ライフサイエンスコーパス: blister

1 uman COL7 transgene and induced subepidermal blisters.

2 goid have been reported to have itch without blisters.

3 ude mice neither produced autoantibodies nor blisters.

4 e period delayed autoantibody production and blisters.

5 findings of bullous pemphigoid, itch, and no blisters.

6 cause loss of keratinocyte cell adhesion and blisters.

7 and break the epidermal cohesion, leading to blisters.

8 antibodies against desmoglein 1 (Dsg1) cause blisters.

9 epidermal cells appear before intraepidermal blisters.

10 induces cutaneous erythema, edema and micro-blisters.

11 s to type VII collagen causing mucocutaneous blisters.

12 3) IgG autoantibodies cause life-threatening blistering.

13 prophylactic IL-1ra administration prevented blistering.

14 adjunctive therapy for control of pemphigus blistering.

15 expression, and GM-CSF blockade reduced skin blistering.

16 educed fibulin-2 and did not appear to cause blistering.

17 dermis of wounds, characterized by extensive blistering.

18 -mediated inhibition of DSG3 binding to skin blistering.

19 bsequent MC degranulation, and ultimately BP blistering.

20 r/Thr), also bound Dsg1 and blocked the skin blistering.

21 lustrated in a patient with mucosal-dominant blistering.

22 nocyte layer), leading to cell fragility and blistering.

23 epidermal cell detachment (acantholysis) and blistering.

24 ak of p38MAPK activation but failed to block blistering.

25 desmoglein-1-specific autoantibodies induce blistering.

26 rmolysis bullosa simplex with intraepidermal blistering.

27 to induce painful cutaneous inflammation and blistering.

28 late onset of mild skin fragility and acral blistering.

29 icantly reduced PAO-induced inflammation and blistering.

30 rsenicals-induced cutaneous inflammation and blistering.

31 In early resolvers, blister 15-epi-LxA(4) and leukocyte ALX were low, but in

32 in pemphigus vulgaris patients leads to skin blistering (acantholysis) and oral mucosa lesions.

33 ey become irreversible, leading to epidermal blistering (acantholysis), when AMA synergize with anti-

34 Finally, we also demonstrate that the blistering activity associated with pederin and other me

35 mide, psymberin does not display irritant or blistering activity.

36 Mice with epidermal p38alpha deficiency blister after passive transfer of PV mAbs; however, acan

37 e nerve agents GA, GB, and VX as well as the blister agent HD.

38 in the epidermis, however, resulted in skin blister and hair follicle phenotypes that were considera

39 rast, other instabilities of sheets, such as blistering and cracking, break the homogeneity of shape

40 ries, V-series, and "new" nerve agents), and blistering and incapacitating warfare agents.

41 hanism underlying lewisite-induced cutaneous blistering and inflammation and describe its novel antid

42 hyria and (2) cutaneous porphyrias with skin blistering and photosensitivity: porphyria cutanea tarda

43 l substrate and a protective oxide can cause blistering and spallation of the scale.

44 ility of pathogenic pemphigus IgGs to induce blistering and that both p38 mitogen-activated protein k

45 molysis bullosa (EB) is associated with skin blistering and the development of chronic nonhealing wou

46 Integrin loss in vertebrate skin leads to blistering and wound healing defects.

47 rotected mice from developing intraepidermal blisters and clinical disease induced by PF IgG.

48 ectron microscopy revealed that the nitrated blisters and edge-like carbon structures, enabling highl

49 oped an acute eruption of oral and cutaneous blisters and erosions 2 days after receiving a diphtheri

50 antibodies are related to the occurrence of blisters and erosions may encourage further studies on t

51 pidermal keratinocyte adhesion, resulting in blisters and erosions of the skin and mucous membranes.

52 epidermal junction and, clinically, by tense blisters and erosions on skin or mucous membranes close

53 elong generalized trauma-induced spontaneous blisters and erosions, particularly around the ankles.

54 Cellular infiltrate was isolated by suction blisters and examined by flow cytometry.

55 nti-BP180 IgG failed to develop subepidermal blisters and exhibited a drastic reduction in p38 MAPK p

56 Individuals with RDEB develop painful blisters and mucosal erosions, and currently, there are

57 cts and secretory portions were dilated, and blisters and papules formed on the skin surface in the k

58 Formation of water blisters and phase separation at the adhesive/dentin int

59 mi-lethality; adult survivors developed wing blisters and were flightless due to a lack of intercellu

60 int pain, joint swelling, vesicular lesions (blisters), and rashes from days 1 to 42.

