ライフサイエンスコーパス: UVB

1 UVB irradiation (290-320 nm) is used to treat skin disea

2 UVB irradiation alone and UVB with heat rekindling are t

3 UVB irradiation significantly increased vitamin D levels

4 UVB irradiation significantly upregulated the expression

5 UVB is a component of solar radiation primarily responsi

6 UVB light is considered the major environmental inducer

7 UVB radiation exposure also increased cell growth as ass

8 UVB skin exposure leads to cGAS-activation and both loca

9 UVB stimulated CRH gene and protein expression in the br

10 UVB stimulated plasma levels of CRH, Ucn, beta-END, ACTH

11 UVB wavelengths of light induce the formation of photopr

12 UVB wavelengths of light induce the formation of photopr

13 l, whereby mice were exposed to 180 mJ/cm(2) UVB two times per week for 28 weeks, we determined the e

14 R4(+/+)) mice were subjected to 90 mJ cm(-2) UVB radiation locally, DNA damage in the form of cyclobu

15 of simulated sunlight exposure (5100 J/m(2) UVB and 1.2 x 10(5) J/m(2) UVA), neither MALDI-TOF-MS no

16 increases in 25(OH)D concentrations after 4 UVB treatments and largest decreases in 25(OH)D concentr

17 -filtered FS-40 sun lamps (approximately 60% UVB and 40% UVA).

18 6-formylindolo[3,2-b] carbazole (FICZ), is a UVB photoproduct of tryptophan and a powerful UVA chromo

19 Using a UVB initiation-promotion protocol, whereby mice were exp

20 Hypophysectomy abolished UVB stimulation of plasma, but not of skin CORT levels,

21 utophagy inhibitor 3-methyladenine abrogated UVB-induced cell growth.

22 Knockdown of rictor but not raptor abrogated UVB-induced mitophagy responses.

23 anoyl-phorbol-13-acetate treatment and acute UVB exposure.

24 ermal cyclopyrimidine dimers following acute UVB exposure are equivalent in the presence or absence o

25 veral recurring UV mutations following acute UVB radiation affecting multiple genes including HRNR, T

26 als new UV mutation features following acute UVB radiation and identifies novel UV mutation hotspots

27 After UVB treatments, rs10741657 in CYP2R1 and rs4588 in GC pr

28 ylating agent, 5-aza-2'-deoxycytidine, after UVB exposure.

29 role of Dsg1 in aiding differentiation after UVB damage was tested.

30 cyclobutane pyrimidine dimers 24 hours after UVB radiation.

31 analysis of the skin of IL1r(-/-) mice after UVB exposure showed decreased gene expression of proinfl

32 of TLR4(+/+) mice than TLR4(-/-) mice after UVB exposure.

33 eased expression of both HMGB1 and MX1 after UVB exposure.

34 ucing a signal for cellular protection after UVB carcinogenesis provocation.

35 ht to test whether skin barrier repair after UVB damage is dependent on the activation of TLR3.

36 lied DHA potentiate cellular defense against UVB-induced skin inflammation and photocarcinogenesis th

37 excellent protectors of melanocytes against UVB-induced pathology.

38 d gene expression program to protect against UVB-, chemotherapy- and vemurafenib-induced apoptosis.

39 lsalicylic acid [ASA]) could protect against UVB-induced DNA damage and skin carcinogenesis.

40 esults indicate that ASA can protect against UVB-induced inflammation in skin and reduce UVB-induced

41 in natural amalgamation, may protect against UVB-mediated skin carcinogenesis.

42 xygenase-1 in the skin and protected against UVB-induced oxidative stress, inflammation and papilloma

43 powder-mediated protective response against UVB-induced skin cancer was accompanied by enhanced DNA

44 n (UVR) indicators and stratified by ambient UVB of residence and body mass index (BMI).

45 n sub-analyses of subjects with high ambient UVB of residence and of subjects with BMI < 25 kg/m(2).

46 tly increased after toll-like receptor 2 and UVB treatment in lupus keratinocytes, and neutralization

47 ng ultraviolet B (UVB) irradiation alone and UVB irradiation with heat rekindling.

48 UVB irradiation alone and UVB with heat rekindling are translational models of inf

49 l concentrations between oral vitamin D3 and UVB groups (difference in median of oral vitamin D3 minu

50 ow that LITE-1 directly absorbs both UVA and UVB light with an extinction coefficient 10-100 times th

51 peaks of the ZnO-NPs existed in both UVA and UVB region.

