ライフサイエンスコーパス: posttransfusion

1 nal metabolic stress, were compared pre- and posttransfusion.

2 , respectively, which were compared pre- and posttransfusion.

3 s will have a satisfactory platelet recovery posttransfusion.

4 lated acute lung injury (TRALI) is a form of posttransfusion acute pulmonary insufficiency that has b

5 No stroke occurred posttransfusion after a mean follow-up of 6.1 years.

6 Posttransfusion antibody screening confirmed development

7 donor and recipient HVR1 sequences 7.9 weeks posttransfusion, but donor and recipient sequences diver

8 in-10, and interleukin-1 receptor antagonist posttransfusion compared with controls.

9 Age of blood was not associated with posttransfusion hemoglobin or ferritin change.

10 Posttransfusion, hemoglobin and hepcidin increased, and

11 of the rbc storage lesion as storage-related posttransfusion hemolysis producing Hb-driven pathophysi

12 in the differential diagnosis of unexplained posttransfusion hemolytic anemia or fever, regardless of

13 Patients with posttransfusion hepatitis C are at greater risk of cirrh

14 Several reports suggest that posttransfusion hepatitis C causes more aggressive histo

15 Patients with posttransfusion hepatitis C were more likely to develop

16 , has been reported in patients with non-A-G posttransfusion hepatitis in Japan.

17 Although GBV-C is associated with acute posttransfusion hepatitis, it is not clear if the virus

18 se members (SENV-D and SENV-H) are linked to posttransfusion hepatitis.

19 ish that SEN-V might be a causative agent of posttransfusion hepatitis.

20 ve been found, some with an association with posttransfusion hepatitis.

21 By multiple regression, pre- and posttransfusion hepcidin concentrations were both associ

22 e been used in the past and have resulted in posttransfusion increments for more than 24 hours after

23 nd TRALI have emerged as important causes of posttransfusion morbidity and mortality.

24 sured in chronically transfused SCD pre- and posttransfusion (N = 25), in nontransfused SCD (N = 26),

25 hils (mean +/- SD) resulted in a mean 1-hour posttransfusion neutrophil increment of 2.6 +/- 2.6 x 10

26 from a patient (H) during the acute phase of posttransfusion non-A, non-B hepatitis, which had been t

27 d resulted in 5 STRs occurring 9 to 24 hours posttransfusion; none of these STRs had been reported by

28 The posttransfusion nosocomial infection rate was 14.3% in 4

29 of TA-GVHD in recipient mice over a 10-week posttransfusion observation period: peripheral blood cel

30 ra collected during the 4th through 8th days posttransfusion; only 2 of the 67 sera were still RNA no

31 an change within each group from the pre- to posttransfusion period for Pg-Paco2 gap and gastric intr

32 t-by-time analysis or comparing the pre- and posttransfusion periods either for Pg-Paco2 gap (mean di

33 The mean 1-hour posttransfusion platelet corrected count increment (CCI)

34 for PCT and conventional platelets, although posttransfusion platelet count increments and days to ne

35 ip between LCTAB levels in the recipient and posttransfusion platelet count increments.

36 and duration of platelet storage, can affect posttransfusion platelet increments, but it is unclear w

37 modest impact on both absolute and corrected posttransfusion platelet increments, they have no measur

38 amphotericin were associated with decreased posttransfusion platelet responses.

39 g idiopathic thrombocytopenic purpura (ITP), posttransfusion purpura (PTP), drug purpura (DP), and X-

40 natal alloimmune thrombocytopenia (NAIT) and posttransfusion purpura (PTP).

41 and neonatal alloimmune thrombocytopenia and posttransfusion purpura.

42 platelet storage led to a markedly improved posttransfusion recovery and hemostatic function of plat

43 , is associated with a reduction in platelet posttransfusion recovery and hemostatic function.

44 chlorophenylhydrazone (CCCP), led to reduced posttransfusion recovery in mice, an effect that directl

45 rance, as their inhibition markedly improved posttransfusion recovery of both the mitochondria-injure

46 rage duration was associated with decreasing posttransfusion red cell recovery (P = 0.002), decreasin

47 51-Chromium posttransfusion red cell recovery studies were performed

48 iter blood volume, and experienced a smaller posttransfusion reduction in erythropoiesis and hepcidin

49 sted for GBV-C markers in pretransfusion and posttransfusion samples.

50 Donor lymphocytes were detected in posttransfusion specimens using a quantitative Y-chromos

51 nor-specific HLA haplotypes were detected in posttransfusion specimens, consistent with one or more d

52 difications during storage that reduce their posttransfusion survival and functionality.

53 d that TACE activity correlates with reduced posttransfusion survival of these cells.

54 s) in immunocompetent recipients 3 to 5 days posttransfusion (tx).

55 Other major late effects included posttransfusion viral hepatitis, eight patients; CNS tox

56 e such antibodies (Abs) (six neonatal; three posttransfusion) were examined in the presence and absen