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731.
MT Sullivan ; AE Williams ; CT Fang ; EP Notari ; BJ Poiesz ; GD Ehrlich 《Transfusion》1993,33(7):585-590
Interviews and laboratory testing were conducted for 168 contacts referred by former blood donors identified as seropositive for antibody to human T-lymphotropic virus type I (HTLV-I) or type II (HTLV-II). Thirty-two (28%) of 114 heterosexual contacts of seropositive donors, including 12 women and 20 men, were found to be antibody positive. None of 40 offspring (except one adult man who reported sexual contact in Puerto Rico) or 14 other (nonspousal) family members were seropositive. Thirty-one of the seropositive contacts were typeable as having either HTLV-I (52%) or HTLV-II (48%). Assessment of couples found that the median duration of the sexual relationship was significantly longer (p = 0.03) for those in which both partners were infected than in discordant pairs. Analysis of risk history data for 22 infected couples revealed that, in three cases, risk factors (Japanese ancestry or sexual contact with an injecting drug user) could be identified in the women, but not in their male partners. Among couples in which the male had the greater risk history, the risk factor was either a history of transfusion, birth or sexual exposure in an endemic area, or injected drug use. Counseling strategies for individuals with HTLV-I or HTLV-II infection should take into account the relatively high seroprevalence in their partners and should address the potential for sexual transmission in both directions. 相似文献
732.
Mr James H. Cicman BHS RRT Vinson F. Skibo AE CBET James M. Yoder BA 《Journal of clinical monitoring and computing》1993,9(2):104-111
This second article in a 2-part series on the operation of principal components within Narkomed anesthesia systems describes the function and compensation mechanisms of the Dräger 19.n vaporizer, the operating principles of the anesthesia ventilator-electronic, the structure and mechanics of the pressure limit control, and the 3 basic monitoring systems built into the anesthesia system. Part II of this series builds on the data published in part I (J Clin Monit 1992;8:295–307). 相似文献
733.
Rh E/e genotyping by allele-specific primer amplification 总被引:1,自引:0,他引:1
Faas BH; Simsek S; Bleeker PM; Overbeeke MA; Cuijpers HT; von dem Borne AE; van der Schoot CE 《Blood》1995,85(3):829-832
It has been shown that the Rhesus (Rh) blood group antigens are encoded by two homologous genes: the Rh D gene and the Rh CcEe gene. The Rh CcEe gene encodes different peptides: the Rh C, c, E, and e polypeptides. Only one nucleotide difference has been found between the alleles encoding the Rh E and the Rh e antigen polypeptides. It is a C-- >G transition at nucleotide position 676, which leads to an amino acid substitution from proline to alanine in the Rh e-carrying polypeptide. Here we present an allele-specific primer amplification (ASPA) method to determine the Rh E and Rh e genotypes. In one polymerase chain reaction, the sense primer had a 3'-end nucleotide specific for the cytosine at position 676 of the Rh E allele. In another reaction, a sense primer was used with a 3'-end nucleotide specific for the guanine at position 676 of the Rh e allele and the Rh D gene, whereas the antisense primer had a 3'-end nucleotide specific for the adenine at position 787 of the Rh CcEe gene. We tested DNA samples from 158 normal donors (including non-Caucasian donors and donors with rare Rh phenotypes) in these assays. There was full concordance with the results of serologic Rh E/e phenotyping. Thus, we may conclude that the ASPA approach leads to a simple and reliable method to determine the Rh E/e genotype. This can be useful in Rh E/e genotyping of fetuses and/or in cases in which no red blood cells are available for serotyping. Moreover, our results confirm the proposed association between the cytosine/guanine polymorphism at position 676 and the Rh E/e phenotype. 相似文献
734.
Analysis of hematopoietic stem and progenitor cell populations in cytomegalovirus-infected mice 总被引:1,自引:0,他引:1
We have studied the effects of murine cytomegalovirus (MCMV) infection on bone marrow stem and progenitor cell populations to find an explanation for the defects in hematopoiesis that accompany CMV infections in patients. Sublethal MCMV infection of BALB/c mice resulted in a 5- to 10-fold decrease in the numbers of myeloid (colony- forming unit-granulocyte-macrophage [CFU-GM]) and erythroid (burst- forming unit-erythroid [BFU-E]) progenitor cells in the marrow, but not in primitive myeloerythroid progenitor cell (colony-forming unit-spleen [CFU-S]) numbers. In contrast, we observed a 10- to 20-fold reduction in CFU-S as well as CFU-GM and BFU-E in lethally infected mice. Depletion of marrow CFU-GM was less severe in C57BL/10 and C3H/HeJ mice, which are more resistant to the effects of MCMV infection. Treatment of bone marrow cells with MCMV preparations in vitro did not reduce the numbers of CFU-GM, although up to 10% of the cells were productively infected. This finding suggests that CFU-GM were not susceptible to lytic MCMV infection in vitro and are probably not eliminated by lytic infection in vivo. Increases in the frequencies of Sca-1+Lin- marrow cells, a population that includes cells with the characteristics of pluripotential stem cells, were observed in MCMV- infected BALB/c, C57BL/10, and DBA/2J mice. Increases in the frequencies of c-kit+Lin- marrow cells were only seen in DBA/2J mice. MCMV infection did not impair the function of pluripotential stem cells because transplantation of marrow from MCMV-infected donors into irradiated recipient mice resulted in successful reconstitution of the T, B, and myeloid cell lineages. 相似文献
735.
