bluuebunny/crossref_metadata_2025_split huggingface dataset:
Adoptive chemoimmunotherapy using Ex vivo activated memory T‐cells and cyclophosphamide: Tumor lysis syndrome of a metastatic soft tissue sarcoma
Authors: Gold Jay E. , Malamud Stephen C. , Larosa Felicia , Osband Michael E. 
Published: February 2007

AbstractAdoptively transferred immune cells in combination with chemotherapeutic agents form the basis for adoptive chemoimmunotherapy (ACIT) of neoplastic disease. Autolympho‐cytes (ALT‐cells) are ex vivo activated peripheral blood lymphocytes (PBL) from tumor‐bearing hosts (TBH) that consist primarily of tumor‐specific CD45RO+ (memory) T‐cells. These ALT‐cells combined with cimetidine (CIM) as autolymphocyte therapy (ALT), have previously been demonstrated to be a safe and active form of outpatient adoptive immunotherapy (AIT) in human TBH with metastatic renal cell cancer (RCC). We have previously described an effective ACIT protocol using ALT and cyclophosphamide (CY) for patients with relapsed and refractory non‐RCC solid tumors. We now report a case of a patient with a metastatic gastric leiomyosarcoma to the liver, who developed a clinical picture consistent with a tumor‐lysis syndrome (TLS), following salvage therapy for his tumor with ACIT using ALT and CY. TLS is a well‐known complication resulting from the treatment of rapidly proliferating hematopoietic tumors such as Burkitt's lymphoma and acute lymphocytic leukemia. TLS has also been rarely described in chronic lymphocytic leukemia, as well as certain solid tumors such as breast cancer, small cell lung cancer, and medulloblastoma. However, there have been no previous reports of TLS occurring either secondary to immunotherapy or in sarcomas. The nature of these unusual findings is discussed. © 1993 Wiley‐Liss, Inc.
Phosphatidylserine in the outer leaflet of red blood cells from β‐thalassemia patients may explain the chronic hypercoagulable state and thrombotic episodes
Authors: Yashar Vered Borenstain‐Ben , Barenholz Yechezkel , Hy‐Am Esther , Rachmilewitz Eliezer A. , Eldor Amiram 
Published: February 2007

AbstractInvestigation of red blood cells from β‐thalassemia patients by means of prothrombinase assay reveals phosphatidylserine in the outer leaflet of the plasma membrane. This might explain their elevated susceptibility to phagocytosis by macrophages and the chronic hypercoagulable state, frequent thrombotic events, and life‐long platelet activation that are found in thalassemic patients. © 1993 Wiley‐Liss, Inc.
Phase II trial of recombinant interferon alfa‐2 in the treatment of primary systemic amyloidosis
Authors: Gertz Morie A. , Kyle Robert A. 
Published: February 2007

AbstractPrimary systemic amyloidosis (AL) is a rare disorder characterized by production of an aberrant monoclonal light chain. This insoluble light chain, or a fragment thereof, deposits in tissues as amyloid and results in disruption of organ function and, ultimately, death. Although melphalan and prednisone were reported to benefit subsets of patients with the disease, many patients showed no benefit; the median survival with the disease is ∼2 years. There is a need to develop new agents for patients who fail to respond to a trial of cytotoxic chemotherapy. A study was undertaken of interferon alfa‐2 in the treatment of 15 patients with AL because of its reported benefits in the induction and maintenance therapy for patients with multiple myeloma, a disease that has many characteristics in common with AL. None of the patients showed any objective regression of their disease; the median survival of the entire group was 26.3 months. This survival is not superior to that reported with other agents used for this disease. We conclude that interferon alpha‐2 is not a valuable agent in the treatment of AL. © 1993 Wiley‐Liss, Inc.
Growth retardation in homozygous sickle cell disease: Role of calorie intake and possible gender‐related differences
Authors: Modebe Onyechi , Ifenu Stella A. 
Published: February 2007

AbstractTo evaluate the possible role of inadequate food intake in the pathogenesis of the growth retardation of patients with sickle cell anemia, we determined the daily intake of calories and macronutrients and measured several anthropometric indices in 20 patients with sickle cell anemia aged 17–35 years and in 15 of their normal siblings of similar age. Compared to the control groups, the male patients, but not the females, had a significantly lower mean weight, body mass index, midarm circumference, and triceps and subscapular skinfold thicknesses. Also, while the male patients consumed significantly less total calories, proteins, carbohydrates, and fats per day than their control group, no difference was noted between the daily intake of calories or macronutrients in the female patients and their control group. However, when the intake of calories and macronutrients was corrected for body weight, there was no statistically significant difference between the intake of nutrients in the male patients and their control subjects or between the female patients and their control group. These results suggest a sex‐related difference in the somatic growth of adolescent and adult patients with sickle cell anemia and also suggest that, although an inadequate food intake may be partly responsible for the impaired somatic growth in sickle cell anemia, other factors are also probably important. © 1993 Wiley‐Liss, Inc.
Tracing iron and transferrin in the macrophage by visual means
Authors: Haurani Farid I. , Ryter Antoinette 
Published: February 2007

