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1 relatives were particularly likely to report sunburn.
2 e solar spectrum that does not readily cause sunburn.
3 lla nor sunscreen alone completely prevented sunburn.
4 biopsy specimens 48 hours after experimental sunburn.
5 in indoor tanning had experienced at least 1 sunburn.
6 f hyperthermia, hypothermia, dehydration, or sunburn.
7 ing effects on the skin beyond the immediate sunburn.
8 rns: OR = 2.0 (95% CI 1.0-4.0) for 4+ severe sunburns.
9 3.1 (95% CI 1.7-5.3) for 4+ severe childhood sunburns.
10 y 4% per year of age and by 6% per number of sunburns.
11  higher lifetime number of severe/blistering sunburns.
12 75% of the patients and was characterized by sunburn after brief sun exposure.
13 d the association between indoor tanning and sunburn among US high school students.
14                                              Sunburn, an acute inflammatory response to UVB-induced c
15                           Sunscreens prevent sunburn and may also prevent skin cancer by protecting f
16 ular surface disease, and, in some patients, sunburn and neurological degeneration.
17                            They also suggest sunburn and NMSC etiologies are immunologically linked.
18 udies have assessed the relationship between sunburn and risk of different skin cancers (melanoma, sq
19                                      Because sunburn and skin cancer are causally related, we investi
20 y of individuals with blonde and red hair to sunburn and skin cancer.
21 d, and childhood UVR exposure and history of sunburn and sunlamp use.
22  reduce the prevalence of indoor tanning and sunburn and thus prevent future cases of skin cancer.
23 ians to assess a person's risk of developing sunburn and, by extension, the need for sun protection t
24 s of sun behavior in the US reveal extensive sunburning and use of tanning beds in adolescents and ad
25  previous UVR exposure (represented by prior sunburns and signs of actinic skin damage identified by
26  Sunscreen users reported significantly more sunburns and sunbathing vacations and were more likely t
27 n (ie, sun-safety practices and the risk for sunburn) and alerted users to apply or to reapply sunscr
28 ection (ie, protection practices and risk of sunburn) and alerts (to apply or reapply sunscreen and g
29 ma, higher number of nevi, history of severe sunburn, and light hair color were each associated with
30 ide critical protection against skin cancer, sunburn, and photoaging, a genome-wide perspective of ge
31 olet B light (290 to 320 nm) associated with sunburn, and ultraviolet AII light (320 to 340 nm), and
32 ling for age, sex, lifetime number of severe sunburns, and skin type [BCC: odds ratio (OR), 0.7; 95%
33 r; green, hazel, or blue eyes; a tendency to sunburn; and north European ancestry.
34 = 2.0 (95% CI 1.2-3.1) for 4+ severe teenage sunburns; and OR = 3.1 (95% CI 1.7-5.3) for 4+ severe ch
35 causally related, we investigated UV-induced sunburn apoptosis and erythema in mouse skin as a functi
36              Interestingly, we observed that sunburn apoptosis, inflammatory cytokine induction, and
37 53, which is known to control the process of sunburn apoptosis.
38 adiation on the time course for induction of sunburn (apoptotic) cells and expression of proteins kno
39            These data suggest that childhood sunburns are important in the etiology of nevi.
40 of extremity moles, higher susceptibility to sunburn as a child/adolescent, and higher lifetime numbe
41 that UVA makes a greater contribution toward sunburn at temperate latitudes than under the laboratory
42 ancer risk associated with history of severe sunburns at different body sites (face/arms, trunk, and
43 tle is known about the association of severe sunburns at different body sites with skin cancer risk.
44  not risk of SCC and BCC, when compared with sunburns at other body sites (face/arms and lower limbs)
45 ors often exhibited a concurrent tendency to sunburn, avoid sun protection, and avoid skin cancer scr
46 ors often exhibited a concurrent tendency to sunburn, avoid sun protection, and avoid skin cancer scr
47 llment were also independent predictors, but sunburns, baseline sun exposure, and other sun-protectiv
48 ls after ultraviolet radiation (UVR) through sunburn cell (apoptotic keratinocyte) formation is thoug
49 n epidermal cyclobutane pyrimidine dimers or sunburn cell (SBC) formation were observed between pigme
50 0-320 nm) exposure, thus implicating CHOP in sunburn cell (SBC) formation.
