PCA and PS exposure of stored RBCs increased during storage and showed significant positive correlation. PCA of long-term stored RBCs may not be reversed by transfusion.
BackgroundThis study assessed the health related quality of life of family caregivers (FCs) of leukemia patients by using the health utility scores derived from the EuroQol five-dimensional (EQ-5D) questionnaire.MethodsA cross-sectional survey was undertaken on 306 family caregivers of leukemia patients to assess their health utility using the EQ-5D-3L. Participants were recruited from three hospitals in China’s Heilongjiang province. The health utility scores of the participants were estimated based on the Chinese EQ-5D-3L value set and compared with those of the local general population. Factors predicting the health utility scores were identified through the Kruskal-Wallis analysis of variance and median regression analyses.ResultsFCs had lower health utility scores than the general population (p < 0.001). The participants with a lower socioeconomic status had lower utility scores and reported more problems than those with a higher socio-economic status. Better family function and higher social support were associated with higher health utility scores. The type of leukemia, household income, and social support are significant predictors of health utility scores of the FCs. Chronic lymphocytic leukemia, low socio-economic status, and low social support are associated with lower health utility scores of the FCs.ConclusionsFCs for leukemia patients have lower health utility scores than the local general population, as measured by the EQ-5D-3L. There is an immediate need to address the health concerns of FCs, who play an important role in the Chinese health care system.Electronic supplementary materialThe online version of this article (10.1186/s12885-018-4855-y) contains supplementary material, which is available to authorized users.
Amniotic fluid (AF) may induce disseminated intravascular coagulation when it enters maternal circulation by breaching the placental-maternal circulation barrier. The precise mechanism of the procoagulant activity of AF is unclear, we speculate that AF cells have procoagulant activity due to the externalization of phosphatidylserine (PS). The present study aims to demonstrate that, in addition to tissue factor (TF), the PS that is externalized on AF cells is important for the procoagulant activity of AF. Ten AF samples from parturient women were analyzed and normal platelets, neutrophils, and lymphocytes were harvested as controls. Lactadherin, a glycoprotein, binds to membranes containing PS, inhibits prothrombinase activity, factor Xase activity, and tissue factor-factor VIIa activity by blocking PS-containing membrane binding. Thus lactadherin was utilized as a PS probe for flow cytometry and confocal microscopy to enable comparison of PS distribution with TF and intrinsic factor Xase complex formation. Procoagulant activity of AF cells was first measured in plasma with AF cells serving as thromboplastin. Activity of AF cells supporting intrinsic and extrinsic factor Xase complexes was measured in purified systems. Lactadherin, as an agent to block exposed PS, inhibited 85% of intrinsic and extrinsic factor Xase activity. Competition binding studies indicated that lactadherin competed for 55% of factor VIII binding sites. However, binding of factor VIII was completely inhibited by PS-containing vesicles and by mAb that recognize the factor VIII C2 domain indicating that all fVIII binding was mediated by the membrane-binding motif or an overlapping epitope. Confocal microscopy identified patches and a rim-pattern indicating a diffuse PS exposure. Lactadherin binding sites and TF distributed to discreet, but overlapping regions of the cells. These results indicate that PS exposure parallels procoagulant activity on AF cells and is required for at least 85% of intrinsic and extrinsic factor Xase activities. However, the topographical pattern of PS exposure differs from the pattern of TF and the pattern of binding site distribution for intrinsic factor Xase complexes. Thus, the results imply that intrinsic factor Xase and extrinsic factor Xase activity are localized to small cell regions where PS exposure coincides with TF and intrinsic factor Xase binding sites, respectively.
Amniotic fluid (AF) may induce disseminated intravascular coagulation (DIC) when it enters maternal circulation by breaching the placental-maternal circulation barrier. The precise mechanism of the procoagulant activity of AF is unclear, but tissue factor (TF) has been proposed to be the main cause. As one constituent of AF, AF cells accumulate and undergo apoptosis continuously. Therefore, we speculate that AF cells have procoagulant activity due to the externalisation of phosphatidylserine (PS). The present study aims to demonstrate that, in addition to TF, the PS that is externalised on AF cells is important for the procoagulant activity of AF. Ten AF samples from parturient women were analysed using lactadherin as the probe for PS. Anti-TF antibody also was used to identify TF and its associated coagulation functions in AF cells. Normal platelets, neutrophils, and lymphocytes were harvested as controls. Confocal microscopy and flow cytometry was used to assess PS expression on AF cells. The procoagulant activity of AF cells was demonstrated by a plasma coagulation assay and further confirmed by factor Xase/prothrombinase assays. PS and TF were present on most AF cells, providing substantial procoagulant activity. Furthermore, factor Xase and prothrombinase assays showed that AF cells substantially enforced the activation of factor X and prothrombin. PS on AF cells is an important procoagulant source for AF. Lactadherin is an ideal anticoagulant for inhibiting the procoagulant activity of AF cells.
Acute promyelocytic leukemia (APL) causes coagulation, which can worsen following initiation of chemotherapy and is improved or corrected by the differentiating agents, all trans retinoic acid (ATRA) and arsenic trioxide (As2O3). The relationship of procoagulant activity to phosphatidylserine (PS) exposure on leukemic cells has not been clarified, although prior studies indicate that APL cells expose tissue factor (TF). Procoagulant activity of leukemic cells was measured in a modified prothrombin time in which leukemic cells replaced thromboplastin. The presence of phosphatidylserine (PS) in neutrophils and mononuclear cells (MNC) from healthy donors and APL cells from patients was investigated by flow-cytometry and confocal microscopy. The assembly of extrinsic tenase, intrinsic tenase and prothrombinase complexes on these cells was studied using enzymatic assays employing plasma or purified proteins. Lactadherin was utilized as a probe to track PS exposure and as an agent to block exposed PS. Isolated APL cells exhibited patches that stained with lactadherin, but neutrophils and MNC did not, indicating more PS exposure on APL cells than the other two cell types. Exclusion of propidium iodide by the leukemic cells indicated that PS exposure occurs in the absence of frank apoptosis. Coagulant activity increased approx 20-fold after cells were exposed to 0.1 μM daunorubicin for 24 hr with 70% of apoptosis and decreased by 85% after 24 hr treatment with 1 μM ATRA or As2O3 with partial differentiation. Inhibition of procoagulant activity by ATRA and As2O3 corresponded to decreased PS and decrease activity for all three enzyme complexes. Lactadherin, which blocks PS binding sites, inhibited Xase and prothrombin conversion by their respective APL-assembled activating complexes. APL cells support all procoagulant reactions leading to robust thrombin formation. This ability results from concomitant PS and TF exposure at the outer leaflet of cell membrane. In contrast, less PS on neutrophils and MNC do not support the coagulation.
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