ライフサイエンスコーパス: footpad

1 in a sterile inflammation model in the mouse footpad.

2 d at pressure-bearing sites of the mammalian footpad.

3 0 s on the bottom surface of a tumor-bearing footpad.

4 of Freund's complete adjuvant into the hind footpad.

5 mor or intracutaneously in the contralateral footpad.

6 ith AdZ.F(RGD) or AdZ subcutaneously via the footpad.

7 eaches the sensory nerve fibers in the mouse footpad.

8 suppressed in another anatomic location, the footpad.

9 swelling when mice received challenge in the footpad.

10 s following CFA injection in the adult mouse footpad.

11 a scaling similar to that of a natural gecko footpad.

12 ensory neurons in the DRG that innervate the footpad.

13 ed with low doses of anti-CD3 Ab s.c. in the footpad.

14 ted HSV-1 replication in the DRG but not the footpad.

15 injection of viable M. leprae into each hind footpad.

16 ed by enumerating the M. leprae bacteria per footpad.

17 ted onto microneedles and delivered to mouse footpad.

18 n after they were sensitized with SRW in the footpad.

19 DLL and propagated it in athymic nude mouse footpads.

20 onstruct and mutant-specific siRNAs to mouse footpads.

21 the tail and, by day 7, a thickening of the footpads.

22 thetic innervation of sweat glands in rodent footpads.

23 st a hotplate, and fiber density in hindlimb footpads.

24 op an autoinflammatory disease with inflamed footpads.

25 exclusively localized to the stress-bearing footpads.

26 ocompetent adult mice inoculated in the rear footpads.

27 after inoculation of guinea pig genitals and footpads.

28 essively up-regulated in WT but not in Tabby footpads.

29 itment to draining lymph nodes following the footpad administration of TLR4 and TLR5 agonists, is dra

30 tive growth of Mycobacterium leprae in mouse footpads after 8 weeks of bedaquiline therapy.

31 B, and beta 2 receptors are expressed in rat footpads; alpha 1 and beta 2 receptors are localized spe

32 tually eliminated L. major parasites in both footpad and dermal infection sites.

33 density of nonpeptidergic nociceptors in the footpad and exhibit enhanced sensitivity to mechanical f

34 in eliciting disease, delivery of Ag in the footpad and tailbase results in poor induction.

35 with virulent EEE virus in their right rear footpad and were followed in a time-course study for 4 d

36 odels of carrageenan-induced inflammation in footpads and air pouches.

37 leprosy bacilli could be propagated in mice footpads and detected using an in vivo imaging system (I

38 d susceptible C3H/HeJ (C3H) mice in the hind footpads and monitored arthritis development for 21 days

39 l structures indicated by absence of ventral footpads and presence of supernumerary ventral nails.

40 tin-3 impaired neutrophil recruitment in the footpads and the draining lymph nodes 1 d following infe

41 postinoculation (hpi) at the injection site (footpad) and as early as 72 hpi in the brain.

42 noma cells were implanted into the subcutis, footpad, and pancreas of syngeneic IFN-gamma(+/+) and IF

43 infected neutrophils than inoculation of the footpad, and these higher frequencies were associated wi

44 th additional abnormalities in whisker pads, footpads, and eyes.

45 tion of claws, interdigital webbing, reduced footpads, and trans-differentiation of sweat glands into

46 neous vaccination with live parasites in the footpad are even greater than previously appreciated.

47 ting bands encircle the tail and digits, the footpads are thickened and scaled, and loricrin staining

48 mice ultimately had lower parasite burden in footpads as compared with wild-type mice, demonstrating

49 TH response to mycobacterial proteins in the footpad assay, indicating that the accumulation of blood

50 Shepard's mouse footpad assay, therefore, was truly a breakthrough in le

51 by increased viral load in the contralateral footpad at 1 day post-infection, and significantly reduc

52 sferred with recipient APC into a SCID mouse footpad, CD4(+) T cells were hyporesponsive in DTH to do

53 12, or 24 h prior to an otherwise lethal VEE footpad challenge were completely protected from death,

54 Moreover, following infection of the footpad, changing the expression kinetics of VP5 from le

55 te topographically segregated targets in the footpad; cholinergic sympathetic axons innervate sweat g

56 ng, transgenic GFP skin tissue grafting, and footpad DC injection.

