Archives for Dermatological Research (ARCH DERMATOL RES)
In 1869 the Archives of Dermatological Research was founded as Archiv für Dermatologie und Syphilis by H. Auspitz and F. J. Pick. Continued and edited by A. Neisser L. v. Zumbusch J. Jadassohn W. Pick. Vols. 1-127 (1920) published by Braunmüller Vienna; as of Vol. 128 (1921) by Springer Berlin. From 1921 until 1973 organ of the Deutsche Dermatologische Gesellschaft (Vereinigung deutschsprachiger Dermatologen). As of Vol. 201 (1955) published as Archiv für klinische und experimentelle Dermatologie. As of Vol. 240 (1971) as Archiv für Dermatologische Forschung/Archives for Dermatological Research. As of Vol. 253 (1975) as Archives for Dermatological Research/Archiv für Dermatologische Forschung. As of Vol. 261 (1978) as Archives of Dermatological Research/Archiv für Dermatologische Forschung. As of Vol. 264 (1979) as Archives of Dermatological Research. Archives of Dermatological Research publishes original contributions in the field of experimental dermatology including papers on biochemistry morphology and immunology of the skin. Papers describing new techniques and methods are welcome if they contribute to the further understanding of skin problems. Archives of Dermatological Research guarantees rapid publication of: Original papers · Short communications · Letters to the editor. Archives of Dermatological Research is a highly rated journal with a large international readership. All of the articles are written in English.
- Impact factor2.28Show impact factor historyHide impact factor history
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Other titlesArchives of dermatological research (Online), Archiv für dermatologische Forschung
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Publications in this journal
Article: Studien über Aktinomykose[show abstract] [hide abstract]
ABSTRACT: 1. Die Eigenvaccinebehandlung ist bei der echten refraktären Aktinomykose erfolgreich gewesen, und zwar mit der R-Variante, die stets die stärkste Cutireaktion gab. 2. Bei der Acne actinomycotica wurden die bisherigen guten Eigenvaccineerfolge mit der S-Variante weiterhin bestätigt. 3. Aus Menschenblutascitesagar gelang es bisher stets, den Erreger herauszuzüchten. 4. Wir konnten keine strenge Trennung von aerob und anaerob bei den pathogenen Stämmen machen, da die anaeroben auch zum Teil aerob wachsen können. Umgekehrt gelang es nicht, die aeroben Stämme der Gräser an anaerobes Wachstum zu gewöhnen. 5. Wir züchteten die anaerobe S-Variante von Roggenähren aus verschiedenen Gegenden und können uns vorläufig noch nicht auf einen endogenen Infektionsmodus festlegen, obgleich wir der S-Variante keine ausschlaggebende Bedeutung bei der Entstehung der Aktinomykose beimessen. 6. Die fusiformen Stäbchen und Leptothricheen sind in den Vordergrund getreten und werden in Zukunft unser Arbeitsgebiet neben den Actinomyceten beherrschen. 7. Die aus 14 Fällen gezüchtete R-Variante konnte bisher noch nicht saprophytär aus normalen Mundhöhlen oder außerhalb des menschlichen Körpers gefunden werden. 8. Die Möglichkeit des Virulentwerdens der Proactinomyceten wird erwogen, die Frage der Symbiose von Actinomyceten und fusiformen Stäbchen, bzw. Leptotricheen wird ventiliert und die Beeinflussung des einen Keimes durch Abtötung des anderen für möglich gehalten.Archives for Dermatological Research 05/2012; 185(3):468-492.
Article: Beitrag zur Erythroplasie QueyratArchives for Dermatological Research 05/2012; 185(1):162-187.
Archives for Dermatological Research 05/2012; 62(2):339-350.
