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1 t antimicrobial strategies, leading to fatal staphylococcal infection.
2 bers of neutrophils, the key defense against staphylococcal infection.
3  and IL-22 protects against severe pulmonary staphylococcal infection.
4 andidiasis predisposes the host to secondary staphylococcal infection.
5 ORAI1/2-deficient mice highly susceptible to staphylococcal infection.
6 nt complication of non-Staphylococcus aureus staphylococcal infection.
7 n and thus contribute to the pathogenesis of staphylococcal infection.
8 sal carriage is a documented risk factor for staphylococcal infection.
9 mans, which in turn may diminish the risk of staphylococcal infection.
10  infection to reduce bacterial burden during staphylococcal infection.
11 nd of increasing risk for coagulase-negative staphylococcal infection.
12 as been associated with an increased risk of staphylococcal infection.
13 ad spectrum of superantigens released during Staphylococcal infection.
14 e revealed a critical role for MntABC during staphylococcal infection.
15  multiplex PCR protocol for the diagnosis of staphylococcal infection.
16 l subset 2 and is frequently associated with staphylococcal infection.
17 major source of inflammatory cytokines after staphylococcal infection.
18 ungoides, were studied for the occurrence of staphylococcal infection.
19 evelop better strategies to tackle foodborne staphylococcal infections.
20 that improve our understanding of persistent staphylococcal infections.
21 n important contributing factor to recurrent staphylococcal infections.
22  implications for the effective treatment of staphylococcal infections.
23 nly 1 initiated CAS; 67% (8/12) of these had staphylococcal infections.
24 a rise in enterococci and coagulase-negative staphylococcal infections.
25 gnificant clinical implications for relapsed staphylococcal infections.
26 nd develop therapeutic approaches to control staphylococcal infections.
27  for attenuating current multidrug resistant staphylococcal infections.
28  potential treatment for multidrug-resistant staphylococcal infections.
29 he development of novel targets for treating staphylococcal infections.
30 ctams with approved clinical indications for staphylococcal infections.
31 ng into question the role of Agr in invasive staphylococcal infections.
32 rtality, and economic impact associated with staphylococcal infections.
33 omplement resistance and the pathogenesis of staphylococcal infections.
34 e agents for the management and treatment of staphylococcal infections.
35 al resistance highlights their importance in staphylococcal infections.
36 n important role in cardiovascular and other staphylococcal infections.
37 hway holds potential for managing persistent staphylococcal infections.
38  assay should improve clinical management of staphylococcal infections.
39 amamelitannin may be used as a suppressor to staphylococcal infections.
40 at interferons play a protective role during staphylococcal infections.
41  activation and the protection of hosts from staphylococcal infections.
42 ibutions of prophages to the pathogenesis of staphylococcal infections.
43 herapeutic agents for preventing or treating staphylococcal infections.
44 sues and for the establishment of persistent staphylococcal infections.
45 itor can eliminate medical device-associated staphylococcal infections.
46 s an important aspect of the pathogenesis of staphylococcal infections.
47 e responsible for approximately 70% of human staphylococcal infections.
48 cts with the TLR2 Arg753Gln polymorphism had staphylococcal infections.
49 n the only uniformly effective treatment for staphylococcal infections.
50 intracellular survival in the persistence of staphylococcal infections.
51 hylococcus aureus plays an important role in staphylococcal infections.
52  simplex infections, neonatal varicella, and staphylococcal infections.
53 urther consideration as a potential drug for staphylococcal infections.
54 o, and potential role in the pathogenesis of staphylococcal infections.
55 is an integral part of the innate defense to staphylococcal infection and comprises a well-coordinate
56 d laboratory evidence support roles for both staphylococcal infection and environmental allergens in
57           Abscess formation is not unique to staphylococcal infection and purulent discharge has been
58 mial bacterial sepsis and coagulase negative staphylococcal infections, and thus should not be used i
59                                              Staphylococcal infections are a major source of global m
60 fforts to harness these viruses to eradicate staphylococcal infections are also highlighted.