52 OH chemistry (e.g. VOC photolysis in UVA and UVB) is not sufficiently represented under some conditio

53 -simulated UVR (ssUVR), a mixture of UVA and UVB, are not well characterized.

54 reduce the transmittance of incident UVC and UVB light by up to 90%, and UVA transmittance by up to 2

55 eak intensities of radiation in both UVC and UVB range while remaining visible-blind, and a high sign

56 s on 25(OH)D concentrations after artificial UVB irradiation and supplementation by vitamin D(3)-fort

57 trations in the same manner after artificial UVB-induced vitamin D and consumption of vitamin D(3)-fo

58 centrations after a given dose of artificial UVB irradiation and 25 single nucleotide polymorphisms l

59 ere cultivated during exposure of artificial UVB.

60 type and exposed to a gradient of artificial UVB.

61 uggest that N.oceanica exposed to artificial UVB could be used as a new natural source of vitamin D(3

62 clusion, we demonstrated that Rg1 attenuated UVB-induced GC insensitivity.

63 ts were well correlated to the daily average UVB light intensity corrected for light screening incorp

64 vitamin D in response to ultraviolet type B (UVB) light.We tested the hypothesis that, in vitamin D-d

65 te machinery that responds to ultraviolet B (UVB) and functions critically to convert the keratinocyt

66 idemiological studies suggest ultraviolet B (UVB) component (290-320 nm) of sun light is the most pre

67 s of inflammatory pain, using ultraviolet B (UVB) irradiation alone and UVB irradiation with heat rek

68 In response to sublethal ultraviolet B (UVB) irradiation, human keratinocytes transiently block

69 nflammatory pain that involve ultraviolet B (UVB) irradiation, which can employ peripheral and centra

70 Ultraviolet B (UVB) light is the principal aetiological factor associat

71 ming human telomeric DNA with ultraviolet B (UVB) light results in the formation of anti cyclobutane

72 ated secondary to exposure to ultraviolet B (UVB) radiation (whether from the sun or from an artifici

73 Ultraviolet B (UVB) radiation is a natural nonchemical stressor posing

74 cancer development induced by ultraviolet B (UVB) radiation is dependent on its gene dose.

75 found that the proportion of ultraviolet B (UVB) radiation-induced C>T transitions differed signific

76 urated fatty acids (PUFAs) on ultraviolet B (UVB)-induced skin inflammation and photocarcinogenesis u

77 Ultraviolet (UV) B (UVB, 280-310 nm) results in isomerization of 7-dehydroch

78 d the epidermis of untreated and narrow band UVB (NBUVB)-treated human vitiligo skin.

79 s for vitiligo repigmentation is narrow-band UVB (NBUVB), but how the hair follicle melanocyte precur

80 (n = 60) and those who received narrow-band UVB exposure (n = 58) </=6 mo.There was no difference in

81 ells from 12 patients undergoing narrow-band UVB phototherapy and 12 corresponding healthy controls r

82 n and vitiligo skin treated with narrow-band UVB.

83 pin splitting of the uppermost valence band (UVB) and the lowermost conduction band (LCB) in bulk and

84 d expression of ATF4 and CHOP protein before UVB irradiation significantly enhanced apoptosis, sugges

85 There were strong associations between UVB exposure and post-holiday levels of T-T dimers and v

86 to chemically induced double strand breaks, UVB and ionizing radiation.

87 gulator of immune responses, is activated by UVB irradiation in the skin.

88 NOX1 is uniquely present and activated by UVB radiation with biphasic expression of the enzyme imm

89 e that aqueous photochemical aging (aging by UVB and UVA photolysis; as well as OH oxidation), as wel

90 eral sensitisation in both species driven by UVB irradiation, with a clear mechanical and thermal hyp

91 t protection against the effects elicited by UVB radiation; however, there was no efficient protectio

92 fy mechanisms regulating body homeostasis by UVB through activation of the HPA axis that originate in

93 Potentially mutagenic DNA lesions induced by UVB (wavelengths 280-320 nm) are important risk factors

94 xpression of ATF4 or CHOP was not induced by UVB as compared with traditional ISR activators.

95 Loss of eIF2alpha-P induced by UVB diminished G1 arrest, DNA repair, and cellular senes

96 y barrier repair following injury induced by UVB irradiation.

97 ative stress after corneal damage induced by UVB irradiation.

98 vitamin D2 production in dried mushrooms by UVB irradiation.