Article: Association of haptoglobin phenotypes with the development of Kaposi’s sarcoma in HIV patients[show abstract] [hide abstract]
ABSTRACT: Kaposi’s sarcoma (KS) is a rare cutaneous tumor caused by human herpes virus-8 (HHV-8) infection that preferentially develops in case of severe immunosuppression, such as in HIV/AIDS disease. Haptoglobin (Hp), a polymorphic multifunctional plasma protein, exerts several immunomodulatory effects and is characterized by a genetic polymorphism leading to three major phenotypes (Hp 1-1, Hp 2-1 and Hp 2-2). This study investigated the influence of Hp genetic polymorphism on the development of KS in HIV-positive patients. 661 HIV patients were enrolled in the study with a median age of 35years and a median follow-up time of 57months. Hp phenotyping was performed using hemoglobin-supplemented starch gel electrophoresis. In case of low Hp concentration high pressure gel permeation chromatography (HPGPC) was used. The Hp 1-1 phenotype was associated with a significant higher risk of KS compared to the combined group of Hp 2-1 and Hp 2-2 patients (p<0.0005) which remained significant after adjustment for possible confounding variables (age, gender and AIDS status) (p<0.001). In contrast, the Hp 2-1 phenotype carried the lowest risk. These findings point to the involvement of Hp phenotypes in the pathogenesis of KS, which may be due to a difference in skin immunosurveillance between the Hp phenotypes. KeywordsGenetic polymorphism–Haptoglobin–HIV–Kaposi’s sarcomaArchives for Dermatological Research 05/2012; 303(10):763-769.
Article: RETRACTED ARTICLE: Gln50Ter Polymorphism of Fcγ receptor IIB gene associated with genetic susceptibility to human systemic lupus erythematosus in Chinese populations[show abstract] [hide abstract]
ABSTRACT: The aim of this study was to investigate the role of FcγRIIB gene in susceptibility to systemic lupus erythematosus (SLE) using family-based association methods. In total, 119 patients The aim of this study was to investigate the role of FcγRIIB gene in susceptibility to systemic lupus erythematosus (SLE) using family-based association methods. In total, 119 patients with SLE from 95 nuclear families, aged from 14 to 78years, who met the American College of Rheumatology (ACR) 1997 criteria, with SLE from 95 nuclear families, aged from 14 to 78years, who met the American College of Rheumatology (ACR) 1997 criteria, were recruited, as were 316 family members of these patients. A family-based association analysis was used to explore the were recruited, as were 316 family members of these patients. A family-based association analysis was used to explore the relationship between gene polymorphism and SLE. We studied three single-nucleotide polymorphisms (SNPs, rs10917661, rs5017567, relationship between gene polymorphism and SLE. We studied three single-nucleotide polymorphisms (SNPs, rs10917661, rs5017567, and rs1050499) encoding non-synonymous substitution in the FcγRIIB gene with respect to genetic susceptibility to SLE in collection of 435 subjects from 95 nuclear families. We performed the and rs1050499) encoding non-synonymous substitution in the FcγRIIB gene with respect to genetic susceptibility to SLE in collection of 435 subjects from 95 nuclear families. We performed the genotyping using PCR-restriction fragment length polymorphism method. Among 119 SLE patients, the frequencies of FcγRIIB Gln/Gln,Gln/Ter and Ter/Ter genotypes were 12.7, 60.7 and 26.6%. Univariate (single-marker) family-based association tests (FBATs) demonstrated that genotyping using PCR-restriction fragment length polymorphism method. Among 119 SLE patients, the frequencies of FcγRIIB Gln/Gln,Gln/Ter and Ter/Ter genotypes were 12.7, 60.7 and 26.6%. Univariate (single-marker) family-based association tests (FBATs) demonstrated that variant alleles at a SNP, rs10917661, in exon 2 of FcγRIIB gene were significantly associated with genetic susceptibility to SLE in additive model (exon 2, Z=3.444, P=0.00057). transmission/disequilibrium test (TDT) and sibship disequilibuium test (SDT) analysis showed an excess of the variant alleles at a SNP, rs10917661, in exon 2 of FcγRIIB gene were significantly associated with genetic susceptibility to SLE in additive model (exon 2, Z=3.444, P=0.00057). transmission/disequilibrium test (TDT) and sibship disequilibuium test (SDT) analysis showed an excess of the alleles of 50Ter from heterozygous parents to affected offspring (χ2=10.88, P=0.0013). However, the rs5017567 and rs1050499 SNPs were not found in Chinese population. Our findings provide strong evidence alleles of 50Ter from heterozygous parents to affected offspring (χ2=10.88, P=0.0013). However, the rs5017567 and rs1050499 SNPs were not found in Chinese population. Our findings provide strong evidence suggesting that a FcγRIIB–Gln50Ter loci might be the susceptible factor of SLE in Chinese population. suggesting that a FcγRIIB–Gln50Ter loci might be the susceptible factor of SLE in Chinese population. KeywordsFcγRIIB-Polymorphism-Single nucleotide-Lupus erythematosus-Systemic-Susceptibility-Chinese-Family-based association test (FBAT) KeywordsFcγRIIB-Polymorphism-Single nucleotide-Lupus erythematosus-Systemic-Susceptibility-Chinese-Family-based association test (FBAT)Archives for Dermatological Research 05/2012; 299(1):47-51.
