ライフサイエンスコーパス: burst size

1 (+) T cell cultures to be determined (clonal burst size).

2 frequencies increases burst fraction but not burst size.

3 the right half of cosN, does not affect the burst size.

4 ) and accompanied by a fourfold reduction in burst size.

5 ically reduce noise in mRNA copy numbers and burst size.

6 hnique for measuring protein copy number and burst size.

7 ations as the transcription rate and protein burst size.

8 per genome) and (ii) an 80% drop in average burst size.

9 T cell TCR binding, signal transduction, and burst size.

10 deoffs between phage latent period and phage burst size.

11 e linear relationship between lysis time and burst size.

12 whose virion production rate maximizes viral burst size.

13 tion rates lower than the one that maximizes burst size.

14 l gene expression, cytopathic effects and/or burst size.

15 beta-globin gene with modest stimulation of burst size.

16 phages, which are cosN+, also had wild-type burst sizes.

17 stimuli caused a rapid and acute increase in burst sizes.

18 t extents and hence produce different photon-burst sizes.

19 marked change in the distribution of photon-burst sizes.

20 ractal properties, with power-law scaling of burst sizes across a remarkable 5 orders of magnitude an

21 ation confocal spectroscopy and fluorescence burst size analysis are used to individually count and s

22 The concentration dependence, fluorescence burst size analysis, and fluorescence correlation analys

23 CCK reduced burst size and cluster size, whereas bombesin reduced bu

24 blocking plaque formation, sharply reducing burst size and enhancing the survival of host cells foll

25 The expected phage burst size and fitness curve were predicted from these m

26 or necrosis factor alpha (TNF) only modulate burst size and frequency along a constrained trend line

27 amics of primary B-cells, but modulates both burst size and frequency in response to gamma-interferon

28 wo key parameters of protein expression--the burst size and frequency--can be either determined direc

29 y meaningful properties, such as the average burst size and frequency.

30 Ag-specific CD8 T cells negatively regulated burst size and TCR avidity in vivo.

31 ey variables that heavily influence effector burst size and the persistent memory pool size: the cell

32 nitude and a scale-free relationship between burst sizes and durations.

33 tions, allowing us to estimate transcription burst sizes and extrinsic noise strength and calculate t

34 idual phage growth parameters-latent period, burst size, and adsorption rate.

35 per-plaque burst number versus per-infection burst size, and based on analysis of existing models of

36 infectivity, much greater stability, higher burst size, and decreased induction of cellular interfer

37 For each phage strain, the lysis time, burst size, and fitness (growth rate) were determined.

38 BCs, RBC age preference, RBC infection rate, burst size, and within-RBC interference.

39 The lysis times, burst sizes, and relative fitness were empirically deter

40 "slow" or if burst sizes are large, (ii) if burst sizes are already large, or (iii) if virion bindin

41 The histograms of the burst sizes are generated in <3 min with <1 pg of DNA.

42 ly, (i) if virion adsorption is "slow" or if burst sizes are large, (ii) if burst sizes are already l

43 but only if adsorption is otherwise slow or burst sizes are large.

44 bacterial densities are especially high, or burst sizes are large.

45 on" and "off" transitions, together with the burst sizes, are modulated in single cells to increase g

46 This suggested burst size as a neural code for stimuli optimality (and

47 lysis-timing mutants, should increase phage burst sizes, as more time is available for phage-progeny

48 with a mathematical model, the in vivo viral burst size averaged 4.0 x 10(4) and 5.5 x 10(4) virions

49 Burst size [B = alpha(mu - nu)], the number of phages re

50 cts of food deprivation and concentration on burst size (BS), burst number (BN), and other parameters

51 ritable variations in gene function--such as burst size, burst frequency, cell cycle-specific express

52 n be modulated by altering burst fraction or burst size, but how regulatory elements control bursting

53 s demonstrated that hok/sok decreased the T4 burst size by 40%, increased the time to form mature pha

54 Second, if increases in burst size can contribute to plaque size (i.e. larger pl

55 cle that are not captured in an SCA, such as burst size, cell-to-cell transmission, or infected-cell

56 o glucose (increased total intake, increased burst size, decreased number of pauses), relative to fru

57 ptional activators alter burst frequency and burst size, depending on the expression level of the loc

58 Reduction in burst size depends on efficient expression of the EGS co

59 As expected, burst size did not vary with stimulus orientation in the

60 High-quality burst size distribution histograms were obtained for DNA

61 Burst-size distributions are, in addition, shaped by mRN

62 plex multiprotein regulation can have peaked burst-size distributions in contrast to the geometric di

63 the recBCD(+) host cell cytoplasm and a low burst size due, at least in part, to a decreased ability

64 l pool is a direct consequence of the clonal burst size during the primary response may no longer be

65 ith one-step growth curves revealing reduced burst sizes for the generalist phages.

