ライフサイエンスコーパス: multiple infection

1 arly half of the infected spiders exhibiting multiple infection.

2 h facilitates the treatment of patients with multiple infections.

3 ndosymbiotic bacteria and frequently exhibit multiple infections.

4 other and therefore represented evidence of multiple infections.

5 tion depending on the presence or absence of multiple infections.

6 fect cross-immunity has on the prevalence of multiple infections.

7 d, senescent states ("Hayflick limit") after multiple infections.

8 re enhanced among older women and women with multiple infections.

9 tion and thus appeared to result solely from multiple infections.

10 d beneficial fitness effects associated with multiple infections.

11 ls the multiplicity of subtypes results from multiple infections.

12 selection of more-resistant C. albicans over multiple infections.

13 with patients often displaying a history of multiple infections.

14 % [n=97]; isolated thoracotomy, 0.02% [n=5]; multiple infections, 0.6% [n=130]).

15 timing is discussed from the perspectives of multiple infection and life-history trait evolution.

16 widespread use as vaccine platforms against multiple infections and cancers, and multiple serotypes

17 withstand parasitic infections, the role of multiple infections and the trade-off in multiple defenc

18 Analyses of viral load need to address multiple infections and type attribution to evaluate whe

19 ger women with low-grade histology/cytology, multiple infections, and the highest viral load.

20 isolates from three continents, we find that multiple infections are common, especially in regions wi

21 , the mechanisms that lead to such extensive multiple infections are not understood.

22 gs) play an important role in the CNS during multiple infections, as well as autoimmune inflammation,

23 in a single-round infectivity assay and in a multiple-infection assay in H9 and CEMx174 cells.

24 at MHC heterozygote superiority emerges over multiple infections because MHC-mediated resistance is g

25 Multiple infection control improvements led to the reduc

26 s, a similar distribution was observed after multiple infection cycles, and among recombinant sequenc

27 yping directly from tissue sections resolved multiple infections detected in exfoliated cells to a si

28 The proportion of multiple infections detected increased with the PGMY09/1

29 and the ARLG Master Protocol for Evaluating Multiple Infection Diagnostics (MASTERMIND) initiative f

30 d MASTERMIND (Master Protocol for Evaluating Multiple Infection Diagnostics) for advancement of infec

31 We also find that multiple infections do not influence viral dynamics when

32 If multiple infections do occur, then only a single haploty

33 a mode of HIV transmission that can lead to multiple infection events per target cell.

34 vs. susceptibility to infection, we included multiple infection experiments including one with consta

35 s between the single-infection group and the multiple-infection group regarding the number of DNA sub

36 Also, patients who had multiple infections had lower CD4 counts than those with

37 PQS is required for virulence in multiple infection models and has been found in the lung

38 Multiple infections occurred significantly more frequent

39 f viruses, which increased the likelihood of multiple infection of a host cell and ultimately enabled

40 if one virus is transferred per synapse, and multiple infection of cells increases susceptibility.

41 virus population to anti-viral drugs through multiple infection of cells, contributing to low-level v

42 irus to overcome the antiviral state through multiple infection of cells.

43 assortment of influenza through simultaneous multiple infection of individual hosts and the generatio

44 rger numbers of transferred viruses, because multiple infection of the same cell wastes viruses that

45 Multiple infections of Agaricus may represent a diverse,

46 o study the immune response that occurs with multiple infections of C. trachomatis in the female uppe

47 The high incidence of multiple infections of cells by HIV sets the stage for r

48 The patient had a history of multiple infections of central vascular catheters with o

49 Multiple infections of different bacteria in a single ho

50 itional survival costs to aphids of carrying multiple infections of symbiont species or strains, and

51 d provide key insights into the influence of multiple infections on HIV dynamics.

52 ients were significantly more likely to have multiple infections over time than HIV- patients, highli

53 ought to investigate the effect of single or multiple infections (pathogen burden) on atopy and wheez

54 and experimentally validate the model using multiple infections per cell by cell-free HIV in the pre

55 We propose a model whereby multiple infections per cell lead to reduced sensitivity

56 was to identify the strains responsible for multiple infections, presumably through recent transmiss

57 common HPV types but were probably due to a multiple infection rather than to a cross-reaction.

58 Yet how HIV dynamics proceeds with multiple infections remains poorly understood.

59 the results of our study show that even when multiple infections seem to have no effect on a host, th

60 Escalation was associated with multiple infection sites (2.54, 1.34-4.83) and a positiv

61 ng hormone as a signal to differentiate into multiple infection structure and thus time the infection

62 may explain why extant models, which ignore multiple infections, successfully describe viral dynamic

63 at in vitro phenotypes should be examined in multiple infection systems to fully understand their rol

64 time PCR format that has been used to detect multiple infection targets.

65 Hence, multiple infection via synapses does not simply lower tr

66 In a murine model of multiple infections, we show that exposure of mice to re

67 f wheeze and atopic outcomes with single and multiple infections were analyzed by means of logistic r

68 Multiple infections were found to be more common than ex

69 While multiple infections were more common in young women and

70 Multiple genotypes (implying multiple infections) were detected in tissues from 8 of

71 Children with multiple infections with Cryptosporidium were more likel

72 Multiple infections with different strains of Mycobacter

73 Multiple infections with HPV genotypes of different risk

74 Multiple infections with the attenuated plasmid-deficien