ライフサイエンスコーパス: skin infection

1 hogenicity of herpes simplex virus type 1 in skin infection.

2 s; 42.1% women), 22.0% reported a history of skin infection.

3 cause systemic infection in a mouse model of skin infection.

4 lence of USA300 in necrotizing pneumonia and skin infection.

5 key source of IL-17 in the early hours after skin infection.

6 romote host innate defense against S. aureus skin infection.

7 ntion for individuals with a disseminated VV skin infection.

8 rodent models of CA-MRSA USA300 pneumonia or skin infection.

9 d with increased dermonecrosis in a model of skin infection.

10 n rodent models of necrotizing pneumonia and skin infection.

11 e lesion size in a murine model of S. aureus skin infection.

12 ce in a humanized mouse model of superficial skin infection.

13 mouse model was used to measure superficial skin infection.

14 che, while Vsp2 is associated with blood and skin infection.

15 S virulence in a murine model of necrotizing skin infection.

16 ial function in the diagnosis and therapy of skin infection.

17 wt bacteria and increases severity of murine skin infection.

18 ntly more tissue damage in a murine model of skin infection.

19 may enhance susceptibility to staphylococcal skin infection.

20 ilm in vivo in a murine model of superficial skin infection.

21 utrophils were dispensable for resistance to skin infection.

22 trophils and increasing tissue damage during skin infection.

23 masome activation and immunopathology during skin infection.

24 lammation in a mouse model of staphylococcal skin infection.

25 olling the host innate response to S. aureus skin infection.

26 ss-reactive immune responses occur following skin infection.

27 cally to clear vaccinia virus from a primary skin infection.

28 rmal barrier defects and recurrent microbial skin infections.

29 s and a propensity for Staphylococcus aureus skin infections.

30 most common organism isolated from purulent skin infections.

31 taphylococcus aureus is the leading cause of skin infections.

32 ylococcus aureus (MRSA) is a common cause of skin infections.

33 rtant antiviral granule component in in vivo skin infections.

34 ccines designed to moderate severe S. aureus skin infections.

35 non-biocide virulence inhibitors in treating skin infections.

36 hogenesis in mouse models of lung and burned skin infections.

37 AD, but not psoriasis, suffer from frequent skin infections.

38 ten triggered by bacterial, fungal, or viral skin infections.

39 AS166 were isolated from experimental murine skin infections.

40 tes from temperate countries as well as from skin infections.

41 and the initiation of group A streptococcal skin infections.

42 and the development of group A streptococcal skin infections.

43 the molecular pathogenesis of streptococcal skin infections.

44 ing, as evident in both in vitro and in vivo skin infections.

45 al agent for the treatment of staphylococcal skin infections.

46 as a dose-response relationship was seen for skin infections.

47 A safety outcome was number of skin infections.

48 evaluated in a mouse model of staphylococcal skin infections.

49 Exophiala species are mostly responsible for skin infections.

50 in as a topical antibacterial agent to treat skin infections.

51 common colonizer of persons with and without skin infections.

52 erbation and flare, and preventing secondary skin infections.

53 evelopment, disease chronicity, or recurrent skin infections.

54 antimicrobials currently used to treat MRSA skin infections.

55 which in turn impairs control of herpesvirus skin infections.

56 ibed a role in immunity after resolved viral skin infections.

57 fections (UTIs, 1.41; 95% CI, 1.35 to 1.45), skin infections (1.50; 95% CI, 1.45 to 1.55), septicemia

58 ds ratio 6.21, 95% CI 3.25-11.85), recurrent skin infections (2.87, 1.10-7.45), and severe pneumonia

59 promoter showed increased resistance to GAS skin infection (50% smaller necrotic ulcers and 60% fewe

60 In a model of MRSA skin infection, ACE 10/10 mice had 50-fold less bacteria

61 , P:=0.04) and had more often had a previous skin infection (adjusted OR [95% CI]=3.5 [0.7 to 17], P:

62 moisturizer often used in the prevention of skin infections after ambulatory surgeries and as a main

63 Although a common cause of community-onset skin infections among Indigenous populations in northern

64 component alone is ineffectual in preventing skin infection and bacteremia due to CovR/S mutants but

65 matory skin disease associated with frequent skin infection and impaired skin barrier function.