99 ant response is that ATF4 mRNA is reduced by UVB, and despite its ability to be preferentially transl

100 ipid barrier formation and down-regulated by UVB radiation.

101 melanoma-competent MCSCs upon stimulation by UVB, which induces MCSC activation and translocation via

102 loped multiple epidermal cysts after chronic UVB exposure.

103 mous cell carcinoma onset induced by chronic UVB.

104 t in the presence or absence of LCs, chronic UVB-induced p53 mutant clonal islands expand more readil

105 ir and innate immune response after damaging UVB exposure.

106 advanced glycosylation end product decreased UVB-induced resistance to apoptosis (P < 0.05).

107 in we show that LC-intact epidermis develops UVB-induced tumors more readily than LC-deficient epider

108 ison of UV mutation profiles under different UVB radiation conditions revealed that T > C transition

109 sphorylated STAT3 after exposure to low dose UVB.

110 n cell proliferation in response to low dose UVB.

111 ppm wt/vol, applied on rabbit corneas during UVB irradiation and healing (UVB doses 1.01 J/cm(2) once

112 The molecular events that occur during UVB-induced skin carcinogenesis are poorly understood la

113 In addition to its panoply of effects, UVB (290-320 nm) radiation can specifically affect vario

114 cyte into a pain-generator cell after excess UVB exposure.

115 a major cause of premature aging, following UVB exposure to human reconstructed skin tissue.

116 ression increases in the epidermis following UVB treatment.

117 in TC-PTP-deficient keratinocytes following UVB irradiation.

118 SR is deleterious in keratinocytes following UVB.

119 epithelial cells in wild-type mice following UVB treatment.

120 yed a delay in skin barrier repair following UVB damage.

121 the inhibition of DNA replication following UVB irradiation.

122 ir rate, apoptosis, and senescence following UVB exposure, here we used cultured human keratinocytes

123 uate the roles of PTK6 in the skin following UVB-induced damage, we exposed back skin of Ptk6 +/+ and

124 gnificantly reduced cell viability following UVB exposure in comparison with untreated TC-PTP-deficie

125 lational control reduced viability following UVB that was alleviated by cycloheximide (CHX), indicati

126 enterococci and E. coli after correcting for UVB light screening, suggesting that although the exogen

127 on, however, mast cells were dispensable for UVB-induced immune suppression, whereas basophil-derived

128 ed into greater chemopreventive efficacy for UVB-induced squamous cell carcinoma than melanoma mouse

129 Our data show that AREG is essential for UVB-induced CHS suppression.

130 n mouse skin, SIRT1 is haploinsufficient for UVB-induced DNA damage repair and expression of xeroderm

131 rea, we have developed an in vitro model for UVB-induced skin cancer using immortalized human epiderm

132 activation in mitochondria is necessary for UVB-induced mitophagy.

133 itative adverse outcome pathways (qAOPs) for UVB.

134 al for use as a chemopreventive strategy for UVB radiation-induced malignancies.

135 ne-thrombocytopenic patients when tested for UVB tolerance.

136 Furthermore, SFN rescued cells from UVB-induced toxicity in dose-dependent fashion, which wa

137 and its metabolites protect melanocytes from UVB-induced DNA damage and oxidative stress through acti

138 ate consumption will reduce photodamage from UVB irradiation and alter the composition of the skin mi

139 Skin from UVB-irradiated C57BL/6 mice receiving 0.4 mg ASA daily b

140 corneas during UVB irradiation and healing (UVB doses 1.01 J/cm(2) once daily for four days).

141 larger bullseyes are associated with higher UVB incidence.

142 hich is responsible for DNA demethylation in UVB-exposed skin.

143 PTK6 activation was detected in UVB-induced tumors, and this correlated with increased a

144 ated the anti-inflammatory effects of Dex in UVB-irradiated mouse skin.

145 d to contribute to the gender differences in UVB-induced vitamin D production and to its reversal of

146 e p38alpha is restricted to the epidermis in UVB-exposed skin, and that p38alpha ablation targeted to

147 An SD increase in UVB exposure at age 14 to 19 years (OR, 0.81; 95% CI, 0.

148 stored Dex responsiveness to inflammation in UVB-irradiated HaCaT cells.

149 prabasilar epidermis, yet the role of LCs in UVB-induced carcinogenesis is largely unknown.

150 icantly decreased the number of mutations in UVB-irradiated keratinocytes.