57 bacilli cells in DDS-resistant infected mice footpads decreased by the DPC4, and no bacilli were foun

58 on of adjuvants (CFA or Pam(3)CSK(4)) in the footpad decreases experimental autoimmune encephalomyeli

59 e lungs following intratracheal challenge or footpad delayed type hypersensitivity).

60 ory, SDR-MEM mice responded with an enhanced footpad delayed-type hypersensitivity response, and more

61 One such system, footpad delivery of Venezuelan equine encephalitis virus

62 In this study, we have used footpad delivery of VRP to probe the constituents of thi

63 Wild-type and drug-resistant mouse footpad-derived strains that included three folP1, two r

64 Footpad dermatitis (FPD) is used in the poultry industry

65 zed to the somatotopic representation of the footpad dermatome within the dorsal root ganglia and spi

66 With the unique robot footpad designs that integrate microstructured adhesives

67 is implemented with different adhesive robot footpad designs, allowing vertical and inverted surface

68 ferences that may contribute to differential footpad DTH responses using wildtype and four core genot

69 protection almost exclusively to the treated footpad during vitiligo, which was not possible by local

70 gnificantly in murine sweat gland-containing footpads during the time period when the gland innervati

71 with an ED40 of 16 mg/kg in the carrageenan footpad edema (CFE) assay and caused no gastrointestinal

72 with an ED40 of 7.1 mg/kg in the carrageenan footpad edema (CFE) assay.

73 mPRCs) and ameliorated inflammation in mouse footpad edema and pneumonia models.

74 ells and protected mice from both ET-induced footpad edema and systemic ET-mediated lethality.

75 mice, VSV, injected subcutaneously into the footpad, entered the proximal lymph node, where it repli

76 sociated with rete ridge-like prominences in footpad epidermis and in dorsal lingual epithelium.

77 by confirming previous observations made in footpad epidermis by showing that the full-length involu

78 RHBDF2 (iRHOM2) regulates thickening of the footpad epidermis through its interaction with K16.

79 gered the formation of sebaceous glands from footpad epidermis, in regions normally devoid of hair fo

80 odeling, we demonstrate that in normal mouse footpad epidermis, transition of KCs from basal epiderma

81 ated peptide-positive, free nerve endings in footpad epidermis.

82 Soluble footpad extracts induced the same changes in NBFL neurob

83 cholamine production in neurons treated with footpad extracts.

84 njected into the subcutaneous space of mouse footpads, film-embedded IgG were retained locally, with

85 also reveal similarities in propatagial and footpad form between basal paravians and modern birds, e

86 generated following s.c. immunization in one footpad generate secondary responses to soluble Ag given

87 Using a model of footpad HSV-1 infection in Rag1(-/-) mice, we observed t

88 h the pVR1012-Ag2 construct mounted a strong footpad hypersensitivity and their spleen cells secreted

89 coccidioidomycosis and elicited delayed-type footpad hypersensitivity responses in Coccidioides-immun

90 he recombinant Ag2-GST protein did not mount footpad hypersensitivity to C-ASWS or the recombinant Ag

91 directly into the lumen of the loop prior to footpad immunization.

92 the popliteal lymph nodes of mice following footpad immunization.

93 d in response to oral and i.p., but not s.c. footpad, immunization.