Article: Comparison of stress-induced PRINS gene expression in normal human keratinocytes and HaCaT cells[show abstract] [hide abstract]
ABSTRACT: Psoriasis is a chronic inflammatory skin disease that affects approximately 2–4% of the population. We recently described a novel non-coding RNA, psoriasis susceptibility related RNA gene induced by stress (PRINS), that was overexpressed in non-lesional psoriatic epidermis, and its expression was induced by various stress factors such as serum starvation, contact inhibition, ultraviolet (UV)-B irradiation, viral infection and translational inhibition in HaCaT cells. In the present work we set out to compare the stress and microbial agent-induced PRINS expression in normal human keratinocytes (NHKs) and HaCaT cells. Since nuclear factor-κB (NF-κB) is involved in the cellular stress response, we sought to explore whether there is a connection between the NF-κB and PRINS-mediated signal transduction pathways in NHKs and HaCaT cells. We found that the PRINS expression responded differentially to various stress signals and microbial agents in HaCaT cells and in NHKs: after translational inhibition and UV-B treatment, similar induction of PRINS expression occurred with different time courses while after microbial agent treatment, the PRINS expression was significantly induced in HaCaT cells, whereas we could not detect similar changes in NHKs. To explore whether the known NF-κB abnormalities in HaCaT cells could be related to this differential PRINS expression, we silenced the PRINS gene expression with small interfering RNA (siRNA) in both HaCaT cells and in NHKs and monitored NF-κB signal transduction after lipopolysaccharide (LPS) treatment. Silencing of PRINS had no effect on LPS-induced NF-κB activity either in HaCaT cells or in NHKs. Our results indicate that PRINS probably affects keratinocytes functions independently of NF-κB signalling. KeywordsNon-coding RNA–PRINS expression–NF-κB–HaCaT cells–Normal human keratinocytes–PsoriasisArchives for Dermatological Research 04/2012; 303(10):745-752.
Archives for Dermatological Research 04/2012; 179(5):421-462.
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ABSTRACT: In routine clinical phototesting and in basic research, naked eye dermatological assessment is the “gold standard” for determining the patient’s minimal erythemal dose (MED). In UV-B testing with a divergent, radially attenuating beam of characterised dosimetry, laser Doppler perfusion imaging has been previously used to give quantitative description of reactivity to doses above the MED in addition to a “single-dose” objective determination of the MED itself. In the present paper, the recently developed tissue viability imaging (TiVi) technology is presented for the first time as a reliable, easily applicable, high-resolution alternative to LDPI in the divergent beam testing concept. Data obtained after provocation with a range of doses was analysed in order to determine the reaction diameter, which can be related to the MED using field dosimetry. The dose–response features of exposure above the MED and the relationship between naked eye readings and the diameter were determined from the image data. TiVi data were obtained faster than LDPI data and at a higher spatial resolution of 100μm instead of 1mm. A tool was developed to centre over the erythema area of the acquired image. Response data could be plotted continuously against dose. Thresholding of processed images compared to naked eye “gold standard” readings showed that the normal skin value+4 standard deviations produced a good fit between both methods. A linear fitting method for the dose–response data provided a further method of determination of the reaction diameter (MED). Erythemal “volume under the surface (VUS)” for the reaction provided a new concept for visualising information. TiVi offers advantages over LDPI in the acquisition and analysis of data collected during divergent beam testing. An increased amount of data compared to traditional phototesting is easily and more objectively obtained which increases applicability in the clinical and research environment. KeywordsPhoto-testing–Tissue viability imaging–UV-B–Microcirculation–Polarization spectroscopy–Minimal erythemal doseArchives for Dermatological Research 04/2012; 303(2):79-87.