AbstractThe purpose of the study was to investigate the movement of iron and transferrin in the macrophage using light and electron microscopy. First, depicted here are the phagocytosis of antibody sensitized murine red cells by the murine bone marrow derived macrophage and the formation of red cell phagosomes. Second, we show the fusion of the lysosomes with the red cell phagosome to form a lysophagosome and the lysis of the red cell using acid phosphatase as a lysosome marker. Third, by autoradiography, the presence of 55Fe silver grains in the phagocytosed red cells and its delivery to the organelles of the macrophage are demonstrated. Fourth a transferrin species is shown in red cells of all ages, in the phagocytosed as well as the non‐phagocytosed, and in the phagocytosed as well as the non‐phagocytosed, and in the macrophage itself. Transferrin was detected using immunogold and fluorescence labelling. These studies suggest that iron, using vesicles as means of transport, moves from the effete red cells inside the macrophage to the outside possibly bound to transferrin. © 1993 Wiley‐Liss, Inc.
Efficacy of intravenous immunoglobulin in the treatment of autoimmune hemolytic anemia: Results in 73 patients
Authors: Flores Glenn , Cunningham‐Rundles Charlotte , Newland Adrian C. , Bussel James B. 
Published: February 2007

AbstractTo determine whether warm‐antibody autoimmune hemolytic anemia (AIHA) responds to treatment with intravenous gammaglobulin (IVGG), we conducted separate pilot studies at three institutions enrolling a total of 37 patients. We combined these results with a review of 36 cases of AIHA treated with IVGG reported in the literature. Sixteen clinical variables were examined to determine associations with response to IVGG. Overall, 29 of 73 patients (39.7%) responded to IVGG therapy. Two variables were strongly related to a good response to IVIG: the presence of hepatomegaly (with and without splenomegaly) and a low pre‐treatment hemoglobin. A trend towards a better response was observed in the 11 children. Overall, IVGG provided acute benefit in only 1/3 of patients and therefore cannot be recommended as standard therapy for AIHA. It may, however, be useful as adjunctive treatment in selected cases, such as in those with a pre‐treatment hemoglobin < 6–7 gm/dl or those with hepatomegaly, and in clinical settings where the toxicity of other treatments may be an important consideration. © 1993 Wiley‐Liss, Inc.
Decreased fibrinolytic potential in patients with idiopathic avascular necrosis and transient osteoporosis of the hip
Authors: Van Veldhuizen Peter J. , Neff James , Murphey Mark D. , Bodensteiner David , Skikne Barry S. 
Published: February 2007

AbstractA thrombotic etiology has been suggested as the cause of idiopathic avascular necrosis of the hip, although the underlying pathophysiological mechanisms are unknown. Transient osteoporosis of the hip has also been suggested to represent bone marrow edema that may be related to ischemia. We evaluated four patients with idiopathic avascular necrosis and one patient with transient osteoporosis of the hip for thrombotic potential placing a special emphasis on the fibrinolytic system. All five patients had identifiable abnormalities of fibrinolysis. Four patients had elevated levels of plasminogen activator inhibitor (PAI‐1) and one patient had an inadequate increase in tissue plasminogen activator (tPA) post venous occlusion. Serum triglycerides were increased in three of the patients. These findings suggest an association between decreased fibrinolytic potential and the subsequent development of avascular necrosis and transient osteoporosis of the hip. These patients should have an evaluation of the fibrinolytic system with tPA and PAI‐1 levels as well as a lipid profile. © 1993 Wiley‐Liss, Inc.
Regulation of megakaryocyte colony forming cell numbers and ploidy by dideoxynucleosides in immunodeficient mice
Authors: Chow Fung‐Phing R. , Ordóñez José V. , Sutton Patricia A. , Hamburger Anne W. 
Published: February 2007