EUI IM M.D. BYEONG‐KEUK KIM M.D. YOUNG‐GUK KO M.D. AE‐YOUNG HER M.D. HYUN HEE CHOI M.D. DONG‐HO SHIN M.D. JUNG‐SUN KIM M.D. DONGHOON CHOI M.D. YANGSOO JANG M.D. MYEONG‐KI HONG M.D. Ph.D. 《Journal of interventional cardiology》2013,26(4):378-383
Objectives
Long‐term clinical outcomes were evaluated in long coronary artery stenosis treated with different types of drug‐eluting stents.Background
Long‐term follow‐up data to compare clinical outcomes between Resolute? zotarolimus‐eluting stent (R‐ZES) versus sirolimus‐eluting stent (SES) implantation for long coronary artery stenosis is insufficient.Methods
A total of 254 patients (307 lesions) treated with R‐ZES and 265 patients (303 lesions) treated with SES for long coronary lesions (total stent length ≥30 mm) were enrolled, and long‐term (3 years) clinical outcomes were compared between the 2 groups. Efficacy (target lesion revascularization [TLR]) and safety (the composite occurrence of cardiovascular death, target lesion–related myocardial infarction, or target lesion–related definite stent thrombosis) were assessed.Results
The 2 groups had similar baseline characteristics except for the duration of dual antiplatelet therapy (23.4 ± 11.2 months in R‐ZES‐treated patients vs. 27.4 ± 13.9 months in SES‐treated patients, P < 0.001). Total stent length was similar in R‐ZES‐treated patients (45.0 ± 19.0 mm) and SES‐treated patients (45.4 ± 18.6 mm) (P = 0.464). The cumulative TLR rate was 4.6% in R‐ZES‐treated patients versus 4.6% in SES‐treated patients (P = 0.911). For safety parameters, R‐ZES‐treated patients showed a significantly lower rate of the composite occurrence of cardiovascular death, target lesion–related myocardial infarction, or target lesion–related definite stent thrombosis than SES‐treated patients (0.4% vs. 2.4%, P = 0.042). Particularly, the occurrence of target lesion–related definite stent thrombosis was significantly lower in R‐ZES‐treated patients than in SES‐treated patients (0.0% vs. 2.0%, P = 0.028).Conclusions
R‐ZES stents showed superior long‐term safety than SES for treating long coronary lesions, while maintaining a similar clinical efficacy.736.
Kerst JM; Sanders JB; Slaper-Cortenbach IC; Doorakkers MC; Hooibrink B; van Oers RH; von dem Borne AE; van der Schoot CE 《Blood》1993,81(2):344-351
To study the receptors involved in the interaction between extracellular matrix proteins and hematopoietic progenitor cells, we analyzed the expression of beta 1 integrins on CD34+ bone marrow cells by means of immunoflowcytometry. Alpha 4 beta 1 and alpha 5 beta 1 were expressed, whereas alpha 1 beta 1, alpha 2 beta 1, alpha 3 beta 1, alpha 6 beta 1, and alpha v beta 1 were virtually absent. Furthermore, we assessed the alpha 4 and alpha 5 expression on committed myeloid progenitor cells. These colony-forming cells were detected in the alpha 4 dull fraction and the alpha 5 dull fraction. During myeloid differentiation, both in vivo and in vitro, a differential expression of alpha 4 beta 1 and alpha 5 beta 1 was observed. alpha 5 beta 1 was found to be lost at the myelocytic-metamyelocytic stage, before the loss of alpha 4 beta 1, at the band stage. Functional studies showed no binding of erythroid progenitor-depleted, CD34+ bone marrow cells to fibronectin. However, protein kinase C activation strongly induced fibronectin binding (68% of the cells). Inhibition experiments with specific antibodies and peptides showed the binding to be mediated by both alpha 4 beta 1 and alpha 5 beta 1. Also, colony-forming cells of granulocytes and macrophages were demonstrated to adhere to fibronectin in an activation-dependent way. During granulocyte colony-stimulating factor-induced in vitro maturation, the activation-dependent fibronectin binding capacity is gradually lost. We conclude that: (1) CD34+ bone marrow cells express alpha 4 beta 1 and alpha 5 beta 1; (2) the expression of alpha 4 beta 1 and alpha 5 beta 1 is differentially expressed during myeloid differentiation; and (3) binding of CD34+ bone marrow cells to fibronectin is activation dependent. 相似文献
737.