151 data demonstrate that LCs have a key role in UVB-induced cutaneous carcinogenesis and suggest that LC

152 ere we determined whether AREG has a role in UVB-induced, Treg cell-mediated suppression of CHS react

153 r Hmga2 in the skin plays a critical role in UVB-mediated melanomagenesis.

154 m intakes are low with little seasonality in UVB-exposure.

155 s consistent with the dual roles of SIRT1 in UVB-induced skin tumorigenesis.

156 ntion of oxidative and nitrosative stress in UVB irradiated corneas, which may represent a novel prop

157 o profile single nucleotide substitutions in UVB-irradiated primary human keratinocytes.

158 g inhibition of chromosomal DNA synthesis in UVB-irradiated keratinocytes.

159 ither photoaction spectra or total, incident UVB irradiance.

160 on from different damaging factors including UVB.

161 in ex vivo and indicate that SP may increase UVB mutagenesis and skin cancer risk in certain individu

162 Increased UVB exposure was associated with reduced myopia, particu

163 how that honokiol has the ability to inhibit UVB-induced immunosuppression in preclinical model and,

164 Honokiol application also inhibited UVB-induced DNA hypermethylation and its elevation of th

165 Interestingly, UVB initiated a prosurvival mitophagy response by mitoch

166 After intermittent UVB exposure, melanocytes treated with the JAK inhibitor

167 in gaining valuable mechanistic insight into UVB-induced skin carcinogenesis, identification of novel

168 are photosensitive and ultraviolet B light (UVB) exposure worsens cutaneous disease and precipitates

169 y the lower "damaging" wavelengths of light (UVB and UVA from 300-400 nm) but instead is maximally in

170 As a likely UVB photoproduct of intracellular tryptophan, FICZ repre

171 Local UVB radiation of the skin influences systemic immune rea

172 e report that dietary grape powder mitigates UVB-mediated skin carcinogenesis in an SKH-1 hairless mo

173 chanism to minimize the risk of mutagenesis, UVB-irradiated cells also activate a checkpoint signalin

174 nhibits the removal of potentially mutagenic UVB-induced DNA photolesions by nucleotide excision repa

175 rea, using solar simulated UVR or narrowband UVB (311 nm).

176 efit in AA, and phototherapy with narrowband UVB was shown to be effective especially in vitiligo.

177 ach highlights the genetic evolution and non-UVB mutational signatures associated with melanoma devel

178 Together, these novel, UVB-transformed progression model cell lines can be very

179 C57BL/6 mice was exposed to 400 mJ cm(-2) of UVB or was sham irradiated.

180 Direct DNA absorption of UVB photons in a spectral range of 290-320 nm of terrest

181 ce of LL-37, suggesting that the capacity of UVB exposure to promote both double-stranded RNA and LL-

182 ate immunity in promoting the development of UVB-induced p53 mutations, immune suppression, and skin

183 Development of UVB-induced skin carcinoma is a multistep and complex pr

184 R) mice exposed to a single neonatal dose of UVB.

185 Ptk6 -/- SENCAR mice to incremental doses of UVB for 30 weeks.

186 ubrious effects of suberythemogenic doses of UVB irradiation for the skin barrier.

187 The effect of UVB dose on the growth and biochemical composition of th

188 oassays were used to quantify the effects of UVB at multiple levels of biological organization.

189 Effects of UVB light were analyzed in a murine model of CNS autoimm

190 s conducted to revisit the lethal effects of UVB on crustaceans, generate new experimental evidence t

191 Little is known about the efficiency of UVB emitting LEDs tuned to different wavelengths for pro

192 Formation of UVB-induced lesions is not random, and conformational fe

193 kin prostaglandin E(2) levels and indices of UVB-induced DNA damage and delayed squamous cell carcino

194 Induction of UVB-derived mutations yields highly aggressive tumors wi

195 nt difference in the levels of inhibition of UVB-induced immunosuppression amongst mice that were tre

196 TTG transitions, and genome-wide mapping of UVB-induced DNA photoproducts (pyrimidine dimers) showed

197 anical and thermal stimulation in a model of UVB irradiation and in a model of UVB irradiation with h

198 a model of UVB irradiation and in a model of UVB irradiation with heat rekindling.

199 t monocytes and in vivo on a murine model of UVB-induced skin burns.