AbstractWe have recently demonstrated that azidothymidine (AZT) elevates the levels of circulating platelets in mice made immune deficient by infection with LP‐BM5 murine leukemia virus (MAIDS mice). In an attempt to elucidate the mechanisms of the AZT platelet elevating effect, we examined the number of splenic and bone marrow megakaryocyte colony‐forming cells (CFU‐mk) and the ploidy of megakaryocytes derived from CFU‐mk using fluorescence cytophotometric methods. Two other dideoxynucleosides (ddN) 2′3′‐dideoxyinosine (ddL) and 2′3′‐dideoxycytidine (ddC) were assessed to determine the specificity of the effect of AZT. MAIDS mice were given ddN in drinking water for 15 days. AZT was the only ddN that significantly increased circulating platelet levels in MAIDS mice. AZT significantly increased splenic CFU‐mk in MAIDS mice, but bone marrow CFU‐mk were not affected. ddL and ddC failed to change either platelet levels or the numbers of splenic or bone marrow CFU‐mk. The ploidy of megakaryocytes derived from splenic and bone marrow CFU‐mk were examined by first identifying CFU‐mk by staining for acetylcholinesterase, followed by nuclear staining with propidium iodide. The fluorescence of individual cells was then measured using a Perceptics image analysis system. Modal ploidy of CFU‐mk megakaryocytes derived from spleen cells of AZT‐treated immunodeficient mice was shifted upwards from 16N to 32N. Similarly, AZT treatment changed the modal ploidy number of colony megakaryocytes derived from bone marrows of immunodeficient mice from 16N to 32N. The ploidy distribution was also significantly shifted. ddL and ddC failed to significantly alter either modal ploidy number or distribution of megakaryocytes derived from splenic or bone marrow CFU‐mk. These findings suggest that AZT may affect physiological processes that lead to platelet formation. © 1993 Wiley‐Liss, Inc.
Characteristics of zinc binding to human red blood cell membranes
Authors: Brandão‐Néto José , Bell William R. 
Published: February 2007

AbstractThe objective of the present study was to standardize the analysis of zinc binding on human red blood cell (RBC) membranes in 20 normal adults. The displacement studies revealed that at the maximal stable zinc concentration tested (600 μM), 57% (mean) of the bound 85Zn was displaced and to displace half maximal 65Zn, the stable zinc concentration was 300 μM. Scatchard plots revealed two classes of binding sites for zinc on RBC membranes: one with higher affinity, Kd = 1.20 × 10−5 M (site I), and the other with lower affinity, Kd = 2.77 × M (site II). Binding sites occupancy was 97% means and 58.5% means for sites I and II, respectively. The displacement was affected by temperature, membrane protein concentration, freezing, thawing, and dialysis. Other metal cations, including Co+*, Fe++, and Mn++, had very little effect on 65Zn displacement, in contrast copper displaced 65Zn from its binding sites on RBC membranes. Zinc binding to RBC membranes was rapid and readily reversible in a dynamic equilibrium with its binding sites. It is anticipated that this method will be applicable to studies of a wide variety of diseases specifically related to zinc metabolism in humans as well as in animals. © 1994 Wiley‐Liss, Inc.
Direct evidence for systemic fibrinogenolysis in patients with acquired α2‐plasmin inhibitor deficiency
Authors: Okajima Kenji , Kohno Isao , Soe Gilbu , Okabe Hiroaki , Takatsuki Kiyoshi , Binder Bernd R. 
Published: February 2007

AbstractTo examine whether or not acquired α2‐plasmin inhibitor deficiency is associated with systemic fibrinogenolysis, we analyzed the fibrin and fibrinogen degradation products in eight patients with this condition in various disease states. The underlying disease was gastric cancer in three patients, metastatic prostatic cancer in two, acute promyelocytic leukemia in two, and abdominal aortic aneurysm in one patient. In all eight patients, the α2‐plasmin inhibitor level was reduced to less than 50% of normal, and plasmin‐α2,‐plasmin inhibitor complex levels were increased. Immunoblotting of serum using an anti‐fibrinogen antibody detected a 250 kDa protein (corresponding to fragments X or DY) in all eight patients. Fragment Y and D monomer were detected in seven of the eight patients, indicating the occurrence of systemic flbrinogenolysis. However, they were not detected in one patient with metastatic prostatic cancer. To determine whether or not fibrinogen degradation was also occurring in the patient without fragment Y, we characterized the 250 kDa protein in all eight patients. The protein was found to be fragment X in the metastatic prostatic cancer patient without fragment Y, while it was fragment DY in the other seven patients. Thus, systemic fibrinogenolysis was present in all eight patients. In the two patients with metastatic prostatic cancer, the level of α2‐plasmin inhibitor gradually increased with the reduction of tumor size by treatment. Fragment X, fragment Y, and D monomer were not detected when the α2‐plasmin inhibitor level exceeded 60% of normal in both patients. In the other six patients fragment Y and D monomer also disappeared when the α2‐plasmin inhibitor level exceeded 60% of normal.These findings suggest that systemic fibrinogenolysis only occurs when the plasma levels of α2‐plasmin inhibitor falls below 60% of normal due to activation of the fibrinolytic system by various pathological conditions. © 1994 Wiley‐Liss, Inc.
Detection of tumor necrosis factor‐α in bone marrow plasma and peripheral blood plasma from patients with aplastic anemia
Authors: Schultz John C. , Shahidi Nasrollah T. 
Published: February 2007

