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1 ontribute to the activation of CASP11 during gram-negative bacterial infection.
2 PQ exposure causing increased sensitivity to Gram-negative bacterial infection.
3 eness to a broad range of TLR ligands and to gram-negative bacterial infection.
4 hyporesponsiveness to lipopolysaccharide and gram-negative bacterial infection.
5 tes to loss of anabolic enzyme expression in Gram-negative bacterial infection.
6 as master regulators of inflammasomes during Gram-negative bacterial infection.
7 R38 genotype correlated with human sinonasal gram-negative bacterial infection.
8  caused by an excessive TLR4 response during gram-negative bacterial infection.
9 empiric antimicrobial regimens for suspected Gram-negative bacterial infection.
10 f antimicrobial peptide gene induction after gram-negative bacterial infection.
11 pathway of the Imd innate immune response to Gram-negative bacterial infection.
12 member Traf2 is dispensable in resistance to gram-negative bacterial infection.
13 s required for the innate immune response to Gram-negative bacterial infection.
14 t mediates the potentially lethal effects of Gram-negative bacterial infection.
15 ed neutropenic rats from heterologous lethal gram-negative bacterial infection.
16 t component in the innate immune response to gram-negative bacterial infection.
17 ons for the treatment of multidrug-resistant Gram-negative bacterial infections.
18  All trials primarily enrolled patients with gram-negative bacterial infections.
19 ) is a key enzyme targeted by antibiotics in Gram-negative bacterial infections.
20  the treatment of severe multidrug-resistant Gram-negative bacterial infections.
21      Most infections (12 of 22 [54.5%]) were gram-negative bacterial infections.
22  a common source of antibiotic resistance in Gram-negative bacterial infections.
23 ome to produce inflammatory cytokines during gram-negative bacterial infections.
24 on as part of a coordinated host response to gram-negative bacterial infections.
25 ons for modulating innate immunity to combat Gram-negative bacterial infections.
26 f new treatment options for highly resistant gram-negative bacterial infections.
27 , consequently, caspase-11 activation during Gram-negative bacterial infections.
28 st, may be a potential therapeutic agent for gram-negative bacterial infections.
29 able new candidates for the treatment of MDR Gram-negative bacterial infections.
30 lar, enterococcal, mycobacterial, and severe Gram-negative bacterial infections.
31 y/mortality rates with carbapenem-resistant, Gram-negative bacterial infections.
32 tic for the treatment of multidrug-resistant Gram-negative bacterial infections.
33 G and T399I SNPs and the risk and outcome of gram-negative bacterial infections.
34  with or without microbiologically confirmed gram-negative bacterial infections.
35 nfirmed infections, and 463 patients without gram-negative bacterial infections.
36  the clinical characteristics and outcome of gram-negative bacterial infections.
37 AM7 might prove to be important in combating gram-negative bacterial infections.
38 % CI 1.08-4.38; P=0.03) were associated with gram-negative bacterial infections.
39 antly associated with 90-day mortality after gram-negative bacterial infections.
40 ignificantly associated with mortality after gram-negative bacterial infections.
41 ne covariates associated with outcomes after gram-negative bacterial infections.
42 t of this condition and perhaps more broadly Gram-negative bacterial infections.
43  the vascular leak syndromes associated with Gram-negative bacterial infections.
44 tential new antibiotics for the treatment of Gram-negative bacterial infections.
45 velopment of antibiotics in the treatment of Gram-negative bacterial infections.
46 tic for the treatment of multidrug resistant Gram-negative bacterial infections.
47 y inflammatory genes that are induced during gram-negative bacterial infections.
48 PS) is required for efficient recognition of Gram-negative bacterial infections.
49 tic shock and multiple organ failure seen in Gram-negative bacterial infections.
50 lial cell injury/dysfunction associated with Gram-negative bacterial infections.
51 mining the effects of redox imbalance during gram-negative bacterial infections.
52 novel therapies for the management of ocular Gram-negative bacterial infections.
53 portant role in the inflammatory response to Gram-negative bacterial infections.
54 ction and pathologic changes associated with gram-negative bacterial infections.
55 re were 108 with microbiologically confirmed gram-negative bacterial infections, 135 with clinically
56 ation of inadequate antibiotic treatment for Gram-negative bacterial infections (4.4%, 2.1%, and 1.6%
57 sues, lumican has a major protective role in gram-negative bacterial infections, a novel function for
58 lipopolysaccharide recognition may influence gram-negative bacterial infections after liver transplan
59                      Among 108 patients with gram-negative bacterial infections, alcoholic liver dise
60 thritis support the etiological link between Gram-negative bacterial infection and autoimmune disease
61 a mechanism for the etiological link between Gram-negative bacterial infection and autoimmunity.
62  in experimental models of polymicrobial and gram-negative bacterial infection and sepsis, warranting
63  antimicrobial resistance phenotypes, during Gram-negative bacterial infection and will advance our u
64  clinical benefit to neonates suffering from gram-negative bacterial infection and/or endotoxemia.