51  We found that the inhibition of UVR-induced sunburn cell formation in PKCepsilon transgenic mice may
52                                              Sunburn cell formation requires the Trp53 tumor suppress
53                                              Sunburn cell formation was found to be dependent on Fas
54 nduced apoptosis in vitro and in vivo (i.e., sunburn cell formation), whereas it did not affect Fas-i
55 nificant decrease in UV-induced hypertrophy, sunburn cell formation, and apoptosis when the mice were
56 tely 8-fold as measured by both erythema and sunburn cell formation.
57 Xpa-/- mice were 7-10-fold more sensitive to sunburn cell induction than wild-type mice, indicating t
58 dependence was seen for epidermal thickness, sunburn cell numbers, dermal thickness, glycosaminoglyca
59 neum thickening, viable epidermal thickening sunburn cell production), as well as dermal alterations
60 tal effects of acute UV irradiation, namely, sunburn cell/apoptosis, inflammation, and a hyperprolife
61  Their skin was analyzed for the presence of sunburn cells (apoptotic keratinocytes) and for Fas and
62 4/Bcl-2 mice developed about 5-10-fold fewer sunburn cells (ie, apoptotic keratinocytes) in the basal
63 hanced the UVB-induced increase in apoptotic sunburn cells 6 h later by 127% and 563%, respectively.
64 owed a dose-dependent increase in numbers of sunburn cells and TUNEL-positive cells although their pr
65 in the numbers of morphologically identified sunburn cells and TUNEL-positive cells was detected as e
66 anced the UVB-induced increases in apoptotic sunburn cells at 6 h by 214% and 467%, respectively, and
67        The UVB-induced increase in apoptotic sunburn cells in Bax(-/-) mice at 6 h after exposure to
68 ddition to C1q, we detected C3 deposition on sunburn cells in both wild-type and C1q-deficient mice,
69        The UVB-induced increase in apoptotic sunburn cells in p53(-/-) mice at 6-10 h after exposure
70  the inhibition of UVR-induced appearance of sunburn cells in PKCepsilon transgenic mice.
71 lated the formation of UVB-induced apoptotic sunburn cells in the epidermis by 96, 120, and 376%, res
72 p21(WAF1/CIP1)-positive cells, and apoptotic sunburn cells in the epidermis.
73 r the first time that C1q is also present on sunburn cells in vivo.
74 p21(WAF1/CIP1)-positive cells, and apoptotic sunburn cells may play a role in the inhibitory effects
75  three strains, as was apoptosis measured as sunburn cells or as keratinocytes containing active casp
76 o, no difference in the rate of clearance of sunburn cells was found in C1q-deficient mice from three
77 of UVB-induced DNA damage and the numbers of sunburn cells were not significantly different in the EG
78 tosis of ultraviolet-damaged keratinocytes ("sunburn cells").
79 imidone dimer, (2) reduced the appearance of sunburn cells, (3) induced extensive hyperplasia and inc
80 orter wavelengths (320-345 nm) elicited more sunburn cells, although these differences did not reach
81 reases in morphologically distinct apoptotic sunburn cells, and decreases in the number of epidermal
82 d by the formation of CPDs and the number of sunburn cells, was resolved more rapidly in the skin of
83  cell carcinomas and suppressed formation of sunburn cells, which are DNA-damaged keratinocytes under
84 ng by flow cytometry, and/or the presence of sunburn cells.
85 reduces UV-induced apoptotic keratinocytes, "sunburn cells." Consequently, Gadd45a-null mice are more
86 evi: OR = 1.9 (95% CI 0.9-3.9) for 3+ severe sunburns compared with none in the last 5 years; OR = 2.
