ライフサイエンスコーパス: bacterial resistance

1 to ophthalmic practice to deal with changing bacterial resistance.

2 erea, indicating that NHO1 is not limited to bacterial resistance.

3 ter-strategy towards beta-lactamase-elicited bacterial resistance.

4 toxicity to mammalian cells or induction of bacterial resistance.

5 gning glycopeptide antibiotics that overcome bacterial resistance.

6 sign of new antibiotics to combat widespread bacterial resistance.

7 osmotic stress, group 1 ACQOS contributes to bacterial resistance.

8 robials and aims to prevent the emergence of bacterial resistance.

9 g, and assist in spatio-temporal tracking of bacterial resistance.

10 ral years and was associated with increasing bacterial resistance.

11 ogical activities while avoiding or limiting bacterial resistance.

12 f the drugs and higher propensity to develop bacterial resistance.

13 biocides hindered the propensity to develop bacterial resistance.

14 recent years due to a worldwide increase in bacterial resistance.

15 an increased risk of adverse events such as bacterial resistance.

16 esting that peptides were able to neutralize bacterial resistance.

17 creased susceptibility in the development of bacterial resistance.

18 possibility exists for genetic mutations and bacterial resistance.

19 dal at low concentrations and did not induce bacterial resistance.

20 events of antibiotics and the development of bacterial resistance.

21 s were reviewed to identify risk factors for bacterial resistance.

22 y reducing adverse events and development of bacterial resistance.

23 sistant strains and unlikelihood of inducing bacterial resistance.

24 pectrum of action, low toxicity, and limited bacterial resistance.

25 by which AMPs activate PhoP-PhoQ and induce bacterial resistance.

26 osphorylation does not necessarily result in bacterial resistance.

27 resents a considerable risk for promotion of bacterial resistance.

28 activate the PhoP-PhoQ system, and to induce bacterial resistance.

29 ents and pressures toward the development of bacterial resistance.

30 l drug efflux pumps that are responsible for bacterial resistance against a variety of antibiotics.

31 heptose modification pathway contributes to bacterial resistance against gastrointestinal host defen

32 lationship between adverse events, including bacterial resistance against moxifloxacin, and the inves

33 is study, we show that anteiso-BCFAs enhance bacterial resistance against phagosomal killing in macro

34 in the bacterial membrane may contribute to bacterial resistance against the drug.

35 echanisms of action of cationic AMPs and the bacterial resistance against these peptides.

36 infection via a strategy unlikely to promote bacterial resistance and a vaccine candidate against M.

37 sequence-may be a key feature in preventing bacterial resistance and could explain why sequence-func

38 e has been associated with increases in both bacterial resistance and nosocomial infection.

39 time-shift assays revealed temporal peaks in bacterial resistance and phage infectivity, consistent w

40 called carbapenemases), however, can confer bacterial resistance and represent a serious health thre

41 e need for surveillance of pikR1/pikR2-based bacterial resistance and the preemptive development of d

42 olysaccharide is an important determinant of bacterial resistance and toxicity, KdsC is a potential t

43 ry infection, facilitate weaning, and reduce bacterial resistance and use of systemic antibiotics.

44 al mode of action holds a low risk to induce bacterial resistance, and provides valuable information

45 ope as potential solutions to the problem of bacterial resistance as the membrane-active nature impar

46 With bacterial resistance becoming a serious threat to global

47 l in vitro and in vivo differences in innate bacterial resistance between ACE 10/10 and WT mice.

48 tion antibiotic compounds which can overcome bacterial resistance by disrupting cell membranes and it

49 of NO synthase-elicit responses that mediate bacterial resistance by unknown mechanisms.