200 In an acute model of UVB-triggered inflammation, we observed that a single UV

201 Odds ratios (ORs) of UVB, serum vitamin D3 concentrations, vitamin D single-n

202 own, South Africa, has a seasonal pattern of UVB radiation and a predominantly dark-skinned urban pop

203 er increased its activity in the presence of UVB.

204 novel potential target for the prevention of UVB-induced skin cancer.

205 ion and thermoregulation, increased rates of UVB-induced epidermal apoptosis and caused a severe path

206 oteome and thereby preventing the removal of UVB-induced DNA lesions.

207 his study was to determine whether repair of UVB-induced DNA damage is regulated by Toll-like recepto

208 In the setting of UVB-induced DNA damage, we detected time-dependent incre

209 In contrast, the skins of UVB-irradiated invariant NKT cell-knockout (Jalpha18(-/-

210 implications for predicting the hot spots of UVB-induced lesions in nucleic acids.

211 e in median of oral vitamin D3 minus that of UVB: 1.5 mg/dL; 95% CI: -5.0, 7.0 mg/dL).

212 tein A, and we find that its accumulation on UVB-damaged chromatin is partially attenuated in cells w

213 A simple linear regression model based on UVB light intensity appears to be a useful tool for pred

214 ot of skin CORT levels, and had no effect on UVB stimulation of CRH and Ucn levels in the plasma, dem

215 area) had a significant preventive effect on UVB-induced suppression of the CHS response.

216 al found in plants of the genus Magnolia, on UVB-induced immunosuppression using contact hypersensiti

217 ailure to properly suppress DNA synthesis on UVB-damaged DNA templates.

218 D deficiency with either oral vitamin D3 or UVB does not improve the lipid profile.

219 ependent film irradiation with either UVA or UVB dosages upwards of 80 J/cm(2) both reduce UV transmi

220 er different conditions (white light, UVA or UVB for 12 or 24h a day at 18 or 25 degrees C) to maximi

221 steroids, phototherapy (psoralen with UVA or UVB), topical chemotherapy, topical bexarotene, and radi

222 0741657 in CYP2R1 and rs4588 in GC predicted UVB-induced 25(OH)D concentrations as previously shown i

223 ific heterozygous deletion of SIRT1 promotes UVB-induced skin tumorigenesis, whereas homozygous delet

224 tify an essential role for CD1d in promoting UVB-induced cutaneous tissue injury and inflammation.

225 tion of myopia with ultraviolet B radiation (UVB; directly associated with time outdoors and sunlight

226 UVB-induced inflammation in skin and reduce UVB-induced DNA damage in both melanocytes and keratinoc

227 Loss of TC-PTP also reduced UVB-induced apoptosis.

228 ASA reduced UVB-induced 8-oxoguanine and cyclobutane pyrimidine dime

229 ASA similarly reduced UVB-induced sunburn cells, 8-oxoguanine, and cyclobutane

230 and oral consumption of pomegranate reduces UVB-induced skin damage.

231 um C (XPC), a protein critical for repairing UVB-induced DNA damage.

232 ently increases MC1R signaling and represses UVB-induced melanomagenesis in vitro and in vivo.

233 Mechanistically, Rg1 rescued UVB-induced HDAC2 degradation.

234 eous adverse and beneficial effects of solar UVB exposure in holidaymakers.

235 In both species, UVB irradiation produces peripheral sensitisation measur

236 In both species, UVB with heat rekindling produces central sensitisation.

237 the major determinants of vitamin D status (UVB exposure, diet, pigmentation, and genetics).

238 up to 75-fold, and resistance to subsequent UVB-induced apoptosis.

239 We then discuss how the lack of sufficient UVB exposure could have contributed to the rapid increas

240 helial compartment is sufficient to suppress UVB-induced inflammation.

241 attenuates mTORC2 activation and suppresses UVB-induced mitophagy.

242 We conclude that UVB-induced vitamin D synthesis is associated with consi

243 We demonstrate that UVB-transformed HaCaT cells gain enhanced proliferation

244 We demonstrated that UVB exposure exacerbated inflammation and reduced both t

245 We determined that UVB irradiation is a potent inducer of eIF2-P in keratin

246 We previously found that UVB irradiation of the cornea caused the imbalance betwe

247 To test the hypothesis that UVB can activate the hypothalamic-pituitary-adrenal (HPA

248 Combined, our results indicate that UVB-mediated activation of TC-PTP plays an important rol

249 Here, we show that UVB radiation causes nitration and inactivation of MnSOD

250 maintains mitochondrial health and show that UVB-mediated MnSOD inactivation promotes mitophagy and t

251 The UVB-induced reduction in both Dsg1 transcript and protei

252 Inhibition of cGAMP hydrolysis augmented the UVB-triggered IFN-I response.

253 proach for studying XPB and its roles in the UVB DNA damage response in human skin ex vivo and indica

254 COX-2) expression and PGE2 production in the UVB-exposed skin.

255 The spin splittings of the UVB and the LCB near the Gamma-point in the Brillouin zo

256 antly enhanced by increasing the dose of the UVB.

