ライフサイエンスコーパス: 51Cr

1 g level of 125I was twice as high as that of 51Cr.

2 s to the wells and evaluating the release of 51Cr after 4 hours.

3 following intravenous injection of rats with 51Cr and 125I double-labeled Escherichia coli, hepatic 5

4 producible defect in their ability to induce 51Cr and 125I-UdR release from susceptible allogeneic ta

5 Purified human monocytes were labeled with 51Cr, and measured for adherence to human or porcine end

6 itor of cPLA2, also inhibited the release of 51Cr, and we found that the release of [3H]arachidonic a

7 ontribution to the effect of PTHrP, 45Ca and 51Cr-EDTA (as a blood diffusional marker) were administe

8 thelial resistance and transmural passage of 51Cr-EDTA and 3H-mannitol.

9 barrier function was assessed in vitro with 51Cr-EDTA in Ussing chambers and was expressed as the pe

10 echnique studied mucosal integrity by serial 51Cr-EDTA/14C-mannitol permeability tests.

11 ced release of both [3H]arachidonic acid and 51Cr from infected cells.

12 nin, and injury was determined by release of 51Cr from prelabeled cells.

13 ry to HMVEC-L, as measured by the release of 51Cr, increased significantly when HMVEC-L were incubate

14 otin RBC label by comparison to the standard 51Cr label, and used it to study changes that occur in s

15 Using 51Cr-labeled A-NK cells, it was determined that, at best

16 lex, we have injected 125I-labeled b-IgG/ SA/51Cr-labeled b23-RBC in rats.

17 ilar short-term kinetics were observed using 51Cr-labeled cells.

18 NK cell subsets as effectors and a panel of 51Cr-labeled Con A lymphoblasts as targets in the presen

19 ytometry, and for cytolytic activity against 51Cr-labeled Daudi target cells.

20 ection, were tested for cytotoxicity against 51Cr-labeled donor cells.

21 IELs lysed more 51Cr-labeled HT-29 cells when cultured for 72 hours with

22 say; and cytotoxicity production by lysis of 51Cr-labeled HT-29 cells.

23 arterial endothelial injury, the infusion of 51Cr-labeled microparticles resulted in a 3- to 5-fold i

24 4-fold increase in the functional binding of 51Cr-labeled MOLT-4 T cells.

25 om 1D6.1E5-vaccinated mice were able to kill 51Cr-labeled P815 cells in a dose-dependent fashion that

26 Autologous 51Cr-labeled platelet recovery and survival measurements

27 Simultaneous measurement, using 51Cr-labeled red blood cells, was performed.

28 ated peripheral blood mononuclear cells with 51Cr-labeled targets, followed by assay of radiolabel re

29 we analyze experimental data on migration of 51Cr-labeled thoracic duct lymphocytes (TDLs) via major

30 yed for development of NK activity by adding 51Cr-labeled YAC-1 cells to the wells and evaluating the

31 otaxin Abs, blocked the in vivo migration of 51Cr-labeled, skin-derived DCs from footpads to draining

32 Platelet survival, measured by 51Cr labeling, also declined following infection in both

33 e estimated GFR from the plasma clearance of 51Cr-labelled edetic acid (EDTA), and did intravenous ur

34 25I double-labeled Escherichia coli, hepatic 51Cr levels can be used to reliably quantify hepatic pha

35 examined by labeling the injected cells with 51Cr or 5-chloromethylfluorescein diacetate.

36 beling neutrophils (111In) and erythrocytes (51Cr), reinfusing cells 4.5 hrs after burn, and measurin

37 , 5 min after maternal injection of 45Ca and 51Cr, relative accumulation of 45Ca was significantly in

38 ll destruction was assessed in vitro both by 51Cr release and DNA fragmentation using wild-type and l

39 ing of P. carinii was demonstrated by both a 51Cr release assay and a [35S]methionine pulse immunopre

40 rosis in K562 target cells (as determined by 51Cr release assay and confirmed by transmission electro

41 assay was adopted to replace the traditional 51Cr release assay for detection of Brucella-specific cy

42 -gamma enzyme-linked ImmunoSPOT and in vitro 51Cr release assay results showed that HLA-A2-restricted

43 d CTL activity at E:T ratios of > or = 30:1 (51Cr release assay), but were significantly more resista

44 Using a short-term 51Cr release assay, human peripheral blood mononuclear c

45 By the use of a standard 51Cr release assay, these cells were found to have pepti

46 with HLA-G-transfected PAECs as targets in a 51Cr release assay.