94 f sciatic nerves due to a stimulation of the footpad in cohorts of m(+)/db and db/db mice for detecti

95 usly (s.c.) into the dorsal area or the hind footpad in three-dose schedules; the PorB VRP-immunized

96 The comparable levels of parasites in the footpads in the two diet groups and the higher lymph nod

97 activation by deacylation before it left the footpad; in animals that lacked acyloxyacyl hydrolase, t

98 Injection of OSM into the footpad increased CCL21 mRNA expression in the draining

99 st time that L. major infection in the mouse footpad induced influx of iron at the site of infection

100 Injection of EMAP-II into the mouse footpad induces an acute inflammatory response, although

101 ll-established HSV-1 infection models: mouse footpad infection and rabbit ocular infection.

102 ndings were made in experiments with a mouse footpad infection model.

103 displayed decreased virulence in the murine footpad infection model.

104 In vivo footpad infection of C3HeB/FeJ mice for 7 days with L. a

105 Following footpad infection of susceptible mice, ECTV spreads lymp

106 lysis of pathogenesis in the mouse following footpad infection revealed a slight increase in virulenc

107 r) and become activated following a low-dose footpad infection, although the mechanism of activation

108 Additionally, after footpad infection, Mlkl(-/-) mice, but not Ripk3(-/-) mi

109 After footpad infection, natural killer cells and ILC1 cells b

110 y, and in contrast to subcutaneous M. leprae footpad infection, systemic M. leprae-specific gamma int

111 d these mice invariably died after ocular or footpad infection.

112 ILCs, also developed marked arthritis after footpad infection.

113 ow important differences between genital and footpad infections, including independence of spread to

114 tected mice against the development of acute footpad inflammation induced by carrageenan.

115 pontaneous metastasis model originating from footpad injection in severe combined immunodeficient mic

116 o elicit delayed-type hypersensitivity after footpad injection into mice previously immunized against

117 In this study we demonstrate that footpad injection of a recombinant Adv readily targets t

118 ort de novo generation of T(R) upon a single footpad injection of Ag mixed with a classic proinflamma

119 Using a model of intradermal footpad injection of Candida albicans, we observed that

120 After the induction of EIU with a footpad injection of lipopolysaccharide (LPS), female Le

121 Lewis rats were immunized by a single footpad injection of P gamma emulsified in complete Freu

122 biodistribution and serum assays after local footpad injection revealed that the bispecific antibody

123 skin painting and twice more donor DC after footpad injection, whereas migrating DC expressed less C

124 sfer, DTH to H. pylori Ags was determined by footpad injection; gastritis and bacterial colonization

125 the central nervous system of mice following footpad injections.

126 Groups of BALB/c mice were footpad inoculated with either a high dose of POWV with

127 BALB/c mice were footpad inoculated with either a high dose or a low dose

128 SV latency active promoter 2 (vector SLN) by footpad inoculation 2 weeks after STZ administration pro

129 Moreover, mice receiving a VRP footpad inoculation 6, 12, or 24 h prior to an otherwise

130 The mouse hind footpad inoculation model has served as a standard labor

131 Following footpad inoculation of Borrelia burgdorferi, the agent o

132 tion results in enhanced infection following footpad inoculation of cowpox virus, a natural pathogen

133 or anti-B7-2 at the time of sensitization to footpad inoculation of Schistosoma mansoni eggs or induc

134 r results were obtained following ocular and footpad inoculation with KOS/62, a LAT deletion mutant i

135 ce of delayed-type hypersensitivity (DTH) by footpad inoculation with sterile H. pylori sonicate and

136 able to cause lethal neuroinvasive disease (footpad inoculation) whereas KOS caused no disease.

137 ose of these non-neuroinvasive viruses after footpad inoculation, but in cyclophosphamide-suppressed

138 genes was detected by 1 to 3 h following VRP footpad inoculation, reaching peak expression of >100-fo

139 ug susceptibility testing method using mouse footpad inoculation, which requires at least 6 months to

140 maKO/beta2KO mice) were infected with HSV by footpad inoculation.