61 kin barrier defect with epidermal abrasions, blistering, and early postnatal lethality, due to a thin

62 ed disorder characterized by skin fragility, blistering, and multiple skin wounds with no currently a

63 cture of tungsten, leading to bubble growth, blistering, and/or to the formation of fuzz.

64 bly of defects such as scars, pleats, folds, blisters, and liquid crystal ripples.

65 Skin breaks, ulcers, blisters, and skin necrosis were significantly more comm

66 reatening autoimmune skin disease, epidermal blisters are caused by autoantibodies primarily targetin

67 While fever blisters are more common, occasionally the cornea is inf

68 r wild-type littermates, do not develop skin blisters, are fertile, and survive >1.5 years.

69 n, who develop symptoms ranging from painful blisters around their mouths and hands to neurological c

70 mutant neutrophils emigrating into a suction blister at 16 hours was the same as the percentage in pe

71 erized by generalized erythema and cutaneous blistering at birth followed by hyperkeratosis and less

72 e of STAT3 mutant neutrophils migrating into blisters at 16 hours was the same as in peripheral blood

73 ular recruitment in cantharidin-induced skin blisters at 24 and 72 hours.

74 83 (74%) of 112 patients had three or fewer blisters at 6 weeks compared with 92 (91%) of 101 patien

75 oportion of participants with three or fewer blisters at 6 weeks.

76 tromal cells, some of which localised to the blisters at the epidermal-dermal boundary.

77 dults with bullous pemphigoid (three or more blisters at two or more sites and linear basement membra

78 oimmune disease with severe and chronic skin blistering, autoantibodies are directed against type VII

79 pemphigoid (MMP) is a heterogeneous group of blistering autoimmune disorders of unknown etiology.

80 arwinylus marcosi, family Oedemeridae (false blister beetles), that had an earlier gymnosperm (most l

81 ementary DNA library from leaf tissue of the blister blight-resistant tea cultivar TRI2043 and functi

82 independent of the targeted epitopes, induce blisters both ex vivo and in vivo.

83 cell surface and blocked PF IgG-induced skin blisters, both clinically and histologically.

84 hibit spontaneous but not induced suprabasal blisters by PV mAbs in mouse passive transfer models.

85 s a disorder of incurable skin fragility and blistering caused by mutations in the type VII collagen

86 Transient embryonic epidermal blistering causes the characteristic defects of the diso

87 Arsenicals are painful, inflammatory and blistering causing agents developed as chemical weapons

88 K2 is also activated in human pemphigus skin blisters, causing translocation of MK2 from the nucleus

89 rmatitis herpetiformis (DH) is an autoimmune blistering condition seen in the context of celiac disea

90 on, with different phenotypes, including the blistering conditions Stevens-Johnson syndrome (SJS) and

91 FINDINGS: MMP is an uncommon, subepithelial blistering conjunctivitis that is commonly associated wi

92 atment with oral prednisolone for short-term blister control in bullous pemphigoid and significantly

93 with doxycycline gives acceptable short-term blister control while conferring long-term safety advant

94 hat interlayer shearing and sliding near the blister crack tip, caused by the transition from membran

95 pyrolytic graphite, utilizing atomic-scale 'blisters' created in the top layer by neon atom intercal

96 246D and D392N) responsible for a C. elegans blistering cuticle phenotype was also investigated.

97 Subepidermal autoimmune blistering dermatoses (AIBD) are prototypic autoantibody

98 Using an IgA-dependent skin-blistering disease as a model system, we demonstrated co

99 Pemphigus vulgaris is a blistering disease associated with autoantibodies to the

100 the major autoantigen of the autoimmune skin blistering disease bullous pemphigoid.

