ライフサイエンスコーパス: parasite load

1 three traits (host fecundity, host size and parasite load).

2 ihydroartemisinin, substantially reduced the parasite load.

3 ndii in association with an increased tissue parasite load.

4 adoptive transfer of immune B cells reduced parasite load.

5 not on ART or presenting with a high tissue parasite load.

6 ction in vivo led to an increase in cellular parasite load.

7 ise from ecologically driven fluctuations in parasite load.

8 despite high and similar IFNG expression and parasite load.

9 esional pO2 and a concurrent increase of the parasite load.

10 As a result, these phagocytes had decreased parasite load.

11 this correlated with a 100-fold reduction in parasite load.

12 an early stage of infection revealed a high parasite load.

13 ti-CD40 monoclonal antibody markedly reduced parasite load.

14 asion of host cells and consequently reduced parasite load.

15 e having no effect on parasitemia or cardiac parasite load.

16 cted and had a 1000-fold reduction in dermal parasite loads.

17 ng the swimming speed of cells with moderate parasite loads.

18 and density of hosts, as well as within-host parasite loads.

19 associated with a 10-fold increase in early parasite loads.

20 responses, ameliorated lesions, and reduced parasite load (10(5)-fold).

21 ysis than untreated controls and reduced the parasite load 3-fold when inoculated into BALB/c mice.

22 ltaneously, exhibited transient increases in parasite loads, although ultimately they controlled the

23 1-skewed cytokine production to control the parasite load and alter the course of cutaneous leishman

24 of this monocyte subset resulted in elevated parasite load and decreased survival of infected mice, s

25 trypanocidal drug, is effective at reducing parasite load and decreasing the severity of myocarditis

26 nse that is protective to the host, limiting parasite load and dissemination.

27 ed for parasite infection (n = 154), average parasite load and its interaction with pesticide applica

28 tment before infection with L. major reduces parasite load and promotes healing of cutaneous lesions

29 inoculation, an inverse relationship between parasite load and serum immobilizing activity was seen.

30 ment of L. major-infected mice decreased the parasite load and significantly decreased the lesion siz

31 size, body condition, number of bite marks, parasite load and the microhabitat use and diet, of male

32 For example, parasite loads and antibody titres may vary over the cou

33 st, healed animals had significantly reduced parasite loads and higher CD4(+)IFN-gamma(+)/IL-17(+) ra

34 st clinical score values also exhibited high parasite loads and higher concentrations of anti-saliva

35 Organ parasite loads and parasite pick-up by flies were assess

36 Infants with clinical signs had higher parasite loads and were significantly more likely to be

37 regs resulted in enlarged lesions, increased parasite load, and enhanced production of IL-17 and IFN-

38 isms, we evaluated intraocular inflammation, parasite load, and immunological responses using messeng

39 sites, undergoes a treatment to decrease the parasite load, and its natural and parasite-induced mort

40 In all cases, blood parasitemia, tissue parasite load, and survival rates are similar between wi

41 sembled BALB/c mice in terms of lesion size, parasite load, and the production of Th2 cytokines.

42 hly virulent pathogens, which produce larger parasite loads, are more efficiently transmitted horizon

43 e showed defects in Th1 responses and higher parasite loads as compared to WT mice.

44 DC and T-cell activation and reduced tissue parasite loads at 1 and 3 weeks postinfection.

45 challenge leads to chronic lesions with high parasite loads at 10 weeks postinfection.

46 d multifaceted immune response that controls parasite load but is unable to completely clear infectio

47 0 to neonatal mice significantly reduced the parasite load by a mechanism that was independent of imm

48 oups had a 100-fold reduction in peak dermal parasite loads compared with controls.

49 Despite equivalent parasite loads compared with wild-type (WT) mice, mice d

50 However, only parasite load connected resources to epidemic size.

51 The enhanced parasite load correlated with decreased NO production by

52 5) or autophagy protein 9A (ATG9A) decreased parasite loads, demonstrating that autophagy is essentia

53 levels of IL-17A, IL-17F, and IL-6 were less parasite load dependent.

54 Thus, the persistence of a high parasite load despite antileishmanial therapy could be r

55 euteri and challenged with C. parvum cleared parasite loads from the gut epithelium.

56 ith uninfected organs and had geometric mean parasite loads (GMPL) comparable to intracardiac inocula

57 olyprotein-vaccinated animals had comparable parasite loads, greater numbers of neutrophils at the ch

58 berghei lines (Pbvit(-)) show a reduction in parasite load in both liver and blood stages of infectio

59 ed immunosorbent assay, was used to estimate parasite load in different organs.

60 f life between horn length, body weight, and parasite load in environments of different quality.