141 The footpad is relatively transparent, with comparatively fe

142 In contrast, footpads lacked DDCs and Th1-polarizing adjuvants select

143 and Leishmania amazonensis leads to a healed footpad lesion, whereas co-infection of C57BL/6 (B6) mic

144 Krt16-null mice develop footpad lesions that mimic PC-associated PPK, providing

145 astigotes, in which the rapid development of footpad lesions was associated with an increasing number

146 add-backs and single allele knockouts caused footpad lesions.

147 owing inoculation of B. burgdorferi into the footpad, lymph node NK cells from susceptible C3H/HeJ (C

148 responses and unremitting tissue damage upon footpad microabrasion of Ptpn6(spin) mice.

149 inistration of SC-560 in the rat carrageenan footpad model did not affect acute inflammation or hyper

150 isplays a defect at late stages in the mouse footpad model of infection.

151 to block an HSV-1 infection, using the mouse footpad model.

152 es is severely compromised in a BALB/c mouse footpad model.

153 nfiltrate within the draining lymph node and footpad of B6.TNF(-/-) mice resembled that of B6.WT mice

154 s were injected subcutaneously into one hind footpad of C3H (H-2k) mice.

155 e 1 (HSV-1) infections initiated in the hind footpad of C57BL/6 (B6, H-2b) mice is dependent upon the

156 und that B16-F10 melanoma growth in the rear footpad of immunocompetent mice induces marked B cell ac

157 on of the NRF2 activator sulforaphane to the footpad of Krt16-/- mice prevented the development of PP

158 Injection of U1 RNA into the footpad of mice resulted in DC recruitment to draining l

159 pon subcutaneous (s.c.) inoculation into the footpad of mice, a VEE vector containing the complete in

160 ng carcinoma cells into the s.c. site of the footpad of nude mice.

161 The data infer that tumor growth in the footpad of plasminogen-deficient mice is compromised as

162 s on average are active in interdigital hind footpads of albino TH wild-type mice.

163 opolysaccharide (LPS) was injected into hind footpads of C3H/HeN mice; and AqH, collected at 6, 12, 2

164 Cutaneous infection in the footpads of C57BL/6 mice with HSV-1 results in an accumu

165 metacyclic promastigotes inoculated into the footpads of genetically resistant C57BL/6 mice was studi

166 At 4 months, growth of the bacilli in the footpads of GKO mice plateaued a log(10) higher than tha

167 K16 expression is absent in the thinned footpads of irhom2(-/-) mice compared with irhom2(+/+)mi

168 sisting of granuloma Mphi harvested from the footpads of M. leprae-infected athymic nu/nu mice, were

169 with control DCs, isc DCs injected into the footpads of mice demonstrated enhanced migration, which

170 Furthermore, footpads of mice lacking one or both genes contain choli

171 jection of Schistosoma mansoni eggs into the footpads of mice results in a localized Th2 cytokine res

172 To test this, we inoculated the footpads of mice with various amounts of rAAV as well as

173 ion) or coinjected with OVA-pulsed APCs into footpads of naive DO11.10 mice whose draining lymph node

174 We injected the footpads of New Zealand White rabbits with 1.7 or 8.4 nm

175 ers (fLUC and DsRed, respectively), into the footpads of outbred CD-1 mice to simulate transmission b

176 nuclear cells (PBMCs) were injected into the footpads of severe combined immunodeficiency mice to mea

177 cells, but not 3T3control fibroblasts, into footpads of syngeneic and SCID mice results in lesions t

178 e skin and injected one auto-Ag into the two footpads of the same mouse and analyzed the T cell recep

179 ith TAA in vitro and then injected into hind footpads of tumor-immune mice.

180 early passage volar keratinocytes or in vivo footpads of wild-type mice.

181 Following footpad or ocular infection of mice lacking type I IFN r

182 We hypothesized that footpad or ocular inoculation with rAAV8 would result in

183 e-deficient mice were infected with HSV-1 by footpad or ocular routes of infection.

184 eurons by extracts of sweat gland-containing footpads or by leukemia inhibitory factor.