87 orbic acid has been shown to protect against sunburn, delay the onset of skin tumors, and reduce ultr
88 er, the innate immune mechanisms controlling sunburn development are not considered relevant in NMSC
89  of chronically irradiated skin to an acute "sunburn dose" of ultraviolet-B also produced significant
90                                              Sunburn due to cutaneous sensitivity to sunlight exposur
91 7.9%-86.0%) of indoor tanners had at least 1 sunburn during the preceding year compared with 53.7% (9
92 t, hours spent in the summer sun, blistering sunburns during adolescence, and moles, all increased me
93  on whether ultraviolet radiation, including sunburns, early childhood and adolescent sun exposure, a
94                                   In humans, sunburn enhances epidermal expression of TRPV4 and endot
95 traviolet radiation dose-response curves for sunburn/erythema and suppression of the contact hypersen
96                                     Clinical sunburn evaluation of each individual for all exposed bo
97 such as tanning ability and number of severe sunburns experienced throughout life.
98 rradiation, equivalent to a mild to moderate sunburn exposure for intact skin.
99         Individuals with a history of severe sunburns had an increased risk of nevi: OR = 1.9 (95% CI
100 omen who experienced at least one blistering sunburn (hazard ratio = 2.17, 95% confidence interval =
101 novel insights to the existing literature on sunburn history and skin cancer risk.
102 relative risk of SCC associated with painful sunburn history was significantly higher for homozygous
103 VR exposures during childhood and adulthood, sunburn history, and sunlamp use, but we found no signif
104  type, freckle density, age, hair color, and sunburn history.
105 r from 2009 to 2015 and its association with sunburn in 2015.
106 g epidemiological data implicating childhood sunburn in CMM.
107 tes, a single dose of UVR that mimicked mild sunburn in humans induced clonal expansion of the melano
108  In 2015, indoor tanning was associated with sunburn in the adjusted model: 82.3% (95% CI, 77.9%-86.0
109     Thirty-one percent of relatives reported sunburn in the previous summer, compared with 41% of con
110 ion of XRCC1 genotype and lifetime number of sunburns in SCC [likelihood ratio test (2 d.f.), P < 0.0
111 dday sun (days and hours), and the number of sunburns in the last 3 months.
112 e was no significant difference in number of sunburns in the past 3 months (mean, 0.60 in the treatme
113 and minutes) in the midday sun and number of sunburns in the past 3 months were collected.
114 y, as well as more likely to report multiple sunburns in the past year (aPR, 1.21; 95% CI, 1.00-1.45)
115               After adjustment for sex, age, sunburns in the past, and signs of actinic skin damage,
116 RPV4 as a therapeutic target for UVB-induced sunburn, in particular pain.
117                     There was a total of 142 sunburn incidences in the umbrella group vs 17 in the su
118 cholecalciferol) one hour after experimental sunburn induced by an erythemogenic dose of UVR.
119                                              Sunburn is a commonly occurring acute inflammatory proce
120 ed melanomagenesis and strongly suggest that sunburn is a highly significant risk factor, particularl
121                                              Sunburn is characterized by overlapping sequential profi
122 vity of skin types I/II for a given level of sunburn may play a role in their greater sensitivity to
123 elp reduce the risk for skin cancer, prevent sunburns, mitigate photoaging, and treat photosensitive
124      Additionally, lifetime number of severe sunburns modestly altered the effects of the CTLA4 haplo
125                                              Sunburn on all exposed body sites 22 to 24 hours after s
126                                              Sunburn on the trunk appeared to be more closely associa
127 xperimental evidence regarding the effect of sunburns on cutaneous malignant melanoma and the possibl
128 I: 1.00, 1.28; P = 0.051), getting a painful sunburn once (RR = 1.24, 95% CI: 0.98, 1.57; P = 0.073)
129 e beneficial in treating victims from severe sunburn or exposure to other chemical agents known to tr
130 r activities, and number of children who had sunburn or skin irritation.
131 .05; 95% CI, 1.03-1.07; P < .001), number of sunburns (OR, 1.05; 95% CI, 1.00-1.10; P = .047), and hi
132 ; 95% CI, 1.02-1.07; P < .001) and number of sunburns (OR, 1.06; 95% CI, 1.00-1.11; P = .04) were sta
133 % CI, 2.79-11.99]), greater number of severe sunburns (OR, 2.59 [95% CI, 1.31-5.10]), light eye color
134 ction reduces intermediate outcomes (such as sunburn) or skin cancer.