50 y modified superhydrophobic surfaces obviate bacterial resistance common with chemical agents, and th

51 The increase of bacterial resistance demands rapid and accurate diagnosi

52 Bacterial resistance development has become a very serio

53 ings suggest a potential risk of stimulating bacterial resistance development in the animal gut when

54 Bacterial resistance due to the misuse of antibiotics ha

55 phosphotransferases [APH(3')s] are important bacterial resistance enzymes for aminoglycoside antibiot

56 3'-phosphotransferases (APH(3')s) are common bacterial resistance enzymes to aminoglycoside antibioti

57 udomonas syringae pathovar maculicola (RPM1) bacterial resistance gene is completely absent (rpm1-nul

58 Increased bacterial resistance in ACE 10/10 is directly due to ove

59 ents for public sector drugs on the level of bacterial resistance in low-income and middle-income cou

60 llow us to follow the evolution of viral and bacterial resistance in real time, to uncover the huge d

61 in this review suggested that Gram-negative bacterial resistance increases the burden in the ICU as

62 Emergence of bacterial resistance is a major issue for all classes of

63 The current epidemic of bacterial resistance is attributed, in part, to the over

64 Bacterial resistance is often caused by molecular change

65 ence factors, and lower the risk of creating bacterial resistance is undisputed.

66 this plant compound effectively disabled the bacterial resistance mechanism against the berberine ant

67 ent synthesis will enable further studies on bacterial resistance mechanisms and may provide insight

68 ect of dimerization on the action of several bacterial resistance mechanisms that deactivate tobramyc

69 Bacterial resistance mechanisms usually depend on the ch

70 volving both extracellular and intracellular bacterial resistance mechanisms.

71 in response to the progressive evolution of bacterial resistance mechanisms.

72 overcoming the two most common tetracycline bacterial-resistance mechanisms: ribosomal protection (t

73 he other two patients were not attributed to bacterial resistance missed by routine susceptibility te

74 pical antibiotics does not appear to promote bacterial resistance or a discernible change in conjunct

75 ciety for Microbiology, and in the report on bacterial resistance recently issued by the US Office of

76 er white blood cell count at day 14, reduced bacterial resistance, reduced use of SA, and increased w

77 ve of those detected in distillers grains on bacterial resistance selection.

78 ell rigidity, are key factors in determining bacterial resistance/sensitivity to the bactericidal nat

79 Bacterial resistance surveillance (5330 isolates) was co

80 that these peptides are less susceptible to bacterial resistance than traditional antibiotics and co

81 tion is necessary to overcome the problem of bacterial resistance that affects all currently used cla

82 of efflux pumps is an important mechanism of bacterial resistance that results in the extrusion of an

83 ummarize recent developments with respect to bacterial resistance, the identity of the new beta-lacta

84 cular beta-lactamase allele jointly increase bacterial resistance to a clinically important antibioti

85 Biofilms have been shown to increase bacterial resistance to a variety of stresses.

86 etyltransferases is the predominant cause of bacterial resistance to aminoglycosides.

87 inhibit these emerging causes of pathogenic bacterial resistance to aminoglycosides.

88 roteins can interact with porins to increase bacterial resistance to AMPs.

89 g that the disrupted genes were required for bacterial resistance to an IFN-gamma-dependent immune me

90 enes of Salmonella enterica are important in bacterial resistance to anti-microbial peptides and are

91 Bacterial resistance to antibiotic therapy remains a wor

92 The rise in bacterial resistance to antibiotics demonstrates the med

93 The emergence of bacterial resistance to antibiotics is a major health pr

94 The spread of bacterial resistance to antibiotics poses the need for a

95 Bacterial resistance to antibiotics usually incurs a fit

96 Bacterial resistance to antibiotics, particularly plasmi

97 Bacterial resistance to antibiotics, particularly to mul

98 nt class of enzymes that plays a key role in bacterial resistance to antibiotics.

99 e genetic elements responsible for spreading bacterial resistance to antibiotics.

100 ne disruption, and potential contribution to bacterial resistance to antibiotics.