185 y, we demonstrated that coinfection of mouse footpads or rabbit eyes with rAAV vectors and HSV-1 resu

186 ear, subcutaneous (s.c.) inoculation of the footpad, or inoculation of the peritoneal cavity (intrap

187 Viral infection in mouse footpads, peritoneal cavity, brain, and eyes could be de

188 sensory function was assessed by toe pinch, footpad prick, and the toe-spreading reflex.

189 fractionation of rat manchette and epidermis footpad proteins.

190 gG2a, or delayed-type hypersensitivity (DTH) footpad reactions were detected.

191 ot show a decreased response to Ag by either footpad response or in vitro proliferation.

192 of sections of M. leprae-infected nude mouse footpads resulted in strongly positive staining in macro

193 radermal (i.d.) injection of bacteria in the footpad revealed increased Y. pestis-neutrophil interact

194 inoculation by either the intraperitoneal or footpad route.

195 ice after ECTV infection through the natural footpad route.

196 ice after ECTV infection through the natural footpad route.

197 Hypoactivity of NRF2 in Krt16-/- footpad skin correlated with decreased levels or activit

198 coinciding with sex-specific fluctuations in footpad skin glutathione levels.

199 PPK onset is preceded by oxidative stress in footpad skin of Krt16-/- mice and correlates with an ina

200 n lesions and accelerated PPK development in footpad skin.

201 of the suprabasal layer of the rat and human footpad/sole epidermis in both immunoblotting and immuno

202 o-cultures, and extracts of gland-containing footpads stimulated tyrosine phosphorylation of LIFRbeta

203 ermore, extracts from sweat gland-containing footpads suppressed BH4 in cultured mouse sympathetic ne

204 ed by both DNA sequencing of folP1 and mouse footpad susceptibility testing.

205 In WT footpads, sweat gland germs were detected at E17.5.

206 The two sympathetic targets in footpads, sweat glands, and blood vessels lacked substan

207 titers and protection against mortality and footpad swelling after lethal CHIKV challenge.

208 sitivity, CP-481,715 significantly inhibited footpad swelling and decreased the amount of IFN-gamma a

209 type hypersensitivity responses by measuring footpad swelling and measuring in vitro proliferation of

210 in humans and is characterized by persistent footpad swelling and suppurative inflammation.

211 inflammation, as reflected by reduced joint footpad swelling in female CHIKV-infected mice.

212 ens after resolving this infection: enhanced footpad swelling in response to intradermal C. albicans

213 nificantly reduced magnitude and duration of footpad swelling observed in VCAM-1 mutant mice compared

214 ion did not induce local reactogenicity in a footpad swelling test in mice.

215 After 24 h, footpad swelling was assessed as a measure of delayed-ty

216 Footpad swelling was observed after 6 weeks, coincident

217 The magnitude of footpad swelling was significantly reduced in mice recei

218 meters measured, it did cause a reduction in footpad swelling when mice received challenge in the foo

219 dence of arthritis, the arthritis index, and footpad swelling.

220 the disease incidence, arthritis index, and footpad swelling.

221 the disease incidence, arthritis index, and footpad swelling.

222 in these animals reduced L. major titers and footpad swelling.

223 e operative in delayed-type hypersensitivity footpad-swelling reaction and in debilitating meningitis

224 Some groups of animals were footpad tested with C. albicans mannan to assess delayed

225 After their injection into mouse footpads, the gene-transduced IAb+ cells were observed i

226 iters were comparable between viruses in the footpad, there was a significant reduction in virus in t

227 ce were inoculated with CHIKV SL15649 in the footpad, they displayed reduced weight gain and swelling

228 we observed that inflammation as measured by footpad thickness and neutrophil recruitment occurred in

229 The increase in footpad thickness was considered to be edema.

230 somal iron exporter Nramp1 expression in the footpad tissue.

231 the withdrawal responses of the ipsilateral footpad to von Frey hairs and hotplate stimulation.