AbstractPlasma levels of interferon‐gamma (IFN‐γ) and tumor necrosis factor‐alpha (TNF‐α) were determined in healthy individuals and patients with aplastic anemia (ApAn). IFN‐γ was not detected in normal peripheral blood plasma (PBP) or bone marrow plasma (BMP) and was present in PBP from only 2 of 22 patients and in BMP from 1 of 14 patients and the levels were low (< 1.5 U/ml). Elevated levels of TNF‐α were present in BMP and PBP from patients but not in control (healthy donor) PBP and BMP. Eleven of twenty‐four patients had elevated levels of TNF‐α in their PBP and 6 of 13 patients had detectable levels of TNF‐α in their BMP. Only one of the 14 healthy control donors had detectable TNF‐α and the level was very low (7 pg/ml), while 13 of the 27 ApAn patients had detectable TNF‐α (P = .009, chi‐square test). Not surprisingly, the centers of the distributions of TNF‐α concentrations of the controls and ApAn patients differed significantly (P < .017 for control and patient PBP and P < .056 for control and patient BMP, Wilcoxon rank‐sum test). Spontaneous production of IFN‐γ and TNF‐α by cultured bone marrow mononuclear cells was observed in four of seven patients but not in the six healthy controls (P = 0.026). Spontaneous production of IFN‐γ and TNF‐α by cultured peripheral blood mononuclear cells from patients and controls was however similar. Phytohemagglutinin (PHA)‐induced production of IFN‐γ and TNF‐α by cultured mononuclear cells did not differ significantly between ApAn patients and normal controls. The significance of overproduction of TNF‐α in the pathophysiology of ApAn is discussed. © 1994 Wiley‐Liss, Inc.
Splenic lymphoma with circulating villous lymphocytes: Report of seven cases and review of the literature
Authors: Sun Tsieh , Susin Myron , Brody Judith , Dittmar Klaus , Teichberg Saul , Weiner Robert , Lin Jen H. , Felber Norbert 
Published: February 2007

AbstractSplenic lymphoma with villous lymphocytes (SLVL) is a relatively new entity with only a few reports published. We report seven cases of SLVL with detailed clinicopathologic and comprehensive immunophenotypic studies to further characterize this lymphoma, which is frequently confused with hairy cell leukemia and other low‐grade B‐cell lymphoid neoplasms. The diagnostic criteria we used include 1) prominent splenomegaly, 2) insignificant or no lymphadenopathy, 3) lymphocytosis without leukopenia, 4) presence of circulating villous lymphocytes, 5) characteristic cytologic and histologic features, and 6) specific phenotypic and cytochemical findings. Our studies show that SLVL does not represent a pure entity but rather a morphologically heterogeneous group of low‐grade lymphomas with various cytologlc and histologic features. Although immunophenotyping is helpful in differential diagnosis, multiparameter studies are necessary to confirm the diagnosis. In our series, only two patients died of SLVL, who probably developed transformation to a higher‐grade lymphoma. © 1994 Wiley‐Liss, Inc.
Continuous infusion of monoclonal antibody‐purified factor VIII: Rational approach to serious hemorrhage in patients with allo‐/autoantibodies to factor VIII
Authors: Gordon Erlinda M. , Al‐Batniji Fatma , Goldsmith Jonathan C. 
Published: February 2007