61 s CD154 resulted in a remarkable increase in parasite load in IFN-gamma-/- mice infected with Toxopla

62 ody displayed a 25% and 90% reduction in the parasite load in infected salivary glands 14 and 18 days

63 L-17A decreased intraocular inflammation and parasite load in mice.

64 ) mice exhibited reduced mortality and lower parasite load in muscle tissue.

65 r responses was also associated with reduced parasite load in the brain.

66 and transmission of a high percentage of the parasite load in the fly.

67 le immunization with sporozoites reduces the parasite load in the liver so greatly during subsequent

68 on decreased arginase activity induction and parasite load in vitro and in vivo.

69 red the presence of TNF receptor 2 to reduce parasite load in vivo.

70 crophages in vitro and in mice, although the parasite loads in both model systems were modestly reduc

71 nfected CD4(-/-) mice did not exhibit higher parasite loads in comparison to the parental wild-type m

72 Parasite loads in murine macrophages infected with each

73 Parasite loads in skin varied from 1428 to 63 058 parasi

74 Furthermore, increased parasite loads in the blood and/or tissue were observed

75 Although the parasite loads in the common bile duct and large intesti

76 leen and leads to a significant reduction in parasite loads in the liver and spleen.

77 clear seasonal pattern and tolerance of high parasite loads in these bats.

78 ar magnetic resonance of RBCs, to infer the 'parasite load' in blood.

79 use peritoneal exudate cells (PECs), and the parasite load increased significantly.

80 The parasite load initially rises in the liver and spontaneo

81 ed that a Wnt5a-Rac/Rho-mediated decrease in parasite load is associated with an increase in F- actin

82 Instead, the influence of a high parasite load is dependent on the presence of a type 2 c

83 t interactions for lamb male body weight and parasite load, leading to a change in the genetic correl

84 CD8(+) T cells expressing CD38, parasite load, lipopolysaccharide (LPS), soluble CD14, m

85 s indicates that the observed aggregation of parasite load may be dynamically generated by random var

86 be explained by an alteration in peritoneal parasite load, nor by increased apoptosis of infected in

87 The enormous discrepancy in parasite loads observed in livers and spleens from mice

88 expression, anti-Leishmania IgG levels, and parasite load occurred independently of the inoculum use

89 examine a nonlinear stochastic model for the parasite load of a single host over a predetermined time

90 st L. infantum infection, with reductions in parasite loads of 99.6%, a level of protection greater t

91 models that posit perfect correlation of the parasite loads of hosts in a square meter of habitat app

92 r than two models that posit independence of parasite loads of hosts in a square meter, regardless of

93 prior to cell transfer (and thus had a high parasite load) or at the time of cell transfer.

94 itiated during VL treatment, and high tissue parasite load (parasite grade 6+) at VL diagnosis.

95 infected for 3 weeks, suggesting that a high parasite load regulates the development of protective im

96 spleen, and sera were investigated to check parasite load, spleen visceralization, cytokine expressi

97 er that high local interhost correlations in parasite load strongly influence the spatial distributio

98 RP10-deficient mice and controls had similar parasite loads, suggesting that DOCK8 promotes local gro

99 tion, restore the immune response and reduce parasite load, supporting a deleterious role of IFN-gamm

100 s a tendency for foreign fish to have higher parasite loads than residents, after controlling for MHC

101 Women who transmitted had higher parasite loads than those who did not (median, 62.0 [int

102 R (65.5% vs 33.9%; P < .001), and had higher parasite loads than those who had lived in infested hous

103 -infected mice displayed an increase in skin parasite load upon secondary infection with Leishmania m

104 The parasite load V can also affect the rate of environmenta

105 term g(E) to account for the increase in the parasite load V within a host due to the continuous inge

106 of both CD8 KO and microMT mice in which the parasite load was even higher.

107 When pLDH could be detected, the parasite load was higher in patients with presumed cereb

108 Accordingly, the parasite load was reduced in mice lacking mannose recept

109 lenged with Leishmania: Both lesion size and parasite load were significantly reduced in the CpG-trea

110 40-/-, CD40 ligand-/-, and SCID) high dermal parasite loads were associated with little or no patholo

111 protection against dermal lesions and their parasite loads were no longer significantly reduced, whe

112 xicity in the host but still suppressing the parasite load when treated with 15.

113 knockout mice presented significantly lower parasite loads when compared with those from wild-type m

114 but develop chronic lesions with persistent parasite loads when they are infected with Leishmania am

115 We determined parasite loads with the use of quantitative PCR testing

116 proinflammatory cytokine milieu, and reduced parasite load within the myocardium during the acute pha

117 ugh there were 1- to 2-log reductions in the parasite loads within the lesions, the parasites continu