ライフサイエンスコーパス: bacterial resistance

1 y reducing adverse events and development of bacterial resistance.

2 sistant strains and unlikelihood of inducing bacterial resistance.

3 tiviral activity, and a low rate of inducing bacterial resistance.

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

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

6 osphorylation does not necessarily result in bacterial resistance.

7 resents a considerable risk for promotion of bacterial resistance.

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

9 ed for strict adherence, and reduced risk of bacterial resistance.

10 ents and pressures toward the development of bacterial resistance.

11 to ophthalmic practice to deal with changing bacterial resistance.

12 urface properties of the implants or promote bacterial resistance.

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

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

15 gning glycopeptide antibiotics that overcome bacterial resistance.

16 lly, the d,l-K(6)L(9) peptides do not induce bacterial resistance.

17 e crucial in addressing the global crisis of bacterial resistance.

18 ple approaches have been developed to combat bacterial resistance.

19 hage cocktails that prevent the emergence of bacterial resistance.

20 ver, mutations in its binding site can cause bacterial resistance.

21 nce, but not for salicylic acid induction or bacterial resistance.

22 imperative to resolve in the face of rising bacterial resistance.

23 on-oxide ceramic compound with known surface bacterial resistance.

24 h-needed new classes of antibiotics to fight bacterial resistance.

25 drug design of antibiotics to tackle rising bacterial resistance.

26 onse towards circumventing the mechanisms of bacterial resistance.

27 as an adjuvant therapy in the fight against bacterial resistance.

28 he infection and also prevent development of bacterial resistance.

29 edical use, such as toxicity, stability, and bacterial resistance.

30 ns that allowed or disallowed development of bacterial resistance.

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

32 ral years and was associated with increasing bacterial resistance.

33 possibility exists for genetic mutations and bacterial resistance.

34 , multi-drug antimicrobial chemotherapy, and bacterial resistance.

35 toxicity to mammalian cells or induction of bacterial resistance.

36 sign of new antibiotics to combat widespread bacterial resistance.

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

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

39 ogical activities while avoiding or limiting bacterial resistance.

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

41 biocides hindered the propensity to develop bacterial resistance.

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

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

44 esting that peptides were able to neutralize bacterial resistance.

45 creased susceptibility in the development of bacterial resistance.

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

47 events of antibiotics and the development of bacterial resistance.

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

49 In the context of emergence of bacterial resistance, a short duration of antimicrobial

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

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

52 The emergence of bacterial resistance against life-saving medicines has f

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

54 Bacterial resistance against phage infection is a topic

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

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

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

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

59 use of antibiotics triggered the process of bacterial resistance and causes major health problems.

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

61 mation of biofilms, decreases the chances of bacterial resistance and is compatible with local delive

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

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

64 , offering a promising avenue for mitigating bacterial resistance and promoting more effective treatm

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

66 Interestingly, this combination prevented bacterial resistance and restored susceptibility of gent

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

68 these cyclic nucleotide phosphates (cNPs) in bacterial resistance and tolerance to antimicrobial trea

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

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

71 g to patient non-adherence, the emergence of bacterial resistance, and infection progression.

72 d skin commensals, do not readily select for bacterial resistance, and possess anti-infective activit

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

74 rocesses, from ATP export in mitochondria to bacterial resistance, and represent a promising platform

75 nvironmental pollution, animal intoxication, bacterial resistance, and sustained occupational exposur

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

77 With bacterial resistance becoming a serious threat to global

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

79 These should not only overcome the existing bacterial resistance but also provide at least interim e

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

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

82 eting, which in turn contributes to avoiding bacterial resistance caused by single-target mutations.

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

84 er, M -NDs show a lower propensity to induce bacterial resistance compared to conventional small-mole

85 s to conventional antibiotics to address the bacterial resistance crisis.

