ライフサイエンスコーパス: Gram-negative bacterial infection

1 hyporesponsiveness to lipopolysaccharide and gram-negative bacterial infection.

2 tes to loss of anabolic enzyme expression in Gram-negative bacterial infection.

3 as master regulators of inflammasomes during Gram-negative bacterial infection.

4 R38 genotype correlated with human sinonasal gram-negative bacterial infection.

5 caused by an excessive TLR4 response during gram-negative bacterial infection.

6 empiric antimicrobial regimens for suspected Gram-negative bacterial infection.

7 f antimicrobial peptide gene induction after gram-negative bacterial infection.

8 pathway of the Imd innate immune response to Gram-negative bacterial infection.

9 member Traf2 is dispensable in resistance to gram-negative bacterial infection.

10 s required for the innate immune response to Gram-negative bacterial infection.

11 t mediates the potentially lethal effects of Gram-negative bacterial infection.

12 ed neutropenic rats from heterologous lethal gram-negative bacterial infection.

13 t component in the innate immune response to gram-negative bacterial infection.

14 eness to a broad range of TLR ligands and to gram-negative bacterial infection.

15 st, may be a potential therapeutic agent for gram-negative bacterial infections.

16 able new candidates for the treatment of MDR Gram-negative bacterial infections.

17 lar, enterococcal, mycobacterial, and severe Gram-negative bacterial infections.

18 tic for the treatment of multidrug-resistant Gram-negative bacterial infections.

19 f new treatment options for highly resistant gram-negative bacterial infections.

20 G and T399I SNPs and the risk and outcome of gram-negative bacterial infections.

21 with or without microbiologically confirmed gram-negative bacterial infections.

22 nfirmed infections, and 463 patients without gram-negative bacterial infections.

23 , consequently, caspase-11 activation during Gram-negative bacterial infections.

24 the clinical characteristics and outcome of gram-negative bacterial infections.

25 AM7 might prove to be important in combating gram-negative bacterial infections.

26 % CI 1.08-4.38; P=0.03) were associated with gram-negative bacterial infections.

27 antly associated with 90-day mortality after gram-negative bacterial infections.

28 ignificantly associated with mortality after gram-negative bacterial infections.

29 ne covariates associated with outcomes after gram-negative bacterial infections.

30 t of this condition and perhaps more broadly Gram-negative bacterial infections.

31 the vascular leak syndromes associated with Gram-negative bacterial infections.

32 tential new antibiotics for the treatment of Gram-negative bacterial infections.

33 velopment of antibiotics in the treatment of Gram-negative bacterial infections.

34 y inflammatory genes that are induced during gram-negative bacterial infections.

35 PS) is required for efficient recognition of Gram-negative bacterial infections.

36 tic shock and multiple organ failure seen in Gram-negative bacterial infections.

37 lial cell injury/dysfunction associated with Gram-negative bacterial infections.

38 mining the effects of redox imbalance during gram-negative bacterial infections.

39 novel therapies for the management of ocular Gram-negative bacterial infections.

40 portant role in the inflammatory response to Gram-negative bacterial infections.

41 ction and pathologic changes associated with gram-negative bacterial infections.

42 re were 108 with microbiologically confirmed gram-negative bacterial infections, 135 with clinically

43 ation of inadequate antibiotic treatment for Gram-negative bacterial infections (4.4%, 2.1%, and 1.6%

44 sues, lumican has a major protective role in gram-negative bacterial infections, a novel function for

45 lipopolysaccharide recognition may influence gram-negative bacterial infections after liver transplan

46 Among 108 patients with gram-negative bacterial infections, alcoholic liver dise

47 thritis support the etiological link between Gram-negative bacterial infection and autoimmune disease

48 a mechanism for the etiological link between Gram-negative bacterial infection and autoimmunity.

49 in experimental models of polymicrobial and gram-negative bacterial infection and sepsis, warranting

50 clinical benefit to neonates suffering from gram-negative bacterial infection and/or endotoxemia.

51 e inflammatory response toward extracellular Gram-negative bacterial infections and are vital for the

52 Severe gram-negative bacterial infections and sepsis are major

53 ation and is central to host defense against Gram-negative bacterial infections and to the pathogenes

54 nthase (NOS) increased larval sensitivity to gram-negative bacterial infection, and abrogated inducti

55 I interferons, particularly in patients with gram-negative bacterial infections, and reflect on the m

56 olyclonal antibody production in response to Gram-negative bacterial infection are modulated by acylo

57 Gram-negative bacterial infections are the main cause of

58 was selected for the empirical treatment of Gram-negative bacterial infections as follows: time peri

59 ria by macrophages and host defenses against gram-negative bacterial infection, as shown by increased

60 iotic classes for the empirical treatment of Gram-negative bacterial infections can reduce the occurr

61 titis patients had a significant increase in gram negative bacterial infections compared with the con

62 During Gram-negative bacterial infections, excessive LPS induce

63 Although the host response to gram-negative bacterial infection follows largely from t

64 endent on TLR4 for optimal expression during gram-negative bacterial infection has not been determine

65 nflammasome-based surveillance machinery for Gram-negative bacterial infections has been recently dis

66 are hypersensitive to both Gram-positive and Gram-negative bacterial infections; however, the mechani

67 (anorexia, anhedonia, cachexia) to simulated gram-negative bacterial infections (i.p. lipopolysacchar

68 n receptor for detection and defense against Gram-negative bacterial infection in M. sexta.

69 ndromes associated with antibiotic resistant gram-negative bacterial infection in patients with malig

70 promising efforts to combat life-threatening Gram-negative bacterial infections in hospitals worldwid

71 tion of AR could be a therapeutic target for Gram-negative bacterial infection-induced visual complic

72 Gram-negative bacterial infection is a common cause of s

73 The host response to Gram-negative bacterial infection is influenced by two h

74 l recognized that the immune response during Gram-negative bacterial infection is initiated after the

75 ary neutrophil-mediated host defense against Gram-negative bacterial infection is not understood.

76 the morbidity and mortality associated with gram-negative bacterial infection is the result of patho

77 herapeutically to prevent the development of gram-negative bacterial infection of the respiratory tra

78 at porins play a role in bone destruction in gram-negative bacterial infections of bone.

79 III protein secretion is essential for many gram-negative bacterial infections of host cells and an

80 Gram-negative bacterial infections of the eye can lead t

81 used for the empiric treatment of suspected gram-negative bacterial infections, on the incidence of

82 pirical treatment of suspected or documented Gram-negative bacterial infections, on the occurrence of

83 stepwise regression analysis, we found that gram-negative bacterial infection played a crucial role

84 In neutropenic patients, gram-negative bacterial infections predominate early, wh

85 lones significantly reduced the incidence of gram-negative bacterial infections (relative risk, 0.21;

86 unction of Mkp-1 in host defense during live Gram-negative bacterial infection remains unclear.

87 as an important virulence factor in several gram-negative bacterial infections such as Escherichia c

88 During Gram-negative bacterial infection, the Toll-like recepto

89 Following Gram-negative bacterial infection there is a reduction i

90 In Drosophila the Imd pathway detects Gram-negative bacterial infections through recognition o

91 dime) for the empiric treatment of suspected gram-negative bacterial infections was continued.