Fragility and structure of hemoglobin S fibers and gels and their consequences for gelation kinetics and rheology 总被引:1,自引:0,他引:1
Pathogenesis in sickle cell disease depends on whether red blood cells can pass the microvasculature during the delay time before hemoglobin S gelation and cell rigidification occur. Here we observe individual hemoglobin S fibers by differential interference contrast (DIC) microscopy and show that hemoglobin S gels and fibers are fragile and easily broken by mechanical perturbation, and that breakage results in vast acceleration of gelation kinetics due to the creation of new, growing fiber-ends. Hence, in vivo this may be an important factor, in addition to hemoglobin concentration and degree of deoxygenation, that governs delay time and pathogenesis. Pathogenesis also depends on gel rheology and cell rigidification, which depend on fiber cross-linking. We show different mechanisms by which X-shaped, Y-shaped, and "zippering" cross-links form. Finally, we estimate the "on" rate constant for fiber growth to be about 200 mmol/(L.s) and obtain a value for the heterogeneous nucleation rate at 13.5 mmol/L heme. 相似文献
738.
RM Minchinton ; M de Haas; AE von dem Borne; M Kleijer ; AW Roberts ; EA Gillett 《Transfusion》1995,35(10):874-878
BACKGROUND : Neutrophils from a patient in first remission of acute myeloid leukemia were found to lack NA1 and NA2 alloantigens. This NA null phenotype was converted to the normal phenotype of NA1, NB2 by the transplantation of bone marrow from an HLA-identical sibling. To investigate the inherited or acquired nature of this rare phenotype, a combination of conventional neutrophil serology and recently developed restriction fragment length polymorphism (RFLP) and polymerase chain reaction (PCR) assays was used. STUDY DESIGN AND METHODS : Diagnosis, remission, and posttransplant patient peripheral blood samples were used for neutrophil phenotyping by granulocyte agglutination and immunofluorescence tests. The presence and dose of the gene for neutrophil Fc gamma RIIIb (Fc gamma RIIIB) were tested for with RFLP and Southern analysis and PCR-based RFLP tests. Plasma levels of circulating soluble Fc gamma RIII (sFc gamma RIII) were measured with radioimmunoassay. The sibling bone marrow donor and the patient's parents were also studied. RESULTS : RFLP analysis of DNA obtained from the patient at the time of diagnosis showed that she lacked the Fc gamma RIIIB gene for neutrophil Fc gamma RIII (i.e., Fc gamma RIIIb), but that, in DNA prepared from posttransplant samples, the Fc gamma RIIIB gene was present. Quantitation of plasma levels of soluble FcRIII (sFcRIII) demonstrated a complete absence of sFcRIII in the patient's pretransplant plasma. However, 20 units of sFcRIII were detected in the patient's plasma by 160 days after graft. Hair samples from the patient provided sufficient nonhematopoietic, genomic DNA to confirm that her genotype was NA0NA0. DNA prepared from lymphocytes of both parents and the sibling marrow donor was used to quantitate their Fc gamma RIIIB gene dose. The mother and brother had only one Fc gamma RIIIB gene each, while the father apparently had a normal complement of two Fc gamma RIIIB genes. CONCLUSION : In this case, an inherited absence of Fc gamma RIIIB gene in a patient with acute myeloid leukemia was unintentionally corrected by the transplantation of bone marrow from a sibling donor who himself carried only one Fc gamma RIIIB gene. 相似文献
739.
N Puig ; M de Haas; M Kleijer ; JA Montoro ; A Perez ; JV Villalba ; I Gomez ; AE von dem Borne 《Transfusion》1995,35(8):683-687
BACKGROUND: Fc gamma RIIIb deficiency is a rare defect in which neutrophils do not express Fc gamma RIIIb and therefore the individuals with this defect have an NA null phenotype. Soluble Fc gamma RIII in plasma is severely decreased and almost undetectable. During pregnancy, Fc gamma RIIIb deficiency may cause the formation of maternal Fc gamma RIIIb antibodies, which leads to an isoimmune neonatal neutropenia. The first known case of isoimmune neonatal neutropenia caused by these antibodies in a Spanish child was identified. CASE REPORT: A newborn infant was severely affected by omphalitis; analysis of his blood showed an absolute neutropenia, but he responded well on intravenous immunoglobulin therapy. The maternal antiserum reacted strongly with all tested Fc gamma RIIIb-positive neutrophils. A family study showed that the infant's mother, one of the mother's sisters, and her mother were Fc gamma RIIIb deficient. No neutrophil antibodies were found in the plasma from these other Fc gamma RIIIb-negative women, although both had had numerous pregnancies. The three women were healthy, but one had recurrent otitis. DNA analysis of the family showed the absence of both Fc gamma RIIIB genes in the three Fc gamma RIIIb-negative women. The father of the child and all the children of the Fc gamma RIIIB gene-deficient women were shown to lack one of the Fc gamma RIIIB genes. CONCLUSION: A new case of isoimmune neonatal neutropenia caused by anti-Fc gamma RIIIb is identified. The family study indicates that the Fc gamma RIIIb deficiency is a hereditary genetic defect. In accordance with the location of Fc gamma RIIIB on chromosome 1, an autosomal pattern of inheritance of the Fc gamma RIIIB-deficient allele was observed. 相似文献
740.