86 The increase of bacterial resistance demands rapid and accurate diagnosi

87 Moreover, no bacterial resistance developed to the combined treatment

88 Bacterial resistance development has become a very serio

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

90 exploited via phage steering, where emerging bacterial resistance due to receptor modification could

91 Bacterial resistance due to the misuse of antibiotics ha

92 ull activation of RBOHD, gene expression and bacterial resistance during ETI.

93 l for decreasing the possibility of inducing bacterial resistance during farm animal production.

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

95 3'-phosphotransferases (APH(3')s) are common bacterial resistance enzymes to aminoglycoside antibioti

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

97 orted study to our knowledge to identify key bacterial resistance genes directly from the bloodstream

98 The continued emergence of bacterial resistance has created an urgent need for new

99 stem coupled with prevention of emergence of bacterial resistance highlight the potential of this com

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

101 eutic phage strategies that outsmart evolved bacterial resistance in clinical settings.

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

103 main complementary strategies for mitigating bacterial resistance in phage therapy: minimizing the ab

104 ntial for eATP-induced calcium signaling and bacterial resistance in plants.

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

106 me; safety endpoints were adverse events and bacterial resistance in sputum.

107 of negative urine cultures, and emergence of bacterial resistance in urinary, intestinal and nasal mi

108 of negative urine cultures, and emergence of bacterial resistance in urinary, intestinal, and nasal m

109 Nonetheless, continuous surveillance for bacterial resistance in wild birds is necessary because

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

111 One of the most efficient mechanisms of bacterial resistance involves the expression of efflux p

112 ng antimicrobials, however, the potential of bacterial resistance is a major concern.

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

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

115 The central question remains whether bacterial resistance is driven by the AgNPs, released Ag

116 Bacterial resistance is increasing rapidly, requiring ur

117 Bacterial resistance is often caused by molecular change

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

119 (confers virus resistance), and Bs2 (confers bacterial resistance) leads to oligomerization of their

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

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

122 of the mechanisms of action of biocides, the bacterial resistance mechanisms encompassing both intrin

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

124 Bacterial resistance mechanisms usually depend on the ch

125 (MBL) production is one of the most alarming bacterial resistance mechanisms, conferring broad-spectr

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

127 volving both extracellular and intracellular bacterial resistance mechanisms.

128 s have been developed to block the principal bacterial resistance mechanisms: (i) beta-lactamase inhi

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

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

131 erent ways may be involved in both viral and bacterial resistance of HBECs in asthma.

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

133 ity testing (AST) is critical in determining bacterial resistance or susceptibility to a particular a

134 The bacterial resistance pattern among PWH between 2014 and

135 ory concentrations (MIC), are independent of bacterial resistance pattern, phenotype variations and/o

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

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

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

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

140 acterial agents among the ever-increasing PA bacterial resistance strains.

141 Bacterial resistance surveillance (5330 isolates) was co

142 Bacterial resistance surveillance is one of the main out

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

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

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

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

147 in Bacillus subtilis significantly increased bacterial resistance to 4-HNE in vitro and promoted bact

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

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

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

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

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

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

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

155 Bacterial resistance to antibiotic therapy remains a wor

156 llular S. aureus survival, thereby promoting bacterial resistance to antibiotic treatment.

157 n 41 U.S. states during 1978-2019 to examine bacterial resistance to antibiotics and heavy metals.

158 The rise in bacterial resistance to antibiotics demonstrates the med

159 The emergence and spread of bacterial resistance to antibiotics has developed into o

160 Bacterial resistance to antibiotics has reached critical

161 Bacterial resistance to antibiotics in this clinical set

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

163 Bacterial resistance to antibiotics makes previously man

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

165 Bacterial resistance to antibiotics usually incurs a fit

166 Bacterial resistance to antibiotics, particularly plasmi

167 Bacterial resistance to antibiotics, particularly to mul

168 necessary, it has led to a rapid increase in bacterial resistance to antibiotics.

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

170 nce of phenotypic delay for the evolution of bacterial resistance to antibiotics.

171 lity, altering RNA stability, and conferring bacterial resistance to antibiotics.