66 n and p300/CBP binding are important for VZV skin infection and may be targeted for antiviral drug de

67 ciated with niche-specific infections, i.e., skin infection and pharyngitis-induced acute rheumatic f

68 ve strain in murine models of staphylococcal skin infection and pneumonia, we expanded upon recent st

69 at staphylococcal alpha-toxin promotes viral skin infection and provides a mechanism by which S aureu

70 CA-MRSA PSMs contribute to skin infection and recruit and lyse neutrophils, and tru

71 Staphylococcus aureus is a frequent cause of skin infection and sepsis in humans.

72 that liver infection is predicated on severe skin infection and that death requires significant liver

73 the ORF25 deleted virus infects fish through skin infection and then spreads to internal organs as re

74 MCG-2 strains were mostly obtained from skin infections and affected patients with a mean age of

75 of disease manifestations from pulmonary to skin infections and are notoriously difficult to treat,

76 ayer in cutaneous innate immune responses to skin infections and injury.

77 s aureus (MRSA) has become a common cause of skin infections and invasive infections in community dwe

78 reat potential for topical treatment of MRSA skin infections and lays the foundation for further anal

79 ts role against bacterial strains related to skin infections and mechanism of action is not well unde

80 We investigated whether skin infections and nasal colonization in travelers cont

81 sible for illnesses ranging from superficial skin infections and pharyngitis to severe invasive infec

82 Skin infections and previous infection or inflammation o

83 rovide new insights into the pathogenesis of skin infections and suggest potential roles for MCs and

84 study of adults and children with S. aureus skin infections and their household contacts in Los Ange

85 s and children after treatment for S. aureus skin infections and their household contacts in Los Ange

86 ain developed fatal sepsis, extensive tissue skin infection, and abscess-forming deep-seeded thigh mu

87 itis, joint surgery, hip or knee prosthesis, skin infection, and human immunodeficiency virus type 1

88 bscess, abscess size, the number of sites of skin infection, and the presence of nonpurulent cellulit

89 sion may be important in the pathogenesis of skin infections, and (iv) the molecular interactions in

90 cluding overnight hospitalization, recurrent skin infections, and similar infection in household cont

91 l produce large SAg numbers, consistent with skin infections, and that certain SAgs will be overrepre

92 kin (IL)-6 autoantibodies and staphylococcal skin infection; and anti-IL-17A, anti-IL-17F, or anti-IL

93 nitiation and termination of inflammation in skin infection are incompletely understood.

94 linking epidermal barrier defects and viral skin infection are not well understood.

95 Skin infections are frequently caused by Staphylococcus

96 gh their roles in immunity against localized skin infections are less well defined.

97 Group A Streptococcus (GAS) skin infections are particularly prevalent in developing

98 he dual roles of staphylokinase in S. aureus skin infections as promoting the establishment of infect

99 in identifying acceptable levels of risk for skin infections associated with sand exposures.

100 .2 percentage points; 95% CI, -8.2 to -2.2), skin infections at new sites (3.1% vs. 10.3%; difference

101 e defined as salon customers with persistent skin infections below the knee.

102 Among 588 household contacts, 10% reported a skin infection by month 3 and 13% by month 6.

103 soprostol improved host defense against MRSA skin infection by restoring DC migration to draining lym

104 as targeting the Hla might prevent invasive skin infection by staphylococci.

105 mice, which have increased susceptibility to skin infection by Streptococcus.

106 that enables CA-MRSA to produce necrotizing skin infections by allowing the bacteria to escape from

107 patients are prone to chronic bacteremia and skin infections by Helicobacter and related species such

108 y and are important for host defense against skin infections by some bacterial and viral pathogens.

