bluuebunny/crossref_metadata_2025_split huggingface dataset:
Arachidonic acid metabolites produced by platelet‐depleted human blood monocytes: A possible role in thrombogenesis
Authors: Jones C. Michael , Hall Elizabeth R. , Hester Jeanne P. , Wu Kenneth K. 
Published: February 2007

AbstractThe arachidonic acid metabolites produced by human peripheral blood monocytes were studied to determine which metabolites could have a role in thrombogenesis. Monocytes were found to be free of platelets by scanning electron microscopy and by measurement of 12‐HETE. Human peripheral blood monocytes produce thromboxane as their major metabolite. Thromboxane levels reached a plateau at 12–16 hours of culture. Monocytes produced relatively little prostaglandin E2 or F2. In contrast to our control platelet preparation, neither A23187 (1–10 μM) nor exogenous arachidonic acid (0–40 μM) caused an increase in monocyte thromboxane B2. On the other hand, lipopolysaccharide (20 μg per ml), collagen (2.5 mg per 107 cells), and thrombin (5–10 units per ml) caused a two‐ to fivefold increase in monocyte thromboxane B2 in most donors but had no effect on prostaglandin F1α levels. Blockage of thromboxane synthase by 1‐benzylimidazole abolished thromboxane B2 production but did not increase prostaglandin F1α. Finally, aspirin‐treated platelets from a volunteer donor, which were refractory to 30 μM arachidonate, could be aggregated by isolated blood monocytes.Our data indicate that monocytes are capable of producing thromboxane in large amounts. The regulation of this increase, however, appears to be quite different from platelets. We postulate that monocytes may have a role in hemostasis by virtue of their ability to adhere at sites of vascular injury and release thromboxane, which may enhance platelet aggregation and thrombus formation.
Neutrophil maturation and hypersegmentation promoted in normal bone marrow by a carcinoma‐elaborated protein factor
Authors: Bailey Steven C. , Head Jonathan F. , Greengard Olga 
Published: February 2007

AbstractIn rats with subcutaneously transplanted mammary carcinoma 5A (MC) and 2 to 10‐fold elevations in the blood content of mature neutrophils, 30–50% of the neutrophils showed pronounced hypersegmentation. This phenomenon could be reproduced in liquid culture of bone marrow cells from normal (tumor‐free) animals by 48 hr incubation with the MC host's serum, or with MC‐conditioned medium whose activity was attributable to an over 50,000 MW protein. The effects in vitro, occurring without change in total cell number and accompanied by increases in γ‐glutamyltranspeptidase (GGT) and alkaline phosphatase (AP) activity, included decreases in the percents of progenitors (myeloblasts, promyelocytes, myelocytes, metamyelocytes and bands) and an increase in mature neutrophils 50% of which exhibited obvious hypersegmentation. Much less if any neutrophil hypersegmentation, and no statistically significant decrease in immature cells, occurred in response to the several colony stimulating factors (CSFs) tested, although (in addition to inducing GGT and AP) some CSFs did cause an increase in mature neutrophils.These investigations demonstrate the efficacy of a MC‐elaborated blood‐borne protein to promote myeloid cell maturation, and describe a system for the first time in which neutrophil hypersegmentation can be studied in vitro.
Large granular lymphocytes from B‐chronic lymphocytic leukemia patients inhibit normal B cell proliferation
Authors: Perri Robert T. , Kay Neil E. 
Published: February 2007

AbstractLarge granular lymphocytes (LGL) may exert regulatory influences on B cell immuno‐globulin synthesis. We, therefore, investigated the influence of LGL from controls and B cell chronic lymphocytic leukemia patients (B‐CLL) on control B cell proliferation to costimulation with the F(ab′)2 fragment of goat antihuman μ and B cell growth factor (BCGF). Purified LGL (>90% by morphology) from control and B‐CLL peripheral blood were added in various concentrations to purified control B cells and incubated with anti‐μ, and BCGF for 3 days. [3H]‐thymidine uptake of B cells was then measured. There was no proliferation of control or CLL LGL alone to the costimulatory signals of the F(ab′)2 fragments of goat antihuman μ chain and BCGF. Addition of control LGL to equal numbers of control B cells did not blunt control B cell responsiveness to BCGF (with control LGL 8,649±298 cpm vs. control B cells alone 8,336 ± 556 cpm, mean ± SEM). When control LGL were increased to 10:1 LGL:B cell ratio, the maximal inhibition by control LGL of control B cell proliferative response to BCGF was 23%. In contrast, addition of CLL LGL at a 1:1 LGL:B cell ratio resulted in marked impairment of the control B cell proliferative response to BCGF (with CLL LGL 3,586 ± 954 cpm vs. control B cells alone 8,649 ± 298 cpm). Inhibition by CLL LGL occurred in a cell‐concentration‐dependent manner. No difference in CLL LGL's inhibitory effect on either resting or activated control B cell responsiveness to BCGF was noted. Inhibition of de novo protein synthesis (by cycloheximide inhibition) of CLL LGL did impair CLL LGL's inhibitory capacity for BCGF‐induced B cell proliferation. A possible explanation for these findings includes the possibility that a subgroup of LGL with B cell suppressive activity may have expanded as a host response to the B cell leukemia or as part of the disordered cell regulation in B‐CLL.
Evaluation of the clinical utility of platelet aggregation studies
Authors: Remaley Alan T. , Kennedy Julia M. , Laposata Michael 
Published: February 2007