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ABSTRACT: Exposure to ultraviolet (UV) irradiation has detrimental effects on skin accompanied by the increased metabolism of hyaluronan (HA), a linear polysaccharide important for the normal physiological functions of skin. In this study, the modulation of human keratinocyte response to UVB irradiation by HA (970kDa) was investigated. Immortalized human keratinocytes (HaCaT) were irradiated by a single dose of UVB and immediately treated with HA for 6 and 24h. The irradiation induced a significant decrease in the gene expression of CD44 and toll-like receptor 2 6h after irradiation. The expressions of other HA receptors, including toll-like receptor 4 and the receptor for HA-mediated motility, were not detected in either the control or UVB-irradiated or HA-treated HaCaT cells. UVB irradiation induced a significant decrease in the gene expression of HA synthase-2 and hyaluronidase-2 6h after irradiation. The expressions of HA synthase-3 and hyaluronidase-3 were not significantly modulated by UV irradiation. Interestingly, HA treatment did not significantly modulate any of these effects. In contrast, HA significantly suppressed UVB-induced pro-inflammatory cytokine release including interleukin-6 and interleukin-8. Similarly, HA treatment reduced the UVB-mediated production of transforming growth factor β1. HA treatment also significantly reduced the UV irradiation-mediated release of soluble CD44 into the media. Finally, HA partially, but significantly, suppressed the UVB-induced decrease in cell viability. Data indicate that HA had significant protective effects for HaCaT cells against UVB irradiation. KeywordsHyaluronan–Inflammation–Keratinocyte–Ultraviolet lightArchives for Dermatological Research 04/2012; 303(4):277-284.
Article: The role of KLF4 in UVB-induced murine skin tumor development and its correlation with cyclin D1, p53, and p21Waf1/Cip1 in epithelial tumors of the human skin[show abstract] [hide abstract]
ABSTRACT: The zinc-finger-type transcriptional factor KLF4 is expressed in a variety of tissues including skin. KLF4 can function as either a tumor suppressor or an oncogene, depending on the type of tissue in which it is expressed, by modulating the expression of various factors. To understand the role of KLF4 in human skin cancer and also to evaluate the expression of cyclin D1, p53, and p21Waf1/Cip1 in relation to the expression of KLF4, we evaluated the pattern of KLF4 expression during UVB-induced skin tumor development in SKH-1 hairless mice and in human skin cancer. We also determined whether there are correlations between the expression of KLF4, cyclin D1, p53, and p21 and non-melanoma skin tumors. KLF4 expression was found in the basal layer of non-irradiated control murine skin. Chronic UVB irradiation caused a progressive decrease in KLF4 expression, which was substantially decreased in UVB-induced murine skin tumors. In human precancerous lesions, KLF4 expression was maintained in 64.3% of Bowen’s disease samples and 90.0% of AK samples. In contrast, KLF4 expression was significantly reduced in human cancer lesions (p=0.004). A positive correlation was found between the expression of KLF4 and p21Waf1/Cip1 in AK, whereas there was a negative correlation between the expression of cyclin D1 and p21Waf1/Cip1 in Bowen’s disease. Thus, our results suggest that KLF4 may function as a tumor suppressor in the skin and that the deregulated expression of KLF4 in the context of p21Waf1/Cip1 and cyclin D1 expression may be involved in skin tumorigenesis. KeywordsCyclin D1–Kruppel-like factor 4–p21Waf1/Cip1 –p53–Skin tumorArchives for Dermatological Research 04/2012; 303(3):191-200.
Article: Secretory expression of human ScFv against keratin in Pichia pastoris and its effects on cultured keratinocytes[show abstract] [hide abstract]
ABSTRACT: We have got the humanized antibody with high affinity and specificity against keratin by phage antibody library technology. To improve protein yields and get high affinity and specific anti-keratin antibody, we chose to express it in Pichia pastoris. Anti-keratin ScFv gene from plasmid p3MH/ScFv was subcloned into vector pPIC9K. After confirmed by DNA sequence analysis, the recombinant plasmid pPIC9K/ScFv was transduced into the genome of GS115 P. pastoris. Muts multiple insert transformants were screened by G418 and induced by 5mL/L methanol to express soluble ScFv. After 6days of methanol induction, anti-keratin ScFv was efficiently secreted into the medium. Western blot and ELISA assay proved the expressed protein had specific keratin-binding activity. After purification, we examined its effect on cultured keratinocytes by Cell cycle analysis, Which indicated that human ScFv against keratin 17 can inhibit the proliferation of keratinocytes by influence the synthesize of keratinocyte DNA. The successful expression of anti-keratin ScFv in P. pastoris laid a solid foundation for its further application.Archives for Dermatological Research 04/2012; 301(5):367-372.