109 on of C57BL/6 mice, impairs the clearance of skin infections by Streptococcus pyogenes and Staphyloco

110 mice and provide protection against necrotic skin infection caused by Group A Streptococcus (GAS).

111 We report here a case of disseminated skin infection caused by Mucor velutinosus, a recently d

112 osum virus, a dermatotropic poxvirus causing skin infections common in children and immunocompromised

113 gher in patients with established B. garinii skin infection compared to patients with other Borrelia

114 iotic-induced expression of mecA during MRSA skin infection contributes to immunopathology by alterin

115 ts, skin puncture, extreme temperatures, and skin infections-eg, cellulitis) increase the risk of bre

116 beta-lactam treatment of MRSA skin infection exacerbates immunopathology, which is IL-

117 A murine MRSA skin infection experiment confirmed that simvastatin sig

118 For skin infections, Florida had higher risk-adjusted revisi

119 cormycosis with a high prevalence of primary skin infection following trauma and a prognosis signific

120 in mice that localized vaccinia virus (VACV) skin infection generates long-lived non-recirculating CD

121 reus (MRSA) in the United States, visits for skin infections greatly increased.

122 Patients with AD with skin infections had higher CD4(+) IL-22(+) and IL-17(+)

123 s resulting in this increased propensity for skin infections have been an area of active investigatio

124 Revisit rates varied by diagnosis, with skin infections having the highest rate (23.1% [95% CI,

125 +) skin T(RM) cells are both generated after skin infection; however, CD8(+) T(CM) cells recirculate

126 A history of skin infection identified a state of enhanced susceptibi

127 s in vitro, simulating the superficial human skin infection, impetigo, and providing a model system f

128 tection against lethal group A streptococcal skin infection in a mouse model.

129 We report a case of Macrophomina phaseolina skin infection in an immunocompromised child with acute

130 interleukin-4 in cutaneous inflammation and skin infection in human patients.

131 plex virus (HSV-1) is a major cause of viral skin infection in humans.

132 ctional PTS is not required for subcutaneous skin infection in mice; however, it does play a role in

133 oup A Streptococcus pyogenes (GAS) cutaneous skin infection in mice; this was accompanied by increase

134 site, antibiotic use in the prior year, and skin infection in the prior 3 months.

135 L), could account for the high rates of MRSA skin infection in this region.

136 ia formation translated to severely impaired skin infection in vivo.

137 protein E genes, and the pathogenesis of VZV skin infection in vivo.

138 letion reduced cell-cell spread in vitro and skin infection in vivo.

139 envelopment, efficient cell-cell spread, and skin infection in vivo.

140 e recovered from patients with uncomplicated skin infections in 10 different countries during five ph

141 rapidly and specifically diagnose bacterial skin infections in a contact-less manner, allowing for i

142 This outbreak of MRSA skin infections in an otherwise-healthy, well-defined, m

143 Recurrent skin infections in extrinsic atopic dermatitis (EAD) may

144 by S. aureus, promoted the establishment of skin infections in humans and increased bacterial penetr

145 temic disease in fish but produces localized skin infections in humans.

146 (Hla) contributes to the severity of USA300 skin infections in mice and determined whether vaccinati

147 Agr contribute to the pathogenesis of USA300 skin infections in rabbits, whereas a role for PVL could

148 o have increased exposure to antibiotics and skin infections in the home.

149 tem has a crucial role in the development of skin infections in the most prevalent CA-MRSA strain USA

150 ng the prevention and treatment of bacterial skin infections in the newborn period.

151 ertenue and another bacterium known to cause skin infections in the Pacific islands-Haemophilus ducre

152 Emergency department visits for skin infections in the United States have increased with

153 ely absent, perhaps accounting for recurrent skin infections in this disease.

154 profile, for the treatment of uncomplicated skin infections, including both cellulitis and abscesses

155 Staphylococcus aureus skin infection is a frequent and recurrent problem in ch

156 Thus, the clinical severity of S. aureus skin infection is driven by the inflammatory response to

157 ontribution in a murine model of necrotizing skin infection is largely driven by its ability to neutr

158 for the life cycle of the virus because VZV skin infection is necessary for viral transmission and p

159 at contribute to the pathogenesis of CA-MRSA skin infections is incomplete.