101 Bacterial resistance to antimicrobial agents is a growin

102 on of outbreaks of infection or increases in bacterial resistance to antimicrobial agents is an essen

103 Bacterial resistance to antimicrobial compounds is incre

104 These modifications promote bacterial resistance to antimicrobial peptides and reduc

105 nt infection of mice, possibly by increasing bacterial resistance to antimicrobial peptides.

106 life-threatening disease as a consequence of bacterial resistance to antimicrobials in such a state.

107 Bacterial resistance to arsenic is facilitated by ArsD,

108 Bacterial resistance to beta-lactam agents is often medi

109 A major mechanism of bacterial resistance to beta-lactam antibiotics (penicil

110 Beta-lactamases confer bacterial resistance to beta-lactam antibiotics, such as

111 lysis in such enzymes that is central to the bacterial resistance to beta-lactam antibiotics.

112 beta-lactamases is an important component of bacterial resistance to beta-lactam antibiotics.

113 a lead compound for drug discovery to combat bacterial resistance to beta-lactam antibiotics.

114 f beta-lactamases is the most common form of bacterial resistance to beta-lactam antibiotics.

115 Bacterial resistance to beta-lactam/beta-lactamase inhib

116 Bacterial resistance to beta-lactams is achieved by the

117 or extracellular growth but is essential for bacterial resistance to both normal and CGD PMN.

118 an promote bacterial infection by increasing bacterial resistance to CAMP and reducing LPS recognitio

119 ne translocation (Tat) system contributes to bacterial resistance to cationic antimicrobial peptides

120 The recent increase in bacterial resistance to cell wall active agents has led

121 lifying CTX-M and NDM, two genes that confer bacterial resistance to cephalosporins and carbapenems,

122 sage of NTHi increased both PCho content and bacterial resistance to clearance, and no such increases

123 Bacterial resistance to clinically administered beta-lac

124 In acute pyelonephritis, bacterial resistance to co-trimoxazole predicts treatmen

125 in rural Uganda, an area with high rates of bacterial resistance to co-trimoxazole.

126 xazole prophylaxis, despite locally reported bacterial resistance to co-trimoxazole.

127 tetrasaccharide was associated with enhanced bacterial resistance to complement-mediated killing.

128 tly needed to address the growing problem of bacterial resistance to conventional antibiotics.

129 As bacterial resistance to currently used antibiotics incre

130 lation-division family that is essential for bacterial resistance to drugs and toxic metals.

131 The prevalent mechanism of bacterial resistance to erythromycin and other antibioti

132 -encoding gene led to a phenotype of reduced bacterial resistance to ethanol stress, which was more m

133 With the increasing prevalence of acquired bacterial resistance to existing classes of antibiotics

134 ng developed in response to the emergence of bacterial resistance to existing drugs.

135 antageous antibiotic hydrolytic spectrum for bacterial resistance to extended-spectrum antibiotics.

136 lizines were introduced recently to overcome bacterial resistance to fluoroquinolones.

137 in S. aureus causes a selective increase in bacterial resistance to gIIA PLA(2) and HBD-3, the forme

138 (lipo) teichoic acids of S. aureus increases bacterial resistance to gIIA PLA2 approximately 100-fold

139 ed genes within phagocytic cells and promote bacterial resistance to host antimicrobial proteins.

140 iofilm formation are critical mechanisms for bacterial resistance to host immune factors and antibiot

141 Disruption of cdgR decreased bacterial resistance to hydrogen peroxide and accelerate

142 Gram-negative bacteria, plays a key role in bacterial resistance to hydrophobic antibiotics and anti

143 tamases, have emerged as a puzzling cause of bacterial resistance to inhibitors of beta-lactamases.