Article: Purified proteins from leishmania amastigotes-induced delayed type hypersensitivity reactions and remission of collagen-induced arthritis in animal models[show abstract] [hide abstract]
ABSTRACT: A treatment preparation composed of purified Leishmania (L) antigenic fractions (AS210) induced linear delayed type hypersensitivity (DTH) reactions over a 1–40μg dose range, in guinea pigs. When a DBA-1 mouse collagen induced arthritis (CIA) model was used to compare AS210 treatment against: a polyvalent vaccine (AS110-1), a monovalent vaccine (AS110-2) and placebo, the AS210 treated mice had the least amount of forepaw inflammation and the lowest mean arthritis scores (MAS). When MAS for day(s) 1–40 were analyzed using one way ANOVA, statistically significant (P<0.05) differences were seen for the following study groups: PBS versus Dexamethasone and PBS versus AS210. Subsequently, the ANOVA analysis results were corroborated by the Mann–Whitney test: analysis of the first group (P<0.001) and analysis of the second group (P<0.001). Comparison between dexamethasone and AS210 at different time intervals by Mann–Whitney test were as follows: day 0–day 5 both treatments had equal values (P=1.00), from day-7 to 20 AS210 treatment had lower MAS values than dexamethasone (P=0.037), and from day-21 to 30, AS210 MAS were similar to dexamethasone values (P=0.319). No statistical difference was observed between AS110-1, AS110-2, and placebo groups. KeywordsRheumatoid arthritis-Psoriatic arthritis-Mice collagen model-Immunotherapy-Leishmania-Amastigotes antigensArchives for Dermatological Research 04/2012; 302(8):567-581.
Article: Impaired cutaneous wound healing with excess granulation tissue formation in TNFα-null mice[show abstract] [hide abstract]
ABSTRACT: We examined the effects of lacking tumor necrosis factor α (TNFα) on the healing process of a cutaneous wound in mice using TNFα-deficient mice. A full-thickness circular cutaneous wound 5.0mm in diameter was produced in the dorsal skin of wild-type (WT) or TNFα-null (KO) mice. After specific intervals of healing, the healing pattern was evaluated by macroscopic observation, histology, immunohistochemistry, or real-time reverse transcription-polymerase chain reaction. Effect of Smad7 gene transfer on the healing phenotype of KO mice was also examined. The results showed that loss of TNFα promotes granulation tissue formation and retards reepithelialization in a circular wound in mouse dorsal skin. Immunohistochemistry showed that distribution of macrophages and myofibroblasts in newly generated granulation tissue seemed similar between WT and KO mice. However, lacking TNFα enhanced mRNA expression of TGFβ1 and collagen Iα2 in such tissue. Smad7 gene transfer counteracted excess granulation tissue formation in KO mice. In conclusion, lacking TNFα potentiates Smad-mediated fibrogenic reaction in healing dermis and retards reepithelialization in a healing mouse cutaneous wound.Archives for Dermatological Research 04/2012; 301(7):531-537.
Article: Prevalence and significance of human parvovirus variants in skin from primary cutaneous T cell lymphomas, inflammatory dermatoses and healthy subjects[show abstract] [hide abstract]
ABSTRACT: Primary cutaneous T cell lymphomas (CTCL) represent a heterogeneous group of T lymphomas. Virus involvement in CTCL pathogenesis has been extensively investigated, but no data are available as to a causative role of parvovirus B19. The prevalence of parvovirus variants (B19, LaL1/K71, V9) was investigated by using two nested PCRs and a genotype-2 semiquantitative PCR (Q-PCR). Parvovirus DNA was detected in similar percentage in healthy skin controls (40%; n=42), inflammatory dermatoses (ID) (41%; n=80) and CTCL (34%; n=76). Among variants, genotype-2 was more prevalent in ID (26%) and CTCL (22%) than in normal skin (14%; p<0.05). genotype-3 was never found in normal skin and was rare in ID. The only four pathological skin samples with a quantifiable genome copies/μg DNA values in Q-PCR were ID. In conclusion, despite the skin represent a reservoir for genotype-1, parvovirus infection is not involved in the etiopathogenesis of CTCL.Archives for Dermatological Research 04/2012; 301(9):647-652.