65 e inflammatory response toward extracellular Gram-negative bacterial infections and are vital for the
66 provides critical hints for host response to Gram-negative bacterial infections and development of di
67                                       Severe gram-negative bacterial infections and sepsis are major
68 ation and is central to host defense against Gram-negative bacterial infections and to the pathogenes
69 nthase (NOS) increased larval sensitivity to gram-negative bacterial infection, and abrogated inducti
70 I interferons, particularly in patients with gram-negative bacterial infections, and reflect on the m
71 olyclonal antibody production in response to Gram-negative bacterial infection are modulated by acylo
72                                              Gram-negative bacterial infections are a significant pub
73                          Multidrug resistant Gram-negative bacterial infections are an increasing pub
74                                              Gram-negative bacterial infections are the main cause of
75  was selected for the empirical treatment of Gram-negative bacterial infections as follows: time peri
76 ria by macrophages and host defenses against gram-negative bacterial infection, as shown by increased
77 s particularly effective in the treatment of Gram-negative bacterial infections associated with urina
78  N-hexanoyl-L-homoserine lactone (199 Da), a gram-negative bacterial infection biomarker.
79 on for the treatment of carbapenem-resistant Gram-negative bacterial infections, but polymyxin resist
80 tment of a wide range of multidrug resistant Gram-negative bacterial infections, by both intravenous
81 iotic classes for the empirical treatment of Gram-negative bacterial infections can reduce the occurr
82                          Multidrug-resistant Gram-negative bacterial infections cause significant mor
83 titis patients had a significant increase in gram negative bacterial infections compared with the con
84 e need for effective oral therapies to treat Gram-negative bacterial infections, efforts were directe
85                                       During Gram-negative bacterial infections, excessive LPS induce
86                             The treatment of gram-negative bacterial infections exhibiting resistance
87                Although the host response to gram-negative bacterial infection follows largely from t
88 endent on TLR4 for optimal expression during gram-negative bacterial infection has not been determine
89 nflammasome-based surveillance machinery for Gram-negative bacterial infections has been recently dis
90             The rise in multi-drug resistant Gram-negative bacterial infections has led to an increas
91 nce of drug resistance make the treatment of Gram-negative bacterial infections highly challenging.
92 are hypersensitive to both Gram-positive and Gram-negative bacterial infections; however, the mechani
93 (anorexia, anhedonia, cachexia) to simulated gram-negative bacterial infections (i.p. lipopolysacchar
94 n receptor for detection and defense against Gram-negative bacterial infection in M. sexta.
95 ndromes associated with antibiotic resistant gram-negative bacterial infection in patients with malig
96 promising efforts to combat life-threatening Gram-negative bacterial infections in hospitals worldwid
97 effective in treating both Gram-positive and Gram-negative bacterial infections in mice, attesting to
98 tion of AR could be a therapeutic target for Gram-negative bacterial infection-induced visual complic
99                                              Gram-negative bacterial infection is a common cause of s
100                         The host response to Gram-negative bacterial infection is influenced by two h
101 l recognized that the immune response during Gram-negative bacterial infection is initiated after the
102 ary neutrophil-mediated host defense against Gram-negative bacterial infection is not understood.
103  the morbidity and mortality associated with gram-negative bacterial infection is the result of patho
104 y component of the innate immune response to gram-negative bacterial infections is inflammasome activ
105 herapeutically to prevent the development of gram-negative bacterial infection of the respiratory tra
106 at porins play a role in bone destruction in gram-negative bacterial infections of bone.
107  III protein secretion is essential for many gram-negative bacterial infections of host cells and an
108                                              Gram-negative bacterial infections of the eye can lead t
109  used for the empiric treatment of suspected gram-negative bacterial infections, on the incidence of
110 pirical treatment of suspected or documented Gram-negative bacterial infections, on the occurrence of
111  stepwise regression analysis, we found that gram-negative bacterial infection played a crucial role
112                     In neutropenic patients, gram-negative bacterial infections predominate early, wh
113 lones significantly reduced the incidence of gram-negative bacterial infections (relative risk, 0.21;
114 unction of Mkp-1 in host defense during live Gram-negative bacterial infection remains unclear.
115  as an important virulence factor in several gram-negative bacterial infections such as Escherichia c
116                                       During Gram-negative bacterial infection, the Toll-like recepto
117                                    Following Gram-negative bacterial infection there is a reduction i
118        In Drosophila the Imd pathway detects Gram-negative bacterial infections through recognition o
119  trial of patients with carbapenem-resistant gram-negative bacterial infections treated with colistin
120 dime) for the empiric treatment of suspected gram-negative bacterial infections was continued.
121 cidating the role of pyroptosis in resisting gram-negative bacterial infections, with a particular fo

 
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