AbstractTo determine the diagnostic importance of platelet aggregation studies, we evaluated the clinical utility of these assays by a retrospective review of 188 adult patients initially studied for bleeding abnormalities with platelet aggregation tests at a tertiary care hospital from 1984 to 1987. The primary indications for requesting the tests in our patient population were for the evaluation of a positive bleeding history or abnormal bleeding time (68%), hypercoagulability (17%), thrombocytosis (9%), or a family history of a bleeding disorder (6%). There was a statistically higher incidence of platelet aggregation test abnormalities in patients with highly abnormal bleeding times (40%), in patients with thrombocytosis from myeloproliferative disorders (65%), and in patients with a family history of a bleeding disorder (58%), compared to the other groups studied (16–29%). Of the 64 platelet aggregation tests performed that were abnormal, the following abnormalities were identified: 19 aspirin‐like defects (poor response to arachidonate and decreased second wave responses to weak agonists), which were presumably drug‐induced, ten myeloproliferative‐type disorder defects (abnormal response to epinephrine predominantly) in patients known to have myeloproliferative disease, 34 abnormal patterns not characterized as aspirin or myeloproliferative disorder related, four of which ultimately led to a diagnosis of storage pool disease, and one spontaneous aggregation defect. Our results suggest that platelet aggregation tests rarely lead to the diagnosis of a specific, previously undiagnosed platelet function disorder. Specific recommendations are given for efficient utilization of platelet aggregation tests.
BSF‐2/IL‐6 does not augment lg secretion but stimulates proliferation in myeloma cells
Authors: Tanabe Osamu , Kawano Michio , Tanaka Hideo , Iwato Koji , Asaoku Hideki , Ishikawa Hideaki , Nobuyoshi Masaharu , Hirano Toshio , Kishimoto Tadamitsu , Kuramoto Atsushi 
Published: February 2007

AbstractHuman myeloma cells were highly purified from bone marrow aspirates of 21 patients with advanced immunoglobulin G (IgG)‐type multiple myeloma. B‐cell stimulatory factor 2 (BSF‐2)/interleukin‐6 (IL‐6) was originally characterized as a cytokine that can enhance immunoglobulin secretion from activated normal B cells and increase the expression of secretory‐type Ig mRNA in these B cells, but that does not augment proliferation of activated B cells. However, recombinant IL‐6 (rIL‐6) could not enhance M‐protein (IgG) secretion in freshly isolated myeloma cells in vitro but could augment proliferation of myeloma cells, although myeloma cells constitutively expressed IL‐6 receptors. Furthermore, expression of secretory‐type IgG (γ‐chain) mRNA in myeloma cells was not changed in the presence of IL‐6. These results show that IL‐6 is not an enhancing factor in Ig secretion from myeloma cells, and thus signal transduction through IL‐6 in myeloma cells may be altered as opposed to activated B cells.
Increased circulating endothelial cells in sickle cell crisis
Authors: Sowemimo‐Coker Samuel O. , Meiselman Herbert J. , Francis Robert B. 
Published: February 2007