101 mphigus vulgaris (PV) is a potentially fatal blistering disease caused by autoantibodies (autoAbs) ag

102 a is an incurable, often fatal mucocutaneous blistering disease caused by mutations in COL7A1, the ge

103 ophic epidermolysis bullosa is a devastating blistering disease caused by mutations in the COL7A1 gen

104 mphigus vulgaris (PV) is a potentially fatal blistering disease characterized by autoantibodies again

105 garis (PV) is a potentially fatal autoimmune blistering disease characterized by autoantibodies again

106 pemphigoid is a rare subepidermal autoimmune blistering disease characterized by autoantibodies again

107 s pemphigoid (BP), a subepidermal autoimmune blistering disease characterized by autoantibodies direc

108 Pemphigus vulgaris (PV) is an autoimmune blistering disease characterized by autoantibodies to th

109 Bullous pemphigoid (BP) is a subepidermal blistering disease characterized by IgE and IgG class au

110 ullous pemphigoid (BP) is an autoimmune skin-blistering disease characterized by the presence of auto

111 ead to the severe recessive form of the skin blistering disease dystrophic epidermolysis bullosa (RDE

112 A characteristic feature of the skin blistering disease epidermolysis bullosa simplex is kera

113 at provide care for patients with autoimmune blistering disease in Germany, Italy, Singapore, Israel,

114 mphigus foliaceus (PF) is a human autoimmune blistering disease in which a humoral immune response ta

115 Pemphigus vulgaris (PV) is an autoimmune blistering disease in which antibodies against the desmo

116 gus vulgaris (PV) is an autoimmune epidermal blistering disease in which autoantibodies (IgG) are dir

117 mphigus foliaceus (PF) is an autoimmune skin blistering disease mediated by pathogenic autoantibodies

118 Hailey-Hailey disease is a severe genetic blistering disease of intertriginous skin locations that

119 Pemphigus vulgaris (PV) is an autoimmune blistering disease of skin and mucous membranes caused b

120 sis bullosa acquisita (EBA) is an autoimmune blistering disease of the skin and mucous membranes, cha

121 In the autoimmune skin-blistering disease pemphigus vulgaris (PV), autoantibodi

122 Patients with the genetic skin blistering disease recessive dystrophic epidermolysis bu

123 Patients with autoimmune blistering disease seem to have a lower risk of PCP than

124 potentially fatal IgG autoantibody-mediated blistering disease targeting mucocutaneous keratinocytes

125 These mutant mice develop a progressive blistering disease validated at the gross and microscopi

126 from autoantibody-induced arthritis and skin blistering disease, as well as from the reverse passive

127 sis bullosa acquisita (EBA) is an autoimmune blistering disease, characterized by antibodies to type

128 goid (BP), the most frequent autoimmune skin-blistering disease, involves matrix metalloproteinase 9

129 Bullous pemphigoid (BP), a common autoimmune blistering disease, is increasing in incidence and conve

130 ents with this potentially lethal autoimmune blistering disease.

131 ) is a chronic mucocutaneous autoimmune skin blistering disease.

132 (BP) is by far the most frequent autoimmune blistering disease.

133 n desmoplakin can result in devastating skin blistering diseases and arrhythmogenic right ventricular

134 f genome editing as a therapy for congenital blistering diseases and as an antimicrobial agent, and w

135 ithelial and cardiac muscle cells cause skin-blistering diseases and cardiomyopathies.

136 antibody-induced, cell-mediated subepidermal blistering diseases and identified new therapeutic targe

137 Autoimmune blistering diseases are a heterogeneous group of about a

138 In the blistering diseases bullous impetigo and staphylococcal

139 eing described, diagnosis of most autoimmune blistering diseases can now be achieved using standardiz

140 ) and pemphigus vulgaris (PV) are autoimmune blistering diseases characterized by autoantibodies agai

141 tis prophylaxis for patients with autoimmune blistering diseases does not seem to be warranted.

142 ry care physician to the national Center for Blistering Diseases in The Netherlands.

143 n and have implications for the treatment of blistering diseases of the skin.

144 incidence of PCP in patients with autoimmune blistering diseases receiving no routine prophylaxis.

145 argeted by pathogenic autoantibodies in skin blistering diseases such as pemphigus.

146 A total of 801 patients with autoimmune blistering diseases were included in this study; their m

147 heir differential diagnosis of acute febrile blistering diseases, and be aware that certain patients

148 s bullosa (EB), a group of complex heritable blistering diseases, is the topic of triennial research

149 and its dysfunction is linked to human skin blistering diseases.

150 ntinents dedicating their work to autoimmune blistering diseases.