135 ly of sun sensitivity and teenage and recent sunburns: OR = 2.0 (95% CI 1.0-4.0) for 4+ severe sunbur
136 l factors, time spent in the sun, and severe sunburns over three time periods and were asked to count
137 C tumors associated with a history of severe sunburns (P<0.08).
138 hose with a higher lifetime number of severe sunburns (P(interaction) = 0.0074).
139                           Indoor tanning and sunburns, particularly during adolescence and young adul
140  for epidemiological evidence that childhood sunburn poses a significant risk of developing this pote
141 B (UVB) radiation from the sun can result in sunburn, premature aging and carcinogenesis, but the mec
142                          To directly measure sunburn protection offered by a standard beach umbrella
143 n was strongest among those with tendency to sunburn rather than tan.
144 tify candidate eicosanoids formed during the sunburn reaction in relation to its clinical and histolo
145                                          The sunburn reaction is the most common consequence of human
146                   These patients have normal sunburn reactions and are therefore diagnosed later and
147                  These results indicate that sunburn reactions culminate from inflammatory events tha
148 , we examined whether experimentally induced sunburn reactions in mice could be prevented by blocking
149 es have suggested that repeated inflammatory sunburn reactions, which include the induction of cycloo
150 ts aimed for clinically related targets (eg, sunburn reduction).
151 skin cancer and suggest that the etiology of sunburn-related SCC may be significantly different by XR
152 ental studies with mouse models suggest that sunburn resulting from exposure to excessive UV light an
153 atistically significant increase in clinical sunburn scores compared with baseline and had higher pos
154 d not block infiltration of macrophages into sunburned skin; and (ii) RA did decrease autologous and
155                       Patients with an acute sunburning skin phenotype were less likely to develop co
156 rcinomas in the 5 years prior to enrollment, sunburns, sun sensitivity, and recreational sun exposure
157 ponses to a personal interview on history of sunburns, sunbathing, and time spent outdoors.
158 Family history of melanoma, number of severe sunburns, sunburn susceptibility, hair color, and Fitzpa
159      Originally developed to protect against sunburn, sunscreen has been assumed to prevent skin canc
160 tory of melanoma, number of severe sunburns, sunburn susceptibility, hair color, and Fitzpatrick skin
161  studies on hair color, eye color, number of sunburns, tanning ability and number of non-melanoma ski
162 21.0%Delta; women: -28.5%Delta) and, in men, sunburn tendency was associated with less wrinkling.
163          After supplementation, median (IQR) sunburn threshold (minimal erythema dose) was 28 (20-28)
164 ppression of CHS (P < 0.001), and a moderate sunburn (two minimal erythema doses [2 MED]) was suffici
165  can mitigate ultraviolet (UV) light induced sunburn via unknown mechanisms.
166 ction to first summer sun for 1 hour (severe sunburn vs. tan odds ratio (OR)=12.27, 95% confidence in
167  factors, overall baseline history of severe sunburn was more apparently associated with risk of mela
168            The lifetime number of blistering sunburns was also positively associated with BCC risk (p
169 w that skin aging and reported experience of sunburns was proportional to the degree of penetrance fo
170 ugh the absolute risk of SCC associated with sunburns was similar across genotypes, the relative risk
171 ng factors (e.g., lifetime number of painful sunburns), we found a modest increase in risk of SCC (od
172 o achieve a tan, and history of a blistering sunburn were associated with a higher risk of developing
173                       Furthermore, childhood sunburns were related to nevi independently of sun sensi
174                            Age and number of sunburns were significantly associated with the severity
175 n associated with an increased prevalence of sunburn, which is an established skin cancer risk factor
176                     UV overexposure leads to sunburn with tissue injury and pain.
177 , we compared the protection from cumulative sunburn with two sunscreens labeled SPF 6, but with diff
178 screen, protective clothing, shade; multiple sunburns within the past year; previous full-body skin e
179 screen, protective clothing, shade; multiple sunburns within the past year; previous full-body skin e

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