47 m the immunized mice to kill P815 cells in a 51Cr release assay.

48 ted or uninfected radiolabeled EC targets by 51Cr release assay.

49 lls were tested for in vitro cytotoxicity by 51Cr release assay.

50 ity to lyse virus-infected target cells in a 51Cr release assay.

51 ermeabilize mouse L cells as determined by a 51Cr release assay.

52 city against BN and F344 lymphoid cells in a 51Cr release assay.

53 plement mediated cell lysis was evaluated by 51Cr release assays after incubation of islets for 4 hr

54 Both 51Cr release assays and IFN-gamma enzyme-linked immunosp

55 As assessed using both 51Cr release assays and tetramer staining of in vitro st

56 w but significant cytolytic activity in bulk 51Cr release assays in nonstimulated LCMV-specific splen

57 We performed reverse 51Cr release assays in which the lymphocyte effectors ra

58 tigen-specific cytotoxicity was tested using 51Cr release assays of A/J or third-party targets.

59 In hemolysis and 51Cr release assays, Ehx demonstrated similar efficienci

60 etermined by [3H]thymidine incorporation and 51Cr release assays, respectively.

61 tolytic activities were detected by in vitro 51Cr release assays.

62 specific MAbs (MAb-10H2 and MAb-8H6) inhibit 51Cr release by interfering with an undefined post-L-cel

63 MAb-G5 inhibits 51Cr release by interfering with ISVP attachment (via si

64 with peripheral blood mononuclear cells, and 51Cr release cytotoxicity assay of rNcSRS2-stimulated ef

65 By measuring 51Cr release from cultured endothelial cell monolayers,

66 Measurement of 51Cr release from labeled fresh islets after four hours

67 JCV-specific CTL were detected by either 51Cr release or tetramer staining assay.

68 JH4) exhibited a decreased capacity to cause 51Cr release relative to that of wild-type T3A.

69 10H2 and MAb-8H6) inhibited reovirus-induced 51Cr release when added pre- or post-ISVP attachment to

70 st oxidant-induced cytotoxicity (measured by 51Cr release) and F-actin depolymerization.

71 S Susceptibility to lysis was assayed by 51CR release, and the expression of cPLA2 was assayed by

72 in 1-h [3H]thymidine release, but not in 4-h 51Cr release, assays.

73 thanol sensitivity and the capacity to cause 51Cr release.

74 lize cell membranes as measured by chromium (51Cr) release.

75 H13a-specific tetramers and by chromium-51 (51Cr)-release assay, respectively.

76 mative and safer alternative to the standard 51Cr-release assay most often used to quantify CTL respo

77 rfered with NK lysis of tumor cells in a 5-h 51Cr-release assay, but had no ability to block NK cell

78 ctivity against Pam 212 cells in an in vitro 51Cr-release assay, which was blocked by CTLA-4/Ig fusio

79 by RT-PCR and for target cell specificity by 51Cr-release assay.

80 mbinant protein was determined by a modified 51Cr-release assay.

81 f graft-infiltrating cells was determined by 51Cr-release assay.

82 resistant to TALL-104 cell lysis in longterm 51Cr-release assays but can be totally growth inhibited

83 In short-term 51Cr-release assays, these CTL lysed H-2Kb targets that

84 4 or control tumors did not lyse 9L cells in 51Cr-release cytotoxicity assays, specific cytotoxicity

85 or diluent 1 h before administering 45Ca and 51Cr to the dam.

86 jected dose of b-IgG/SA/b23-RBC labeled with 51Cr was detected in the rat blood cells 1 day after iv