151 Pemphigus is an autoimmune blistering disorder associated with significant morbidit

152 Pemphigus vulgaris (PV) is an epidermal blistering disorder caused by antibodies directed agains

153 EB) is a devastating, often fatal, inherited blistering disorder caused by mutations in the COL7A1 ge

154 ermolysis bullosa (RDEB), a severe heritable blistering disorder caused by mutations in the type VII

155 ermolysis bullosa (RDEB) is a rare monogenic blistering disorder caused by the lack of functional typ

156 implex (EBS) is an incurable, inherited skin-blistering disorder predominantly caused by dominant-neg

157 l epidermolysis bullosa, a lethal hereditary blistering disorder, is usually treated by palliative ca

158 thologic diagnosis of an acquired autoimmune blistering disorder.

159 d healthy volunteers and patients with other blistering disorders such as pemphigus vulgaris.

160 ullosa is a heterogeneous group of heritable blistering disorders with considerable morbidity and mor

161 cally and genetically heterogeneous group of blistering disorders with considerable morbidity and mor

162 rview will focus on the prototypic heritable blistering disorders, epidermolysis bullosa, and related

163 B among the "cell-poor" list of subepidermal blistering disorders.

164 psoriasis, allergic contact dermatitis, and blistering disorders.

165 Using dermal microdialysis, suction blister epidermal samples, and sweat collection, we demo

166 in disorders characterized by intraepidermal blistering, epidermal hyperkeratosis, or abnormalities i

167 Whole-genome microarray analysis of suction-blister epidermis obtained throughout the day revealed a

168 esent a patient with extensive mucocutaneous blisters, epidermolytic palmoplantar keratoderma, nail d

169 in disease manifesting with sub-lamina densa blistering, erosions, and chronic ulcers.

170 dSRF (Blistered) expression in specific regions of the larval

171 biopsy specimens (n = 16), serum (n = 114), blister fluid (n = 23), and primary inflammatory cells f

172 CXCL10 levels were higher in blister fluid (P < .0001) and serum (P < .005) from pati

173 groups when using either serum (P < 0.05) or blister fluid (P < 0.001) specimens from BP patients.

174 ISA (P-ELISA) system, only 2 muL of serum or blister fluid and 70 min were required to detect anti-NC

175 ereas similarities between lipid profiles in blister fluid and epidermis indicated a primarily epider

176 ling lipid mediators in biopsies and suction blister fluid can support studies investigating cutaneou

177 presence of the inhibitory property in burn blister fluid that abrogates the skin extract-mediated a

178 ocesses associated with disease progression, blister fluid, serum, and biopsy specimens were collecte

179 ated a primarily epidermal origin of suction blister fluid.

180 ids, in human dermis, epidermis, and suction blister fluid.

181 f mainly CD15(+) neutrophils was observed in blister fluid.

182 lso showed that abundance of CXCR2 ligand in blister fluids also creates a favorable milieu for the r

183 CVA6 viral particles were identified in the blister fluids and skin lesions by electron microscopy.

184 Blister fluids displayed high levels of IL-6, IL-17, IL-

185 Both sera and/or blister fluids from 14 untreated BP patients were analyz

186 ere, we analyzed cytokines and chemokines in blister fluids of patients affected by dystrophic, junct

187 and CCR2(+) myeloid cells toward EB-derived blister fluids.

188 e dermo-epidermal junction lead to cycles of blistering followed by regeneration of the skin.

189 ed by baseline severity (3-9, 10-30, and >30 blisters for mild, moderate, and severe disease, respect

190 pathogenesis of BP with a specific focus on blister formation and to define conditions inducing derm

191 ymerase-chain-reaction assay, and documented blister formation and wound healing with the use of digi

192 recipitate keratinocyte separation to induce blister formation are unknown.

193 disorders characterized by fragile skin and blister formation as a result of dermal-epidermal mechan

194 ng improved wound healing and a reduction in blister formation between 30 and 130 days after transpla

195 e investigated dominant modification of wing blister formation caused by knock-down of eogt.

196 se of the skin characterized by subepidermal blister formation due to tissue-bound and circulating au

197 ound abundantly in BP lesions, their role in blister formation has remained unclear.

198 e necessary for IgE autoantibody-mediated BP blister formation in a humanized IgE receptor mouse mode

199 mechanisms leading to cell dissociation and blister formation in response to autoantibody binding.

200 ly, inhibiting EGFR prevented PV IgG-induced blister formation in the passive transfer mouse model of

201 ivated eosinophils directly contribute to BP blister formation in the presence of BP autoantibodies.