160 trate that MC presence protects mice from VV skin infection, MC degranulation is required for protect

161 In a murine skin infection model, an insertion mutation in the respo

162 In a skin infection model, expression of phagocyte NADPH oxid

163 Using a murine skin infection model, we compared T helper cell response

164 Using a Candida albicans skin infection model, we have shown that direct presenta

165 ly supported in studies using a low-inoculum skin infection model, where low levels of PVL augmented

166 S. aureus virulence was studied in a murine skin infection model.

167 the size of lesions caused by S. aureus in a skin infection model.

168 vival on skin was tested in an adapted mouse skin infection model.

169 -1 human keratinocyte cell line and a rabbit skin infection model.

170 models; an acute lung infection model and a skin infection model.

171 d had reduced virulence in murine sepsis and skin infection models.

172 y against HSV-1 was examined using the flank skin infection mouse model.

173 ct in the previous month with someone with a skin infection; multiple infiltrates or cavities on ches

174 nage) and matched control subjects without a skin infection (n = 147 each) presenting to 10 U.S. emer

175 Skin infections (n = 103) were reported from 67 individu

176 Although most strains caused severe skin infection, not every strain caused systemic infecti

177 Skin infections occurred in 36/142 (25%) and 39/141 (28%

178 Adverse events, such as skin infection, occurred more frequently with placebo; n

179 d having a roommate in training with a prior skin infection (odds ratio [OR] = 3.44) or having a fami

180 a (odds ratio, 0.76 [CI, 0.64 to 0.91]), and skin infections (odds ratio, 0.64 [CI, 0.46 to 0.89]).

181 injected into mice via an air sac model for skin infection, organisms recovered from the spleens sho

182 During a CO-MRSA skin infection outbreak in Alaska, we assessed risk fact

183 are prescribed commonly and increasingly for skin infections, perhaps due, in part, to lack of experi

184 s causes a variety of human diseases such as skin infections, pneumonia, and endocarditis.

185 e aetiological agent of both respiratory and skin infections, produces numerous exotoxins to establis

186 s recombinant IL-17A injected at the site of skin infection promoted more rapid healing of candidiasi

187 ose that the production of SLS by GAS during skin infection promotes invasive outcomes by triggering

188 te, diabetes, recent hospitalization, recent skin infection, recent cephalexin use, and household S.

189 pe colonizing household contacts were recent skin infection, recent cephalexin use, and USA300 geneti

190 Another review on severe staphylococcal skin infections reminds us of the importance of covering

191 Staphylococcus aureus skin infections represent a significant public health th

192 ential for the development of bacteremia and skin infection, representing major types of acute S. aur

193 ells generated as a result of localized VACV skin infection reside not only in the site of infection,

194 3.1% for those with and without a history of skin infection, respectively (unadjusted hazard ratio (H

195 aused changes in the histological pattern at skin infection sites could be complemented.

196 g the genotypic biomarkers for throat versus skin infection specialists.

197 In skin infections, SPMs enhanced vancomycin clearance of S

198 ration) and larger lesion size in a model of skin infection (subcutaneous administration).

199 oth forms of AD have increased propensity to skin infection, suggesting a novel mechanism for infecti

200 skin neutrophils and are prone to bacterial skin infections, suggesting that allergic inflammation c

201 to determine colonization at enrollment, and skin infection swabs over 17 months were assessed for S.

202 By examining the relationships between skin infection, systemic liver infection, and presumptiv

203 etes are more prone to Staphylococcus aureus skin infection than healthy individuals.

204 the expression of hasA than spyCEP in mouse skin infection than wild-type GAS did.