257 plerenone affected XPB protein levels or the UVB response.

258 in UVA exposed skin and its response to the UVB spectrum of the solar UV flux remains unexplored.

259 This process is independent of UVR8, the UVB receptor.

260 ) have been shown to be responsible for this UVB-induced suppression of CHS.

261 rther into biological tissue, as compared to UVB, UVC and ionizing radiation, and cause longlasting d

262 rbing UV irradiation and might contribute to UVB skin protection.

263 rmal differentiation, it also contributes to UVB-induced injury and tumorigenesis in vivo.

264 target Noxa, and sensitizes the epidermis to UVB-induced apoptosis in vivo, while heterozygous SIRT1

265 ced the DNA repair in melanocytes exposed to UVB and stimulated expression of p53 phosphorylated at S

266 e-stranded RNA from keratinocytes exposed to UVB blocked the capacity of these cells to induce adhesi

267 opose a novel mechanism by which exposure to UVB activates a local HPA axis in skin, which in turn ac

268 N/TERT human keratinocytes upon exposure to UVB and the DNA-alkylating chemicals such as methyl meth

269 Exposure to UVB estimated by combining meteorological and questionna

270 Cutaneous exposure to UVB irradiation is an important source of vitamin D.

271 Upon exposure to UVB irradiation, fat-1 transgenic mice exhibited a signi

272 In keratinocytes, exposure to UVB radiation decreased mitochondrial oxidative phosphor

273 receptor 2, 3, or 4 agonists or exposure to UVB radiation.

274 (HaCaT) cells through repetitive exposure to UVB radiation.

275 ted exposure of human primary melanocytes to UVB results in a sustained senescence response, increase

276 Exposure of thrombocytopenic mice to UVB light provokes cutaneous petechial bleeding.

277 erile inflammation caused by overexposure to UVB irradiation (i.e., sunburn) in the mouse plantar ski

278 ith both mutagenesis and a predisposition to UVB-induced cell death but were unique to SP, because ne

279 d from IL1r(-/-) mice were more resistant to UVB-triggered cell death compared with wild-type cells,

280 eIF2alpha-P is cytoprotective in response to UVB by a mechanism featuring translation of a specific s

281 or eIF2alpha-P cytoprotection in response to UVB in human keratinocytes.

282 is stimulated during the initial response to UVB irradiation, which leads to suppression of keratinoc

283 ver, in male mice, the vitamin D response to UVB was attenuated and mineral and skeletal abnormalitie

284 early phase of the inflammatory response to UVB, but it caused a significant increase in the number

285 Sunburn, an acute inflammatory response to UVB-induced cutaneous tissue injury, represents a clinic

286 systems and abrogated two major responses to UVB-induced DNA damage, including the removal of UV phot

287 by defects in multiple cellular responses to UVB-induced DNA damage, including through a failure to p

288 Wild-type mice were more sensitive to UVB and exhibited increased inflammation and greater act

289 of LL-37 can lead to enhanced sensitivity to UVB radiation in rosacea.

290 In the mouse skin and skin tumors, UVB radiation downregulates E-cadherin.

291 d mushrooms can produce ergocalciferol under UVB irradiation.

292 rate that TC-PTP activity was increased upon UVB exposure, and overexpression of TC-PTP in keratinocy

293 ed electron transfer using longer wavelength UVB radiation.

294 Short-wavelength UVB radiation induces sunburn and is a potent immunomodu

295 his study delineates the mechanisms by which UVB regulates protein synthesis in human keratinocytes a

296 iduals in summer, was highly correlated with UVB exposure, and was associated with greater HIV-1 repl

297 adults, the replenishment of vitamin D with UVB exposure would lower LDL-cholesterol concentrations

298 tamin D3 but significant downregulation with UVB.Correcting vitamin D deficiency with either oral vit

299 radiation of cultured human melanocytes with UVB stimulated ROS production, which was reduced in cell

300 tion of elastase activity did not occur with UVB.