232 SM increased trafficking of BMDC injected in footpads to draining LN by 2-fold (p = 0.016).

233 ation of 51Cr-labeled, skin-derived DCs from footpads to draining LNs by 50% (n = 9, p < 0.005).

234 We have used rodent footpads to study this process because three populations

235 negative effect of plasminogen deficiency on footpad tumor growth was entirely relieved by superimpos

236 ents, single cells, and emboli shed from the footpad tumor were easily distinguished with the labeled

237 in tumors from plasminogen-deficient mice or footpad tumors from mice that also lacked fibrinogen.

238 icrovascular thrombi were commonplace within footpad tumors from plasminogen-deficient mice, whereas

239 Footpad tumors showed no lymphatic or blood vessel growt

240 Mice bearing B16-F10 melanoma footpad tumors were imaged to assess tumor-induced alter

241 node alterations, as macrophages infiltrated footpad tumors, whereas lymphocytes accumulated in tumor

242 ed survival in C57Bl/6 mice with established footpad tumors.

243 ut not to Ag given s.c. in the contralateral footpad unless LPS is coadministered.

244 inflammatory s.c. challenge in contralateral footpads, unlike lymphadenectomized mice lacking the ori

245 We monitored macrophages exiting mouse footpads using a newly developed in situ pulse labeling

246 to mouse skin by intradermal injection into footpads using in vivo bioluminescence imaging over mult

247 Finally, we show that footpad vaccination of NOD mice with LjN6.2-pulsed dendr

248 n(+) versus KOS), anatomical infection site (footpad versus eye) and infectious virus dose (500 versu

249 LLC tumors--T241 fibrosarcoma growth in the footpad was also restricted by plasminogen deficiency in

250 Enhanced swelling of the footpad was associated with high levels of interleukin 1

251 the DLN after injection of Ag and CFA into a footpad was dramatically reduced after FTY720 treatment.

252 ensory and sympathetic fibers arrived in the footpad was not affected, the normal partitioning of axo

253 autonomic innervation of sweat glands in the footpads was significantly reduced in db/db mice compare

254 CHIKV-specific T cells in the spleen and footpad were investigated using IFN-gamma ELISPOT.

255 Mouse footpads were treated with either the Ad-U(L)20 Rz or an

256 After inoculation of footpads, which lack parasympathetic innervation, the vi

257 fter immunization with rrPorB in Ribi in the footpad while the same vaccine given in the dorsal area

258 e we report C57BL/6 WT mice infected via the footpad with 10(3) to 10(6) CFU of Brucella spp. display

259 on of 3-week-old weanling BALB/c mice in the footpad with DENV2 VRP resulted in high levels of DENV-s

260 hindpaw induced by SCS were measured in the footpad with laser Doppler flowmeters.

261 We immunized mice in the footpad with papain and studied leukocyte recruitment an

262 In this study, we injected the mouse footpad with recombinant WEEV (McMillan) or VEEV (subtyp

263 kout (KO) BALB/c mice were sensitized in the footpad with short ragweed (SRW) allergen and challenged

264 Mice were also injected in the footpad with WEEV.McM expressing DsRed (Discosoma sp.) a

265 eek-old wild-type (WT) C57BL/6J mice via the footpad with WT LACV or the Gc N609D variant and found t

266 Mice injected in their footpads with an LmATP7-overexpressing strain showed sig

267 ible C3H/HeJ mice by inoculation in the hind footpads with Borrelia burgdorferi.

268 adjuvant induced a marked edema of the hind footpads with coincident local production of PGE2.

269 y, athymic (nu/nu) mice were infected in the footpads with Mycobacterium leprae and fed a linoleic ac

270 Mice were infected orally or in the hind footpads with reovirus, and the repertoires of TCR beta-

271 cal allodynia developed in the corresponding footpad within two weeks and persisted throughout the ex

272 observed that following low-dose challenge, footpads without apparent lesions provided an efficient