202 MK2-dependent and -independent mechanisms of blister formation using passive transfer of human anti-D

203 ted in the dermis, and epidermal thickening, blister formation, accumulation of T cells and stromal c

204 ed both peaks of p38MAPK phosphorylation and blister formation, consistent with our previous findings

205 lity disorder characterized by injury-driven blister formation, progressive soft-tissue fibrosis, and

206 astase expression, two proteases involved in blister formation, thereof further demonstrating its rol

207 pyrimidine synthesis alleles suppressed wing blister formation, while removal of uracil catabolism al

208 neutrophil granulocytes, a precondition for blister formation.

209 in an inflammatory response and subepidermal blister formation.

210 ytosolic uracil levels, thereby causing wing blister formation.

211 ical Notch signaling pathway suppressed wing blister formation.

212 ne of affected skin, thereby contributing to blister formation.

213 aration, improved wound closure, and reduced blister formation.

214 s in gene expression compared with unexposed blisters, further underscoring the relatively muted resp

215 olysis bullosa (RDEB), a currently incurable blistering genodermatosis caused by loss-of-function mut

216 Fifteen patients with itch without blisters had immunopathologic findings of bullous pemphi

217 volume in both sexes; however, at 72 hours, blisters had only resolved in females.

218 sms of continued autoantibody production and blistering have been well characterized using AIBD anima

219 ulates both autoantibody production and skin blistering in a prototypical organ-specific autoimmune d

220 ogy and suggest novel strategies to suppress blistering in bulbous impetigo and staphylococcal scalde

221 sease in C57Bl/10.s (H2s), (iii) microscopic blistering in DBA/1J (H2q), (iv) only presence of non-pa

222 chemical sulforaphane (SF) ameliorates skin blistering in keratin 14 (K14)-deficient mice, correlati

223 of p38 MAPK phosphorylation and subepidermal blistering in MC-deficient mice.

224 tly, TP abrogated autoantibody-mediated skin blistering in mice and was effective when applied topica

225 keletal reorganization in tissue culture and blistering in pemphigus mouse models.

226 in pemphigus vulgaris, with mucosal-dominant blistering in the suprabasal layer of the epidermis.

227 lar link between IgE autoantibodies and skin blistering in this murine model of BP.

228 APK blocked the ability of PF IgGs to induce blistering in vivo.

229 es of responders to cantharidin-induced skin blisters in male healthy volunteers: those with immediat

230 d in the basal epidermis, develop suprabasal blisters in skin that are histologically identical to th

231 We observed epicardial blisters in the Cx43 KO hearts that suggest defects in e

232 Loss of Pod1 in mice leads to epicardial blistering, increased SM differentiation on the surface

233 he contribution of this signaling pathway to blister induction in an in vivo model of PF.

234 complement activation is a prerequisite for blister induction, this lack of function compared with I

235 stress, demonstrating that splitting at the blister interface in patient tissue is due to compromise

236 These results indicate that PF IgG-induced blistering is dependent on activation of p38 MAPK in the

237 ive transfer mouse model of BP, subepidermal blistering is triggered by anti-BP180 antibodies and dep

238 followed by hyperkeratosis and less frequent blistering later in life.

239 ) in early resolvers using aspirin increased blister leukocyte ALX but reduced cytokines/chemokines a

240 ised generalized scale-crusts and occasional blisters, mostly induced by trauma, as well as mild diff

241 ntified 21 patients who developed widespread blistering mucocutaneous reactions without any suspected

242 = 1; acute respiratory illness, n = 1; foot blisters, n = 1; perianal dermatitis, n = 1).

243 No blistering occurred during the mean 2.2 years of follow-

244 (SEM) showed characteristics of melting and blistering of TD MPs and shredding and flaking of LS MPs

245 gus vulgaris (PV) is a disease that features blistering of the skin and mucous membranes caused by au

246 adherin desmoglein 3 cause potentially fatal blistering of the skin and mucous membranes.

247 state of all major leukocytes was lower, in blisters of females.

248 At 24 hours, cantharidin formed blisters of similar volume in both sexes; however, at 72

249 Predominance of blisters on hands and feet may be a clinical clue to the

250 n clinical features with predominantly tense blisters on hands and feet, resembling dyshidrosiform pe

251 ic infections to those with a mild fever and blisters on infected individuals' hands, feet, and throa

252 ous dermatoses (AIBD), autoantibodies induce blisters on skin or mucous membranes, or both.