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

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

174 Pseudomonas aeruginosa highly increases the bacterial resistance to antimicrobial agents and host im

175 Bacterial resistance to antimicrobial agents is a growin

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

177 Bacterial resistance to antimicrobial compounds is incre

178 These modifications promote bacterial resistance to antimicrobial peptides and reduc

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

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

181 Bacterial resistance to antimicrobials is fast becoming

182 erfamily play significant roles in mediating bacterial resistance to antimicrobials.

183 Bacterial resistance to arsenic is facilitated by ArsD,

184 The increased incidence of bacterial resistance to available antibiotics represents

185 Bacterial resistance to beta-lactam agents is often medi

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

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

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

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

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

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

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

193 Bacterial resistance to beta-lactams is achieved by the

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

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

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

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

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

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

200 Bacterial resistance to clinically administered beta-lac

201 benzalkonium chloride (BC) can contribute to bacterial resistance to clinically relevant antibiotics.

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

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

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

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

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

207 pper homeostasis mechanisms are critical for bacterial resistance to copper-induced stress.

208 As bacterial resistance to currently used antibiotics incre

209 dication rates have fallen due to increasing bacterial resistance to currently used broad-spectrum an

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

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

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

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

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

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

216 genes have been shown to promote high-level bacterial resistance to fluoroquinolone antibiotics, pot

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

218 pment to counter the increasingly widespread bacterial resistance to fluoroquinolones.

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

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

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

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

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

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

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

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

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

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

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

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

231 Emergence of bacterial resistance to macrolide antibiotics, particula

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

233 -containing metal efflux platforms mediating bacterial resistance to metal poisoning.

234 Bacterial resistance to most antibiotics in clinical use

235 Bacterial resistance to multiple antibiotics is increasi

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

237 d that Pla enzymatic activity contributes to bacterial resistance to neutrophil-mediated bacterial ki

238 Furthermore, bacterial resistance to osmotic stress was markedly redu

239 Because bacterial resistance to oxidative stress and CAMP are in

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

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

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

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

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

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

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

247 that FH binding by beta was not required for bacterial resistance to phagocytosis by neutrophils or k

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

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

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

251 Mg2+ limitation enhances bacterial resistance to polymyxin antibiotics like colis

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

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

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

255 t of maternal quinolone use on gram-negative bacterial resistance to quinolones in their offspring.

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

257 f the plasmonic Ag nanoparticles reduces the bacterial resistance to ROS and impairs DNA repair capab

258 , we review the emerging role of cysteine in bacterial resistance to ROS with a link to broader eleme

259 ons within the sil system that contribute to bacterial resistance to silver ions.

260 ke conventional antimicrobials, the study of bacterial resistance to silver nanoparticles (AgNPs) rem

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

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

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

264 Bacterial resistance to the aminoglycoside antibiotic ka

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

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

267 tamase enzymes hydrolyze and thereby provide bacterial resistance to the important beta-lactam class

268 se with negative biopsies and no evidence of bacterial resistance to the phage.

269 Bacterial resistance to the third-generation cephalospor

270 This study sheds evident contrasts of bacterial resistance to the two most common heavy metals

271 resistant bacteria, delay the development of bacterial resistance to them and be suitable for local d

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

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

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

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

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

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

278 The transferability of bacterial resistance to tigecycline, the 'last-resort' a

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

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

281 The rapid rise of bacterial resistance to traditional antibiotics combined

282 Bacterial resistance to vancomycin has been attributed t

283 ulating virulence determinant production and bacterial resistance to vancomycin.

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

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

286 Currently the method for determination of bacterial resistance used in laboratory routine is the a

287 onfirmed leprosy cases were investigated for bacterial resistance using a combination of in vivo test

288 osed by bacteria in the face of growing anti-bacterial resistance via mechanisms that include membran

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

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

291 Emergence of bacterial resistance was evident at the end of the treat

292 No impact on emergence of bacterial resistance was observed.

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

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

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

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