient's cells and control plasma were inconclusive but suggested that the abnormality may reside in the plasma.
Corticosteroid‐induced lymphocytopenia in man: Absence of splenic influence and effect of recipient serum
Authors: Beardsley G. Peter , Cohen Harvey Jay 
Published: February 2007

AbstractPharmacologic doses of corticosteroids produce a profound, transient lymphocytopenia in man. We have studied the role of the spleen and possible induction of cytolytic factors in the generation of this effect. A 200 mg IV dose of hydrocortisone‐21‐hemisuccinate was administered to five normal subjects and five subjects whose spleens had been removed as a result of trauma. Sequential peripheral blood lymphocyte counts and subpopulations were then determined, and the effect of serum (obtained from the recipients at several time points after steroid administration) on autologous lymphocyte viability was assessed in vitro. The asplenic subjects experienced the same marked lymphocytopenia as normal individuals, and post‐steroid serum was not cytotoxic to autologous lymphocytes. The in vitro results support the view that corticosteroid‐induced lymphocytopenia is not the result of lymphocytolysis in man. If lymphocyte redistribution is the cause, as has been suggested, our in vivo results directly demonstrate that the spleen does not play a major role.
Lactic acidosis and diffuse histiocytic lymphoma (DHL)
Authors: Mintz Uri , Sweet Donald L. , Bitran Jacob D. , Ultmann John E. 
Published: February 2007

AbstractFour patients with advanced diffuse histiocytic lymphoma who developed lactic acidosis are described. All four patients demonstrated disturbed liver function tests. In two of the patients, the lactic acidosis was unresponsive to treatment. The third patient responded successfully to the early initiation of combination chemotherapy with achievement of a clinical remission and correction of the lactic acidosis. The fourth patient responded to the initiation of chemotherapy with abatement of his lactic acidosis, but expired probably as the result of a pulmonary embolus. It seems likely that extensive hepatic infiltration may be one of the factors contributing to lactic acidosis in patients with diffuse histiocytic lymphoma. The early initiation of antineoplastic therapy may be important in the mangement of patients with histiocytic lymphoma and lactic acidosis.
Studies on a new variant of the Hermansky‐Pudlak syndrome: Qualitative, ultrastructural, and functional abnormalities of the platelet‐dense bodies associated with a phospholipase a defect
Authors: Rendu Francine , Breton‐Gorius Jeanine , Trugnan Germain , Castro‐Malaspina Hugo , Andrieu Jean‐Marie , Bereziat Gilbert , Lebret Marilyne , Caen Jacques P. 
Published: February 2007

AbstractThe structure and functions of platelets from a patient in whom albinism and hemorrhagic diathesis were associated have been investigated. Electron microscope studies showed a large reduction in the number of dense bodies and this was confirmed by an examination of fluorescent platelets loaded with mepacrine. The rare dense bodies were much bigger than normally observed; their density was diminished and was localized in a peripheral ring. Other platelet constituents were found to be normal. Platelet peroxidase activity was normal in the canaliculi of the dense tubular system; catalase‐positive granules were also present. Serotonin uptake by the patient's platelets was much decreased and reserpine, a potent inhibitor of serotonin accumulation by normal human platelets, did not further decrease this incorporation. The uptake of free 14C‐arachidonic acid by the platelets was greatly diminished, as was its thrombin‐induced liberation from phosphatidylcholine and phosphatidyl inositol. Moreover, platelet phospholipase A1 activity was much reduced and phospholipase A2 activity was undetectable.