253 mice develop normally without signs of skin blistering or muscular dystrophy.

254 lear quadrupole resonance (NQR) signals from blister packs of medicines has been compared.

255 intraepidermal (pemphigus) and subepidermal blistering (pemphigoid diseases and dermatitis herpetifo

256 This junctional blistering phenocopies defects reported in newborn alpha

257 t3 in the mutant background rescued the wing blistering phenotype, whereas expression of another fami

258 osine cross-linking activity, explaining the blistering phenotype.

259 drome in man, which is characterized by skin blistering, premature skin aging and skin cancer of unkn

260 sociated with the occurrence of erosions and blisters (r = 0.985; P = .006) but not urticarial and er

261 the causative agent for severe mucocutaneous blistering reactions mimicking SCAR.

262 pal pathogen of P. lambertiana is white pine blister rust (Cronartium ribicola J.C. Fischer ex Raben.

263 in pine beetle and the non-native white pine blister rust (WPBR).

264 d fibulin-2-null mice display perinatal skin blisters similar to those in alpha3beta1-deficient mice.

265 eralized skin fragility, trauma-induced skin blistering since infancy, and development of remarkable

266 Desmosomes at blister sites were occasionally split, with PV IgG decor

267 ing, the recruitment of therapeutic cells to blistering skin and to more advanced skin lesions remain

268 The autoimmune blistering skin disease pemphigus is caused by IgG autoa

269 ced by autoantibodies from patients with the blistering skin disease pemphigus vulgaris (PV) IgG is r

270 ion is observed in the autoantibody-mediated blistering skin disease pemphigus vulgaris (PV), we appl

271 dler syndrome (KS) is an autosomal recessive blistering skin disease resulting from pathogenic mutati

272 a group of autosomal dominant and recessive blistering skin diseases in which pathogenic mutations h

273 1 and plakogloben in staphylococcal-mediated blistering skin diseases.

274 bullous pemphigoid are autoantibody-mediated blistering skin diseases.

275 epidermolysis bullosa (RDEB) is an inherited blistering skin disorder caused by mutations in the COL7

276 The blistering skin disorder epidermolysis bullosa simplex (

277 Bullous pemphigoid is a blistering skin disorder with increased mortality.

278 eficient epidermal adhesion is a hallmark of blistering skin disorders and chronic wounds, implicatin

279 kievirus A6 (CVA6) DNA was identified in the blistering skin lesions in 6 of 21 patients.

280 lammatory disease characterized by recurrent blistering skin lesions, bronchiolitis, arthralgia, ocul

281 4) and in women who experienced at least one blistering sunburn (hazard ratio = 2.17, 95% confidence

282 r ability to achieve a tan, and history of a blistering sunburn were associated with a higher risk of

283 escent, and higher lifetime number of severe/blistering sunburns.

284 A pressurized blister test and mechanical resonance are used to measur

285 Here we use a pressurized blister test to directly measure the adhesion energy of

286 Results from the circular blister test, however, display seemingly anomalous behav

287 ated upon different joining mechanisms using blister tests.

288 , RDEB individuals manifest unremitting skin blistering that evolves into chronic wounds, inflammatio

289 croarray examination of ex vivo LC from skin blisters that were exposed to live L3 also showed few si

290 rnal gas pressure can become great enough to blister the oxide layer.

291 With regard to skin blistering, the clinicopathological findings expand the

292 n PV, but may function downstream to augment blistering via Dsg3 endocytosis.

293 rolonged sun exposure (for painful burn with blisters vs. practically no reaction, multivariable-adju

294 that flies mutant for rutabaga, period, and blistered were deficient for experience-dependent increa

295 mouse strains developed autoantibodies, but blisters were exclusively observed in mice carrying H2s.

296 Suction blisters were induced in 1 subject, and exudate fluid wa

297 e dermal side of salt-split skin and induced blisters when transferred into healthy mice.

298 s simplex labialis (HSL; cold sores or fever blisters), which is the most common recurring viral infe

299 t3 or RNA interference to pgant3 resulted in blistered wings, a phenotype characteristic of genes inv

300 A biopsy specimen showed subepidermal blistering with prominent inflammatory cells, including