AbstractHemorrhage in a patient with factor VIII inhibitor is associated with increased morbidity and mortality. Treatment with factor IX complex concentrates or recombinant factor VIIA (rVIIa) may not control bleeding and may induce thrombosis. In this study, continuous infusion of a monoclonal antibody‐purified factor VII concentrate (Monoclate‐P) was used successfully in two hemophilic patients with factor VIII alloantibodies and one nonhemophilic patient with a factor VIII autoantlbody. In two patients, hemorrhage was life‐threatening, and, in one, bleeding did not stop with repeated infusions of activated factor IX complex concentrates. The patients' ages ranged from 4 to 15 years, and the inhibitor levels from 6 to 300 Bethesda units/ml. Clinical hemostasis was excellent, and In vivo recovery of infused factor VIII was achieved. When an excess of monoclonal factor VIII was added to the inhibitor plasma in vitro, a stable level of residual factor VIII activity was noted after an initial rapid loss. This second‐order reaction occurs in plasmas of patients with type I factor VIII inhibitors. In one patlent, we showed that the saturation dose of the factor VIII inhibitor predicted in vivo recovery of factor VIII:C. These data emphasize the importance of characterizing the kinetic reactions of the factor VIII inhibitor. Furthermore, we confirm previous reports that continuous infusion of monoclonal factor VIII is a safe and effective treatment of patients with factor VIII inhibitors in whom hemorrhage Is either life‐threatening or refractory to standard treatment. © 1994 Wiley‐Liss, Inc.
Hypofibrinolysis: A common, major cause of osteonecrosis
Authors: Glueck Charles J. , Freiberg Richard , Glueck Helen J. , Henderson Clyde , Welch Michael , Tracy Trent , Stroop Davis , Hamer Tracey , Sosa Felix , Levy Mark 
Published: February 2007

AbstractIn 30 patients with osteonecrosis of the hip (12 idiopathic, 18 secondary), we assessed the role of hypofibrinolysis mediated by high levels of piasminogen activator inhibitor (PAI). We evaluated hypofibrinoiysis as a common, potentially reversible, pathophysiologic cause of idiopathic osteonecrosis. In all 18 patients with secondary osteonecrosis. PAI was normal, as was the ability to activate fibrinoiysis. Nine of the 12 patients with idiopathic osteonecrosis had exceptionally high PA1 levels and could not normally elevate tissue piasminogen activator (tPA‐Fx), the major stimulator of fibrinolysis, after 10 min of venous occlusion at 100 mm Hg. The group of 12 patients with idiopathic osteonecrosis, compared to the 18 with secondary osteonecrosis, had low mean stimulated tPA‐Fx (1.92 vs. 7.6 IU/mi, P .001) and very high stimulated PAI‐Fx (70 vs. 7.6 U/mi, P ⩽ .01). Three of the 12 patients with idiopathic osteonecrosis had both normal PAI and normal Stimulated tPA‐Fx. These three patients and 14 of the 18 with secondary osteonecrosis had high lipoprotein (a) [Lp(a)] (>20 mg/dI). Mean Lp(a) was much higher (60 mg/dI) in the patients with secondary osteonecrosis than Lp(a) (16 mg/dI, P ⩽ .001) in the 12 patients with idiopathic osteonecrosis. These findings suggest that hypofibrinoiysis mediated by high PAI is a common cause of idiopathic osteonecrosis, whereas high Lp(a) may play an etiologic role in secondary osteonecrosis. Prospective studies of patients with high PA1 and/or high Lp(a) should be carried out to assess further their apparently causal roles in osteonecrosis. © 1994 Wiley‐Liss, Inc.
Primary amyloidosis associated with a novel heavy‐chain fragment (AH amyloidosis)
Authors: Solomon Alan , Weiss Deborah T. , Murphy Charles 
Published: February 2007

AbstractPrimary or AL amyloidosis occurs in patients with monoclonal plasma cell‐related disorders and is typically associated with the systemic deposition as amyloid fibrils of the light‐chain portion of the immunoglobulin molecule. Recently, the discovery that heavy chains could be involved in amyloid formation led to the designation of this type of disease process as AH amyloidosis. We have now identified a second example of heavy chain‐associated amyloidosis in a patient (MAD) who had a serum IgG monoclonal gammopathy and Bence Jones proteinuria. In this case, the renal and splenic amylold deposits consisted solely of the VH‐D‐encoded portion of the heavy polypeptide chain, in contrast to the first case, where the amyloid contained an immunoglobulin component composed of the entire heavy‐chain variable and third constant domains. In this respect, the chemical composition of the amyloid protein MAD differed not only from that of the first reported case of AH amyloidosis but from all other structurally abnormal components found in patients with heavy chain‐associated disease. The discovery that certain forms of heavy chains, as well as light chains, can form amyloid provides further information on the chemical basis of amyloidogenicity and the diverse nature of this disease. © 1994 Wiley‐Liss, Inc.