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1 nal metabolic stress, were compared pre- and posttransfusion.
2 s will have a satisfactory platelet recovery posttransfusion.
3 , respectively, which were compared pre- and posttransfusion.
4 ), could be rapidly cleared from circulation posttransfusion.
5 lated acute lung injury (TRALI) is a form of posttransfusion acute pulmonary insufficiency that has b
6                           No stroke occurred posttransfusion after a mean follow-up of 6.1 years.
7                                              Posttransfusion antibody screening confirmed development
8 donor and recipient HVR1 sequences 7.9 weeks posttransfusion, but donor and recipient sequences diver
9 atelet count but was not associated with the posttransfusion change in hemoglobin concentration.
10 in-10, and interleukin-1 receptor antagonist posttransfusion compared with controls.
11 ells showed high HLA class I expression, and posttransfusion complement activation was increased in c
12             Furthermore, the emphasis on the posttransfusion count increment and the platelet count a
13                                 However, the posttransfusion function of CSPs is unknown and it is un
14            The risk of NEC was 11.9 per 1000 posttransfusion hazard periods and 12.7 per 1000 control
15                     Then, the risk of NEC in posttransfusion hazard periods was compared with that in
16 ted with a higher risk of NEC during 72-hour posttransfusion hazard periods.
17 ion of red blood cells (RBCs) should yield a posttransfusion hemoglobin increment of 1 g/dL.
18         Age of blood was not associated with posttransfusion hemoglobin or ferritin change.
19                                              Posttransfusion, hemoglobin and hepcidin increased, and
20 of the rbc storage lesion as storage-related posttransfusion hemolysis producing Hb-driven pathophysi
21 in the differential diagnosis of unexplained posttransfusion hemolytic anemia or fever, regardless of
22                                Patients with posttransfusion hepatitis C are at greater risk of cirrh
23                 Several reports suggest that posttransfusion hepatitis C causes more aggressive histo
24                                Patients with posttransfusion hepatitis C were more likely to develop
25 , has been reported in patients with non-A-G posttransfusion hepatitis in Japan.
26      Although GBV-C is associated with acute posttransfusion hepatitis, it is not clear if the virus
27 se members (SENV-D and SENV-H) are linked to posttransfusion hepatitis.
28 ish that SEN-V might be a causative agent of posttransfusion hepatitis.
29 ve been found, some with an association with posttransfusion hepatitis.
30             By multiple regression, pre- and posttransfusion hepcidin concentrations were both associ
31 factors, including genetic polymorphisms, on posttransfusion increments and other patient outcomes.
32 e been used in the past and have resulted in posttransfusion increments for more than 24 hours after
33 nd TRALI have emerged as important causes of posttransfusion morbidity and mortality.
34 sured in chronically transfused SCD pre- and posttransfusion (N = 25), in nontransfused SCD (N = 26),
35 hils (mean +/- SD) resulted in a mean 1-hour posttransfusion neutrophil increment of 2.6 +/- 2.6 x 10
36 from a patient (H) during the acute phase of posttransfusion non-A, non-B hepatitis, which had been t
37 d resulted in 5 STRs occurring 9 to 24 hours posttransfusion; none of these STRs had been reported by
38                                          The posttransfusion nosocomial infection rate was 14.3% in 4
39  of TA-GVHD in recipient mice over a 10-week posttransfusion observation period: peripheral blood cel
40 ra collected during the 4th through 8th days posttransfusion; only 2 of the 67 sera were still RNA no
41 an change within each group from the pre- to posttransfusion period for Pg-Paco2 gap and gastric intr
42 t-by-time analysis or comparing the pre- and posttransfusion periods either for Pg-Paco2 gap (mean di
43                              Second, 72-hour posttransfusion periods were categorized as hazard perio
44                              The mean 1-hour posttransfusion platelet corrected count increment (CCI)
45               The primary outcome was 1-hour posttransfusion platelet count increment (PCI).
46 for PCT and conventional platelets, although posttransfusion platelet count increments and days to ne
47 ip between LCTAB levels in the recipient and posttransfusion platelet count increments.
48     In this study, we sought to evaluate the posttransfusion platelet function and its predictors for
49 and duration of platelet storage, can affect posttransfusion platelet increments, but it is unclear w
50 modest impact on both absolute and corrected posttransfusion platelet increments, they have no measur
51  amphotericin were associated with decreased posttransfusion platelet responses.
52 g idiopathic thrombocytopenic purpura (ITP), posttransfusion purpura (PTP), drug purpura (DP), and X-
53 natal alloimmune thrombocytopenia (NAIT) and posttransfusion purpura (PTP).
54 and neonatal alloimmune thrombocytopenia and posttransfusion purpura.
55 ated storage, autologous 51-chromium 24-hour posttransfusion RBC recovery (PTR) studies were performe
56  platelet storage led to a markedly improved posttransfusion recovery and hemostatic function of plat
57 , is associated with a reduction in platelet posttransfusion recovery and hemostatic function.
58 chlorophenylhydrazone (CCCP), led to reduced posttransfusion recovery in mice, an effect that directl
59 rance, as their inhibition markedly improved posttransfusion recovery of both the mitochondria-injure
60  unchanged by iron repletion: mean change in posttransfusion recovery was 1.6% (95% confidence interv
61  fresh or stored for 7 days, were tested for posttransfusion recovery, as well as metabolomics and li
62                             Steap3 regulated posttransfusion recovery, contributing to a ferroptosis-
63 sion of long-stored RBCs resulted in reduced posttransfusion recovery, mostly due to SME clearance.
64  stored murine RBCs with l-carnitine boosted posttransfusion recovery, suggesting this could represen
65 ary outcome was the within-subject change in posttransfusion recovery.
66 rage duration was associated with decreasing posttransfusion red cell recovery (P = 0.002), decreasin
67                                  51-Chromium posttransfusion red cell recovery studies were performed
68  for red cell storage quality: a 51-chromium posttransfusion red cell recovery study.
69 iter blood volume, and experienced a smaller posttransfusion reduction in erythropoiesis and hepcidin
70 tively associated with survival and with the posttransfusion rise in the platelet count but was not a
71 sted for GBV-C markers in pretransfusion and posttransfusion samples.
72           Donor lymphocytes were detected in posttransfusion specimens using a quantitative Y-chromos
73 nor-specific HLA haplotypes were detected in posttransfusion specimens, consistent with one or more d
74 difications during storage that reduce their posttransfusion survival and functionality.
75 d that TACE activity correlates with reduced posttransfusion survival of these cells.
76                     Globally considering all posttransfusion time points, the overall crSO2 covariate
77 s) in immunocompetent recipients 3 to 5 days posttransfusion (tx).
78            Other major late effects included posttransfusion viral hepatitis, eight patients; CNS tox
79 e such antibodies (Abs) (six neonatal; three posttransfusion) were examined in the presence and absen