61                                              Staphylococcal infections are ideally treated with biofi
62 means that new vaccine strategies to prevent staphylococcal infections are needed.
63                                In bloodborne staphylococcal infections, bacteria and platelets often
64 ocytes (PMN) are the first responders during staphylococcal infection, but 15-50% of the initial inge
65 lls modulate the development of experimental staphylococcal infections by controlling polymorphonucle
66 ese findings show a novel mechanism by which staphylococcal infections can inhibit Th1 reactions and
67 tion and were more resistant to administered staphylococcal infections compared with MN(-) mice.
68 intact complement pathway in an experimental staphylococcal infection, control and C3-depleted mice w
69 y, abscesses can persist or even reoccur, as staphylococcal infections fail to induce protective immu
70 s from patients with invasive or superficial staphylococcal infections for use in the Tigecycline Eva
71      Differentiating true coagulase-negative staphylococcal infection from contamination has an impor
72     We confirmed the importance of EPHA2 for staphylococcal infection in an EPHA2-knock-out cell line
73 ribe here a novel, spontaneous model of oral staphylococcal infection in double knockout mice, defici
74 thicillin-resistant S. aureus, many cases of staphylococcal infection in the ICU are now classified a
75 minase activity and heightened resistance to Staphylococcal infection in TOC keratinocytes.
76 inhibition by S. aureus in vitro and promote staphylococcal infection in vivo.
77 mpted a change in the approach to therapy of staphylococcal infections in both the outpatient clinic
78 ing truncated AIPs as a means of attenuating staphylococcal infections in species beyond Staphylococc
79  in a large proportion of coagulase-negative staphylococcal infections in very-low-birth-weight infan
80 ort an outbreak of botryomycosis, an unusual staphylococcal infection, in a colony of uPA-deficient m
81 El-K is commonly expressed in the setting of staphylococcal infection, in significant amounts.
82                  We propose that handling of staphylococcal infection is a critical step in the ampli
83                          The pathogenesis of staphylococcal infections is multifactorial.
84 such a devastating impact on chemotherapy of staphylococcal infections--is related to the properties
85 (1) the effect of PVL on the pathogenesis of staphylococcal infection may depend on the level of toxi
86 omparative studies exist in the treatment of staphylococcal infections may also offer effective and l
87 whether host factors released in response to staphylococcal infections may increase cell resistance t
88                                              Staphylococcal infections not only remain an important c
89                        At follow-up, cure of staphylococcal infection occurred in a similar percentag
90                                              Staphylococcal infection of bone marrow-derived osteocla
91                   We focused specifically on staphylococcal infection of bone, one of the most common
92 L does not contribute to the pathogenesis of staphylococcal infection of mice.
93                                   Persistent staphylococcal infections often involve surface-associat
94                                    Mice with staphylococcal infection presented with larger thrombi c
95                            Streptococcal and staphylococcal infections result in significant human mo
96  diabetic db/db mice are more susceptible to staphylococcal infection than their nondiabetic litterma
97 unities are often associated with persistent staphylococcal infections that place a tremendous burden
98                          In a mouse model of staphylococcal infection, the parental strain was able t
99  groups, the mortality rate in patients with staphylococcal infections was significantly higher among
100 Thus, using in vitro models of intracellular staphylococcal infection, we demonstrate that EsxA inter
101 c target of the humoral immune system during staphylococcal infections, we developed a synthetic meth
102  in a pediatric hospital with a high rate of staphylococcal infections were examined for any increase
103                         The worse outcome of staphylococcal infections with a higher vancomycin MIC c
104 icrobial agents and support the clearance of staphylococcal infections with minimal selection pressur
105 lucidate the metabolic pathways required for staphylococcal infection within bone and demonstrate tha

 
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