AbstractTo determine whether increased numbers of circulating endothelial cells, a possible indicator of endothelial injury, are present in subjects with sickle cell disease, we measured circulating endothelial cells in 30 normal subjects and in 23 subjects with sickle cell anemia. Mean circulating endothelial cells were significantly higher (P < 0.025) in the sickle cell subjects than in the normal subjects. Circulating endothelial cells were significantly higher than normal in 10 sickle cell subjects studied during painful crisis (P < 0.01) but not in 13 sickle cell subjects studied while in the steady state. To control for the known stimulatory effect of cigarette smoking on circulating endothelial cells, we analyzed the results for smokers and nonsmokers separately. Mean circulating endothelial cells were not significantly higher in sickle cell subjects who smoked (n = 10) than in normal subjects who smoked (n = 8), but were significantly higher (P < 0.05) in sickle cell nonsmokers (n = 13) than in normal nonsmokers (n = 22). Among nonsmoking sickle cell subjects, mean circulating endothelial cells were significantly higher than normal (P < 0.01) during painful crisis (n = 7), but not in the steady state (n = 6). We conclude that circulating endothelial cells are significantly increased in sickle cell crisis, and may indicate the occurrence of acute endothelial injury during episodes of microvascular occlusion.
Ultrastructure of multinucleated giant myeloma cells: Report of one case
Authors: Kurabayashi Hitoshi , Miyawaki Shuichi , Murakami Hirokazu , Nemoto Kazuo , Sawamura Morio , Kubota Kazuo , Naruse Takuji , Tsuchiya Jun 
Published: February 2007

AbstractThe ultrastructure of multinucleated giant myeloma cells obtained from an IgAk myeloma patient was investigated. The characteristic findings were marked nucleocytoplasmic asynchrony, irregular nuclear indentation, branched mitochondria, and Golgi apparatus surrounded by nuclei. The patient died of renal failure only 6 months after diagnosis.
Renal transplantation from a blood group A1B donor to an A2B recipient: A case report
Authors: Albornoz Gonzalo , Korb Steven , Kolovich Richard , Light Jimmy A. 
Published: February 2007

AbstractThis case report describes the transplantation of a kidney from an A1B donor to a recipient who was blood group A2B. The donor/recipient pair were ABO mismatched but compatible. In the majority of cases, A1 antibodies fail to react at 37°C and are of no clinical significance. However, hemolytic transfusion reactions due to A1 antibodies active at 37°C have been reported but are extremely rare. When the opportunity for transplantation arose for this patient, who had received multiple blood transfusions because of dialysis, the question of safety concerning the subject of transplanting across ABO sub‐grouping mismatches was presented. Inquiries regarding this matter proved fruitless and the transplant was performed mainly due to the lack of preformed anti‐A1 antibodies in the recipient at the time of transplant. It was hoped that the A2B recipient would fail to make an anti‐A1 antibody due to antigen exposure or if it did, would not pose a hazard to the allograft. Therefore we present our experience with a patient who was successfully transplanted across an ABO incompatible sub‐grouping, A1B allograft to an A2B recipient.
History and implications of the neutrophil glycoprotein deficiencies
Authors: Styrt Barbara 
Published: February 2007

AbstractThis review focuses on the initial clinical descriptions and subsequent investigation of the syndrome of recurrent infections associated with neutrophil membrane glycoprotein deficiencies. Characterization of the missing group of three glycoprotein heterodimers and their role in adhesion‐related neutrophil function is summarized. Study of the clinical consequences of these genetically determined membrane glycoprotein defects has also contributed to the understanding of the role of normal neutrophils in both host defense and host tissue damage.
Fibrinogenolysis in thrombotic thrombocytopenic purpura
Authors: Kakishita Eizo , Koyama Tetsuji , Higuchi Mitsuhiro , Kunitomi Osamu , Oura Yoshio , Nagai Kiyoyasu 
Published: February 2007

AbstractCoagulo‐fibrinolytic factors were studied in five patients suffering from thrombotic thrombocytopenic purpura (TTP). The change in coagulation factors in the acute stage was mild compared with that found in disseminated intravascular coagulation (DIC). We observed a slight increase of fibrin‐fibrinogen degradation products (FDP) in the plasma of four patients during the acute stage of TTP, but the level of the D‐dimer remained within normal variation and was extremely low compared with that in 27 samples from patients with DIC showing the same level of FDP. At the same time, both antigen levels of tissue‐type plasminogen activator (t‐PA) and plasminogen activator inhibitor type 1 (PAI‐1) were elevated in three of the four patients tested. Although a similar change was recognized in DIC patients' plasma, the elevation of PAI‐1 in the acute stage of TTP was far higher than in overt DIC. The antigen levels of t‐PA and PAI‐1 were normal in remission, and a mild elevation of PAI‐1 was detected in one of the three patients during the early stage of TTP relapse. Enzymography revealed the appearance of free t‐PA and an increase of a substance with a 110 kD molecule, assumed to be a t‐PA and PAI‐1 complex, in TTP plasma in the acute stage, but the findings were normal for plasma from cases in remission and the early stage of relapse. Enzymography also showed a decrease of urokinase‐type plasminogen activator (u‐PA) only in the acute stage of TTP. These changes in the coagulo‐fibrinolytic factors in the acute stage of TTP suggest that fibrinogenolysis might be induced by t‐PA, released through vascular reaction at an uninvolved area of vascular lesions caused by platelet agglutinates, which would then release large amounts of PAI‐1 inhibiting t‐PA and u‐PA activities at the occlusive lesion.
Platelet survival in patients with beta‐thalassemia
Authors: Eldor A. , Krausz Y. , Atlan H. , Snyder D. , Goldfarb A. , Hy‐Am E. , Rachmilewitz E. A. , Kotze H. F. , Heyns A. Du P. 
Published: February 2007