Article: Immunohistochemical study on topoisomerase IIα, Ki-67 and cytokeratin-19 in oral lichen planus lesions[show abstract] [hide abstract]
ABSTRACT: Oral lichen planus (OLP) is a chronic muco-cutaneous inflammatory disease defined as a precancerous condition. We determined the expression patterns of proliferation markers topoisomerase IIα (topo IIα) and Ki-67 and an intermediated filament protein cytokeratin-19 (CK-19) in atrophic OLP. These markers were selected because our recent microarray analysis indicated they might aid in identification of potentially malignant lesions. The expression patterns were correlated with the DNA content of these lesions shown to be useful in detection lesions at risk for malignant transformation of OLP. A series of 81 formalin-fixed, paraffin-embedded biopsies from 70 patients suffering from atrophic OLP were immunostained with monoclonal antibodies against topo IIα, Ki-67 and CK-19 using standard methods. Of the 70 patients, there were eight patients who had dysplastic changes in OLP lesions. During the follow-up, altogether five patients got cancer in the OLP area even though no dysplastic changes were present in the preceding lesion. On light microscopy, 500 cells were examined in the basal and parabasal epithelial layers of biopsy samples at 400× magnification. All biopsy samples were topo IIα positive and approximately 70% of the counted cells were positive. Strong staining of topo IIα was significantly correlated with dysplasia (P=0.019), basal cell hyperplasia (P=0.005) and ulceration (P=0.008) in the samples. Ki-67 was expressed in all samples but only 36% of the cells were positive. CK-19 positivity was found in 29% of the specimens. Histological parameters were not related to either Ki-67 or CK-19. The comparison of the staining patterns with the DNA content of lesions showed that strongly stained cells with topo IIα were significantly more frequent in the samples with 2.5cER higher than 15% than in those below 15% (P=0.013; Mann–Whitney). The percentage of the measured cells is 2.5cER exceeding the 2.5c value on the DNA scale. We earlier showed that this cut-off value of 2.5cER discriminated DNA aneuploidy. To conclude, topo IIα is a proliferation and also an apoptotic marker in atrophic OLP lesions and it might have a predictive value in oral lichen planus lesions prone to develop malignancy.Archives for Dermatological Research 04/2012; 298(8):381-388.
[show abstract] [hide abstract]
ABSTRACT: Darier’s disease (DD, MIM 124200) is an autosomal dominant inherited disease. It is usually present in teenagers or adults with multiple keratotic papules or plaques in seborrheic areas. Pathogenic mutations in the ATP2A2 gene have been identified. It encodes the sarcoplasmic or endoplasmic reticulum Ca2+ ATPase isoform 2 (SERCA2). Polymerase chain reaction and direct sequencing of the full coding sequence of ATP2A2 gene were performed to identify the mutation in this family. In this report, we identified a novel mutation of ATP2A2 gene in a Chinese family with DD. It is a novel heterozygous nucleotide G→T transition at position 2,282 in exon 15 of the ATP2A2 gene. Our study expands the database on the ATP2A2 gene mutations in DD. KeywordsDarier’s disease-Mutation analysis- ATP2A2 geneArchives for Dermatological Research 04/2012; 302(4):311-314.
Article: The UV response of the skin: a review of the MAPK, NFκB and TNFα signal transduction pathways[show abstract] [hide abstract]
ABSTRACT: The sun emits different types of ultraviolet (UV) light. Our skin is a natural target of UV radiation which is involved in vitamin D3 production in our body. UV radiation at high doses is an environmental carcinogen which can elicit skin damage as well as inducing skin cancer. It can mediate inflammatory and immunological reactions through activation of receptors, DNA/RNA damage and production of reactive oxygen species. It is also involved in the release of pro-inflammatory cytokines, of which TNFα has been implicated in tumorigenic activities. In order to mediate its effects, UV radiation is known to activate multiple signalling cascades such as the p38 MAPK, Jun N-terminal kinase, extracellular signal-regulated kinase 1/2 and NFκB pathways in skin cells. The role each of these pathways plays in mediating the release of cytokines such as TNFα remains to be fully characterized. Once the function of these pathways is known, this information may provide for the formulation of therapy which will prevent the release of immunosuppressive cytokines resulting in a reduction in skin cancer formation.Archives for Dermatological Research 04/2012; 302(1):5-17.
Archives for Dermatological Research 04/2012; 73(2):245-300.
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