144 ing antibiotics, the potential mechanisms of bacterial resistance to LpxC inhibitors remain poorly un

145 sturbing the normal flora, the low chance of bacterial resistance to lysins and their ability to kill

146 sturbing the normal flora, the low chance of bacterial resistance to lysins, and their ability to kil

147 f peptidoglycan is typically associated with bacterial resistance to lysozyme, a muramidase that serv

148 A key mechanism of bacterial resistance to macrolide antibiotics is the dim

149 Emergence of bacterial resistance to macrolide antibiotics, particula

150 We show killing is associated with bacterial resistance to mechanical shear and persistence

151 Bacterial resistance to most antibiotics in clinical use

152 Bacterial resistance to multiple antibiotics is increasi

153 The increase in bacterial resistance to multiple drugs represents a seri

154 Because bacterial resistance to oxidative stress and CAMP are in

155 Formate enhances bacterial resistance to P2, as previously demonstrated,

156 The principal cause of bacterial resistance to penicillin and other beta-lactam

157 TEM-1 beta-lactamase confers bacterial resistance to penicillin antibiotics and has a

158 phage to consider include narrow host range, bacterial resistance to phage and phage-encoded virulenc

159 MDR P. aeruginosa, whereby the evolution of bacterial resistance to phage attack changes the efflux

160 Here, we described a mechanism of bacterial resistance to phage infections.

161 nges such as regulation, limited host range, bacterial resistance to phages, manufacturing, side effe

162 ty and the effect does not appear to involve bacterial resistance to phagocytosis.

163 cteriostatic antibiotic reversibly increased bacterial resistance to PLA2-triggered PL degradation an

164 phosphate groups of lipid A is implicated in bacterial resistance to polymyxin and cationic antimicro

165 eptidoglycan amidase activity, which confers bacterial resistance to protamine and alpha-helical CAMP

166 amidases, encoded by amiA and amiC, elevated bacterial resistance to protamine and alpha-helical pept

167 These results indicate that PCho promotes bacterial resistance to pulmonary clearance early in inf

168 ating the ribosome's function and conferring bacterial resistance to ribosome-targeting antibiotics.

169 of opuABCD, trehalose accumulation increases bacterial resistance to stress in broth and mice.

170 act as an antibiotic efflux pump and mediate bacterial resistance to sulfonamide antimetabolite drugs

171 Expression of tetA confers bacterial resistance to tetracycline (Tc(R)) and also ca

172 Bacterial resistance to the aminoglycoside antibiotic ka

173 ort RNA transcripts whose expression confers bacterial resistance to the antibiotic spectinomycin.

174 as low as 4 nM with significant reduction of bacterial resistance to the combination of cefotaxime/13

175 Bacterial resistance to the third-generation cephalospor

176 class A beta-lactamases is a common cause of bacterial resistance to these agents.

177 in this way are no longer effective, because bacterial resistance to these compounds has developed.

178 range of beta-lactam antibiotics to provide bacterial resistance to these compounds.

179 llins and cephalosporins, thus providing for bacterial resistance to these compounds.

180 We assessed bacterial resistance to these drugs in a subset of patie

181 nded spectrum beta-lactamases (ESBLs) confer bacterial resistance to third-generation cephalosporins,

182 idespread in bacteria and is responsible for bacterial resistance to toxic aromatic cations by proton

183 rved amongst bacteria and is responsible for bacterial resistance to toxic substances.

184 The rapid rise of bacterial resistance to traditional antibiotics combined

185 Bacterial resistance to vancomycin has been attributed t

186 ulating virulence determinant production and bacterial resistance to vancomycin.

187 The sharp increase in bacterial resistance toward these antibiotics in recent

188 The global crisis of bacterial resistance urges the scientific community to i

189 penicillin-binding proteins responsible for bacterial resistance was also the structural basis for a

190 Surprisingly, this bacterial resistance was evident 1 day after infection,

191 For the majority of the mutants, bacterial resistance was significantly increased despite

192 der to discourage the continued evolution of bacterial resistance, whilst maintaining the activity an

193 rmine whether the development of significant bacterial resistance will limit rifaximin use.

194 reciprocal changes in phage infectivity and bacterial resistance within microbial communities of tre