AbstractThromboembolic events associated with significant morbidity and mortality have been observed in patients with beta‐thalassemia major (TM). These include arterial as well as venous thrombosis and the development of early arteriosclerosis. To elucidate the possibility that TM patients may develop a hypercoagulable state we carried out a study of platelet kinetics on ten patients with TM and four patients with thalassemia intermedia (TI). Autologous platelets were labeled with indium‐111‐oxine, and the platelet lifespan (PLS) was determined. A significant shortening of PLS was observed in 13 out of 14 patients examined. The mean PLS (±1 SD) in ten patients (8 TM, 2 TI) who underwent splenectomy was 107 ± 36 hr (control splenectomized 248 + 51 hr) (P < .001) and in four nonsplenectomized patients (2 TM, 2 TI) was 102 ± 64 hr (control 224 + 23 hr) (P < .01). The short PLS in addition to reported findings of increased circulating platelet aggregates and the decreased response of TM platelets to aggregating agents suggests in vivo platelet activation in thalassemic patients.
Effect of hydroxyurea on the rheological properties of sickle erythrocytes in vivo
Authors: Ballas Samir K. , Dover George J. , Charache Samuel 
Published: February 2007

AbstractWe have monitored the rheological effects of hydroxyurea (HU) on erythrocytes obtained from two patients with severe sickle cell anemia who were enrolled in a therapeutic trial of this drug. Erythrocyte membrane stability and whole cell and membrane deformability of red cells from treated and untreated patients and normal controls were determined in room air using an ektacytometer—a laser viscodiffractometer. The percentage of dense cells was quantitated by centrifugation on a discontinuous Stractan density gradient. F reticulocytes (FR), absolute F reticulocytes (AFR), and F cells (FC) were determined by single‐cell radial immunolgic assays. After 1 year of treatment with HU, there was a significant increase in the level of hemoglobin (Hb) F, FR, AFR, and FC. The degree of anemia remained the same, but there was significant increase in the mean cell volume (MCV) and a significant decrease in the mean corpuscular Hb concentration (MCHC). Whole cell deformability improved by twofold, but membrane stability remained within normal limits. The hydration status of sickle erythrocytes improved as was indicated by a change toward normal in gradient osmotic ektacytometry, an increase in RBC K+ content, a decrease in percent of dense cells, and a decrease in the MCHC. The data indicate that, in addition to its effect on the production of Hb F, HU has a salutary effect on whole cell deformability and on the hydration status of sickle erythrocytes. Determination of the rheological properties of erythrocytes may be of value in monitoring the response to HU.
Hemoglobin Athens‐Georgia [α2 β2 40(C6)Arg→Lys] in association with β0‐thalassemia in Tunisia
Authors: Mrad A. , Kister J. , Feo C. , Poyart C. , Kastally R. , Blibech R. , Galacteros F. , Wajcman H. 
Published: February 2007

AbstractWe describe an Hb Athens‐Georgia (Hb A‐Ga)/β0‐thalassemia compound heterozygosity, found in a Tunisian patient. Oxygen binding studies of red cell suspensions of this patient, containing approximately 95% Hb A‐Ga, revealed an almost normal oxygen affinity. Nevertheless, dilute solutions of Hb A‐Ga showed an increased overall oxygen affinity and decreased heme‐heme interaction. This could be explained by a tetrameric hemoglobin with normal oxygen binding properties but with increased dissociation into monomers or dimers, as a consequence of a structural abnormality within the α1β2 interface. Such an interpretation would explain the increased oxygen affinity reported in previous studies performed on heterozygous Hb A/Hb A‐Ga patients.
Leukostasis: A phenomenon of prolymphocytic leukemia
Authors: Megaludis Alexis M. , Winkelstein Alan , Zeigler Zella R. , Miller Thomas R. 
Published: February 2007