66 tic life cycle, including a relatively large burst-size, has evolved to promote survival in the face

67 Photon-burst size histograms were constructed, from which the s

68 Due to influenza's higher burst size, however, the overall cost of a T4 phage infe

69 ng lifetimes, high infection rates and large burst sizes; (ii) large, stable, and high-density popula

70 confirmed by a significantly enhanced virus burst size in cells in which silencing was knocked down

71 These include an increased burst size in multiply infected cells, the saturation of

72 Concomitantly, the average clonal burst sizes in EC-stimulated CTL cultures were significa

73 , had broader host range and produced larger burst sizes in WT compared with P1.

74 T4 rnh null mutations reduce burst sizes, increase sensitivity to DNA damage, and inc

75 The burst size indicates that the dimeric enzyme has a singl

76 sponse to EBV and find that a larger primary burst size is associated with proportionally greater dec

77 will expand its host range if its effective burst size is positive.

78 plaques at normal efficiency even though the burst size is reduced to about half that obtained on the

79 T cell burst size is regulated by the duration of TCR engagemen

80 s in vivo as judged by plaque morphology and burst size measurements.

81 y infected CD4(+) T lymphocytes or the viral burst size must be proportionally higher than previous m

82 Under typical clinical circumstances, burst sizes needed to be 3 to 5 mm in order to be reliab

83 latent phase of approximately 60 min, and a burst size of 20 to 30 particles per cell at 28 degrees

84 (26 h) suggested an 11 h latent period and a burst size of 871 by plaque assay, whereas phageFISH ide

85 The clonal burst size of CD4 T cells is predicted to be less than t

86 absence of efficient antibodies, the optimal burst size of lytic viruses would be only a few virus pa

87 ither kind of EGS construct is used in vivo, burst size of phage lambda is reduced by > or = 40%.

88 is NCK203 to lyse 15 min early, reducing the burst size of phi31 100-fold.

89 ty of the response controlled in part by the burst size of T cells expanded from effector/memory prec

90 hibitor of host RNA polymerase, restores the burst size of T7 phage on udk-overexpressing hosts to no

91 cyclophosphamide treatment and how increased burst size of the mutated virus will affect the growth o

92 decrease from 4 mm to eventually 1 mm if the burst size of the virus is triple that which is currentl

93 The initial burst size of these mutations was similar to that of the

94 lated globin genes are cotranscribed in cis, burst sizes of both genes are comparable.

95 of CD8(+) T cells, BLC-stimulated very large burst sizes of CTL were observed from both naive and mem

96 e body, we estimate an average in vivo viral burst size on the order of 104 virions per cell.

97 of consecutive MSNA bursts; while individual burst size only had a mild influence.

98 th (i) latent period reductions, (ii) larger burst sizes, or (iii) faster virion binding to bacteria.

99 to the early antigen load and initial clonal burst size, persist in the host as a stable pool of memo

100 rulence as measured by in vitro growth rate, burst size, plaque morphology, and interferon-gamma sens

101 ven though they have qualitatively different burst-size statistics and regulatory parameters.

102 We introduce a new concept of effective burst size that accounts for the fact that successful ho

103 nheritable changes in plating efficiency and burst size that depended on which host strain it most re

104 infectious virus with delayed kinetics and a burst size that was significantly decreased for the ICP0

105 Whereas the Sp1BS element regulates burst size, the Inr element regulates burst frequency.

106 include the optimization of effector T cell burst sizes, the use of adjuvants, cytokines and co-stim

107 y, whereas stronger expression loci modulate burst size to increase activity.

108 achieving an order-of-magnitude increase in burst size using a mechanism called lysis inhibition (LI

109 s the human genome, both burst frequency and burst size vary by chromosomal location, and transcripti

110 eriod and the relative contribution of phage burst size versus latent period toward plaque size.

111 P(i) burst size was 0.31, indicating that the equilibrium of

112 oximately 100 supercoils per second (average burst size was 6.2 supercoils).

113 The P(i)-burst size was low (0.46 mol/mol), indicating that the e

114 A linear relation between DNA length and burst size was seen from 564 bp to 27.5 kbp.

115 of A3G (hypermutation and reduction of viral burst size) were necessary to replicate the experimental

116 h of replication cycle, virus half-life, and burst size, will also be important to the process optimi

117 ilibrium is postulated, to reconcile reduced burst sizes with full activity of the mutant enzymes.

118 ne LNCaP and a significant increase of virus burst size, with no reduction in specificity of CV706-ba

119 Quantitation of the "burst size" within naive cells further demonstrated that