205 m is a potentially fatal, disseminated viral skin infection that develops in individuals with atopic

206 eczema vaccinatum (EV), a disseminated viral skin infection that follows inoculation with vaccinia vi

207 e evidence using a murine model of S. aureus skin infection that the effects mediated by rsr reduce d

208 e previously reported outbreaks of S. aureus skin infections that affected newborn infants and were a

209 /-) have severe neutrophilia and spontaneous skin infections that limit their life span.

210 trains have been known to be associated with skin infections, the Nudix hydrolase and its associated

211 We hypothesized that MC help protect against skin infection through the expression of cathelicidin.

212 ing the initiation and progression from mild skin infection to a severe disseminated infection remain

213 During the transition from a throat or skin infection to an invasive infection, GAS must adapt

214 We used a mouse model of skin infection to compare the virulence of methicillin-r

215 ide spectrum of diseases, ranging from minor skin infections to fatal necrotizing pneumonia.

216 ns, causing infections from mild superficial skin infections to lethal bacteremia and endocarditis.

217 aureus causes pathologies ranging from minor skin infections to life-threatening diseases.

218 any infectious diseases, ranging from benign skin infections to life-threatening endocarditis and tox

219 humans, from relatively mild pharyngitis and skin infections to life-threatening necrotizing fasciiti

220 nother acute care hospital varied from 1.3% (skin infection) to 5.1% (septicemia).

221 The response to VV skin infection under conditions of TNF-alpha deficiency,

222 rsus those without a past medical history of skin infection using Cox proportional hazards models.

223 e of and species responsible for a bacterial skin infection using differences in Mie scatter spectra

224 During VZV skin infection, viral gene products down-regulated inter

225 the virulence genes known to be involved in skin infection was examined.

226 the speB gene in group A Streptococcus (GAS) skin infection was studied with a mouse model.

227 in-resistant Staphylococcus aureus (CA-MRSA) skin infections was observed in a population of U.S. mil

228 In a mouse model of S. aureus skin infection, we found that lesion size did not correl

229 In contrast to previous findings of skin infection, we observed that clearance of SA from th

230 odel for infection that closely mimics human skin infection, we show that the vaccine can protect aga

231 occal virulence factors in the initiation of skin infections, we compared the adherence of a wild-typ

232 ntacts, independent predictors of subsequent skin infection were Chicago site, antibiotic use in the

233 ongitudinal study, patients with a S. aureus skin infection were more likely to suffer a recurrence i

234 increased neutrophil recruitment and reduced skin infection, whereas in trans expression of SsE(M28)

235 Deletion of ORF12 had no effect on skin infection, whereas replication of POKADelta11, POKA

236 s and systemic infection in a mouse model of skin infection, while an isogenic acapsular strain did n

237 We enrolled outpatients with uncomplicated skin infections who had cellulitis, abscesses larger tha

238 munity, comparing 34 case patients with MRSA skin infection with 94 control subjects.

239 ealing and decreased IL-17A production after skin infection with C. albicans compared with wild-type

240 g epicutaneous sensitization with hapten and skin infection with Candida albicans.

241 n lead to systemic infection and disfiguring skin infection with extremely high mortality.

242 In this study, we used a skin infection with HSV-1 characterized by the successiv

243 Using a murine model that supports extensive skin infection with Leishmania donovani, spatial analyse

244 At 8 months after surgery, the patient had a skin infection with phaeohyphomycosis due to Alternaria

245 Furthermore, treatment of a USA300 MRSA skin infection with retapamulin ointment resulted in up

246 bility of patients with atopic dermatitis to skin infection with S. aureus.

247 istant S. aureus strains most commonly cause skin infections with abscess formation.

248 to expedite specific treatment of bacterial skin infections with narrow-spectrum antibiotics, rather

249 pneumonias; recurrent Staphylococcus aureus skin infections with otitis externa; recurrent, severe h

250 This review examines neonatal bacterial skin infections with respect to host immunity, bacterial

251 Skin infections with ulceration are a major health probl

252 Using skin infections with vaccinia virus (VacV)-expressing mo

253 aviruses (HPVs) cause near ubiquitous latent skin infection within long-lived hair follicle (HF) kera