AbstractWe are reporting a case of a patient with prolymphoctic leukemia complicated by fatal leukostasis. Multiple leukemic thrombi and leukoaggregales were demonstrated on postmortem examination in both the brain and lungs. This represents the first report pathologically documenting leukostasis in a chronic lymphoid malignancy.
Time‐dependent cleavage of a high‐mannose form of Ii to p25 in an intracellular compartment
Authors: Thomas Lawrence J. , Humphreys Robert E. , Knapp Walter , Nguyen Quoc V. 
Published: February 2007

AbstractThe cleavage of a high‐mannose form of Ii to p25 was demonstrated in an intracellular compartment of B cells. Subcellular fractions of 72 hr‐activated B cells, separated by Percoll density gradient centrifugation, were immunoprecipitated with anti‐class II or anti‐I serum and characterized for 5′‐nucleotidase, acid phosphatase, and radiolabeled transferrin. The cleavage of p25 from li as a C‐terminal fragment occurred from 20 to 60 min after synthesis in an intracellular compartment which was intermediate in density between lysosomal and plasma membrane fractions and coincided with the lighter of two internalized transferrin compartments. Chloroquine or monensin treatments, at maximal nontoxic doses, which block Golgi and lysosomal functions, did not seem to alter the cleavage of 1i to p25. p25 molecules were reduced to about 10,500 daltons by treatment with endoglycosidases F or H. We conclude that p25 was generated from a high mannose form of Ii in the endoplasmic reticulum or cis‐Golgi. This finding could either implicate that site for class II MHC desetope charging with foreign peptides or reflect a mechanism for degradation of “excess” Ii molecules.
Geographic variability of hemophilia‐associated aids in the United States: Effect of population characteristics
Authors: Stehr‐Green Jeanette K. , Jason Janine M. , Evatt Bruce L. 
Published: February 2007

AbstractNational AIDS surveillance suggests that approximately 3.5% of all hemophilic patients in the United States have developed AIDS as of February 1988; however, the cumulative incidence of AIDS among seropositive patients at individual hemophilia treatment centers (HTCs) has been reported to be as high as 12%. The purpose of this study was to examine the reported excess risk of AIDS at selected HTCs. Between July 13 and November 6, 1987, we reviewed medical charts from the 598 hemophilia A and hemophilia B patients receiving comprehensive care as of 1980 at six U.S. hemophilia treatment centers (three identified as low AIDS risk and three identified as high AIDS risk using national hemophilia‐associated AIDS surveillance data). The risk of AIDS among all patients was 8% and among seropositive patients was 18%. At the individual HTCs, the risk ranged from 0% to 14% among all patients and 0% to 25% among seropositive patients. Overall incidence rates were higher than those derived from national surveillance data because national estimates include all hemophilic patients (regardless of severity) whereas this study included only patients receiving comprehensive care (who are more likely to be severely affected by their coagulation disorder and receive concentrated clotting factors). The higher incidence of AIDS in the high‐risk centers was attributable to the older age of the patients in these HTCs, a factor previously associated with an increased risk of AIDS in seropositive patients. These findings do not support geographic variability in the incidence of AIDS and emphasize the importance of patient characteristics when comparing the incidence of hemophilia‐associated AIDS between populations.
Multiple responses of aplastic anemia to low‐dose cyclosporine therapy despite development of a myelodysplastic syndrome
Authors: Litzow Mark R. , Kyle Robert A. 
Published: February 2007

AbstractA 55‐year‐old white woman presented in July 1984 with severe aplastic anemia refractory to anti‐thymocyte globulin, corticosteroids, and danazol. In December 1984, oral cyclosporine therapy was begun, and a partial remission was achieved with persistent thrombocytopenia and transfusion independence. The cyclosporine dosage was tapered and then stopped in May 1986 when the platelet count was 35,000/L. In October 1986 the platelet count was only 16,000/L, and the bone marrow showed evidence of a myelodysplastic syndrome; cytogenetic analysis revealed deletion of the long arm of chromosome 13 (previous cytogenetic findings had been normal). After cyclosporine therapy was resumed, platelet count promptly increased to 36,000/L. A subsequent attempt to taper the cyclosporine dosage resulted in a decreased platelet count. The platelet count responded to cyclosporine again and was maintained at 54,000/L and higher with cyclosporine therapy at only 25 mg/day. This information suggests that, despite the development of a myelodysplastic syndrome, immune mechanisms were still operative in the pathogenesis of our patient's thrombocytopenia. Immune modulation may have an important role in preventing progression of myelodysplastic syndromes to more severe forms or to acute leukemia.