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 signaling in mice increases lesion size and parasite load.

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

4 ti-CD40 monoclonal antibody markedly reduced parasite load.

5 asion of host cells and consequently reduced parasite load.

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

7 ndii in association with an increased tissue parasite load.

8 adoptive transfer of immune B cells reduced parasite load.

9 ei ANKA exhibited up to 70% reduction in the parasite load.

10 ) and occurred in parallel with reduction in parasite load.

11 flammatory cytokine production and increased parasite load.

12 us, attractiveness, body size, condition and parasite load.

13 ulted in enhanced CD8-dependent reduction of parasite load.

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

15 ihydroartemisinin, substantially reduced the parasite load.

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

17 ise from ecologically driven fluctuations in parasite load.

18 despite high and similar IFNG expression and parasite load.

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

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

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

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

23 risk for both species increased with higher parasite loads.

24 1 responses, reduced lesion sizes, and lower parasite loads.

25 of nonnative milkweeds that enhance monarch parasite loads.

26 s results in an ineffective ability to clear parasite loads.

27 ayed bigger lesions with significantly lower parasite loads.

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

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

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

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

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

33 circulating blood, and median total splenic parasite loads 81 (IQR: 14 to 205) times greater, accoun

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

35 tion therapy demonstrated a rapid decline in parasite load and achieved 100% cure, with no reports of

36 1-skewed cytokine production to control the parasite load and alter the course of cutaneous leishman

37 ectives included rate of lesion development, parasite load and analysis of local immune responses by

38 asive slit aspirate method for monitoring of parasite load and assessment of cure in PKDL.

39 parent in differential relationships between parasite load and body condition, potentially reflecting

40 ificantly decrease P. falciparum blood-stage parasite load and consistently exhibit dose-dependent in

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

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

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

44 nhibits EGFR signaling) exhibited diminished parasite load and histopathology in the brain and retina

45 ve effects on proxies of fitness, behaviour, parasite load and immune responses were either additive

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

47 a negative correlation was observed between parasite load and L. tropica specific IgG/ADCP/ADNP in t

48 tudies have established correlations between parasite load and negative effects on their hosts, estab

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

50 which resulted in a drastic reduction of the parasite load and restoration of iron homeostasis.

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

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

53 studies support a direct link between total parasite load and the clinical severity of Plasmodium fa

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

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

56 Higher parasite loads and colder temperatures were associated w

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

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

59 ed to endothelial cells exhibited diminished parasite loads and histopathology in the retina and brai

60 re observed in wet ulcers, lesions with high parasite loads and large wounds.

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

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

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

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

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

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

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

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

69 e the power associated with the use of blood parasite load as a surrogate endpoint to predict clinica

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

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

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

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

74 0 to neonatal mice significantly reduced the parasite load by a mechanism that was independent of imm

75 ation behaviour, oxidative stress status and parasite load by exposing yearling common lizards (Zooto

76 found that a 62-day PFAS exposure increased parasite loads by 42-100% in all treatments relative to

77 the two sites differed in mass by 60% and in parasite loads by nearly two orders of magnitude.

78 that the singular exposure to PFOS increased parasite loads by ~40% compared to a mixture containing

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

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

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

82 The enhanced parasite load correlated with decreased NO production by

83 ands occurred sequentially and in pairs, and parasite loads correlated highly with the number of SAPA

84 Blood parasite loads correlated well with tissue parasite load

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

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

87 ayers of different donors showed a time- and parasite load-dependent leak flux indicated by collapse

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

89 Blood Leishmania parasite load determined by qPCR is a promising early bi

90 Subsequent blood stage parasite loads dictated their cytokine profiles, where l

91 ble parasite levels, a continuing decline in parasite load during the second and third years of infec

92 pture important density-dependent effects of parasite load for parasites with high abundance, and in

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

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

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

96 with positive xenodiagnosis had median skin parasite loads >1 log10 unit higher than those with nega

97 ned clinical cure with a gradual decrease in parasite load; however, 25% relapsed within 18 months of

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

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

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

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

102 plication rate and host response to observed parasite load in individual subjects infected with Plasm

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

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

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

106 Parasite load in slit aspirate was monitored using qPCR.

107 Compound 1 reduced the parasite load in spleen (98.9%) and liver (95.3%) of inf

108 +) CD4(+) T cells concomitant with a reduced parasite load in spleen and liver compared to LdCen(-/-)

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

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

111 main functions: first, it auto-regulates the parasite load in the host; second, the stumpy stage is r

112 Parasite load in the liver and spleen of ela(-/-) mice w

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

114 Reduced parasite load in the retina and brain not only required

115 s shown by better control of lesion size and parasite load in Tlr2(-/-) compared with wild-type infec

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

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

118 We estimated P. falciparum parasite loads in 3 groups of children with malaria infe

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

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

121 outcomes could be established using specific parasite loads in different mouse genetic backgrounds.

122 ite-tailed deer (Odocoileus virginianus) and parasite loads in faecal samples within a hierarchical a

123 or extracellular tachyzoites led to reduced parasite loads in mice with DN EGFR.

124 Parasite loads in murine macrophages infected with each

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

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

127 respectively, impacted BBB permeability and parasite loads in the brain parenchyma.

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

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

130 These mice also had lower parasite loads in the retina and brain after intravenous

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

132 We estimated P. falciparum parasite loads in three groups of children with malaria

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

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

135 The parasite load initially rises in the liver and spontaneo

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

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

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

139 ding cerebral malaria (CM), driven by a high parasite load, leading to parasite sequestration in orga

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

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

142 In a multivariable model, parasite load, nodular lesions, and positive skin micros

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

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

145 ssive pathology, in terms of increased organ parasite load, observed in hosts infected with antimony-

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

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

148 trong experimental evidence of the impact of parasite load of vertebrate hosts on the survival probab

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

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

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

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

153 d parasite loads correlated well with tissue parasite loads (p = 0.80) and with microscopy gradings o

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

155 dictated their cytokine profiles, where low parasite loads preferentially expanded IL-17-producing g

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

157 tion, persistent malaria infections can have parasite loads significantly below the lower limit of de

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

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

160 not IFNAR-/- mice, accumulated higher acute parasite loads, suggesting a protective role of STING se

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

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

163 gs and survival of fledglings in relation to parasite loads, temperature and habitat disturbance asso

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

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

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

167 played significantly higher liver and spleen parasite loads than WT controls and showed impaired hepa

168 fection in some hosts, and the potential for parasite load to change dramatically when health conditi

169 ects on parasitism in individual hosts (e.g. parasite load) translate to effects on population-level

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

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

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

173 he injected dose, we found variation in peak parasite load was due to unobserved individual variation

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

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

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

177 The parasite load was statistically strongly correlated with

178 Blood parasite load was the strongest predictor for VL.

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

180 40-/-, CD40 ligand-/-, and SCID) high dermal parasite loads were associated with little or no patholo

181 ance with the attenuated IFN-gamma response, parasite loads were elevated during the acute phase (d10

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

183 significant differences in peripheral blood parasite loads were observed between lethally and nonlet

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

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

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

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

188 We observed that the increase in parasite load within the liver during the first few week

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

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