Material assignment for proton range prediction in Monte Carlo patient simulations using stopping-power datasets.

Motivation and objective. For each institute, the selection and calibration of the most suitable approach to assign material properties for Monte Carlo (MC) patient simulation in proton therapy is a major challenge. Current conventional approaches based on computed tomography (CT) depend on CT acquisition and reconstruction settings. This study proposes a material assignment approach, referred to as MATA (MATerial Assignment), which is independent of CT scanner properties and, therefore, universally applicable by any institute. MATERIALS AND METHODS: The MATA approach assigns material properties to the physical quantity stopping-power ratio (SPR) using a set of 40 material compositions specified for human tissues and linearly determined mass density. The application of clinically available CT-number-to-SPR conversion avoids the need for any further calibration. The MATA approach was validated with homogeneous and heterogeneous SPR datasets by assessing the SPR accuracy after material assignment obtained either based on dose scoring or determination of water-equivalent thickness. Finally, MATA was applied on patient datasets to evaluate dose differences induced by different approaches for material assignment and SPR prediction. RESULTS: The deviation between the SPR after material assignment and the input SPR was close to zero in homogeneous datasets and below 0.002 (0.2% relative to water) in heterogeneous datasets, which was within the systematic uncertainty in SPR estimation. The comparison of different material assignment approaches revealed relevant differences in dose distribution and SPR. The comparison between two SPR prediction approaches, a standard look-up table and direct SPR determination from dual-energy CT, resulted in patient-specific mean proton range shifts between 1.3 mm and 4.8 mm. CONCLUSION: MATA eliminates the need for institution-specific adaptations of the material assignment. It allows for using any SPR dataset and thus facilitates the implementation of more accurate SPR prediction approaches. Hence, MATA provides a universal solution for patient modeling in MC-based proton treatment planning.

Corrigendum to "Protective Effects of Soy Oligopeptides in Ultraviolet B-Induced Acute Photodamage of Human Skin".

[This corrects the article DOI: 10.1155/2016/5846865.].

The efficacy of fractional carbon dioxide (CO2) laser combined with terbinafine hydrochloride 1% cream for the treatment of onychomycosis.

BACKGROUND: Although systemic and topical antifungal agents are widely used to treat onychomycosis, oral medications can cause adverse effects and the efficacy of topical agents is not satisfying. Currently, laser treatment has been studied for its efficacy in the treatment of onychomycosis. Our study was aimed to evaluate the efficacy of fractional carbon dioxide (CO2) laser treatment combined with terbinafine cream for 6 months in the treatment of onychomycosis and to analyze the influencing factors. METHODS: A total of 30 participants (124 nails) with clinical and mycological diagnosis of onychomycosis received fractional CO2 laser treatment at 2-week interval combined with terbinafine cream once daily for 6 months. The clinical efficacy rate (CER) was assessed from the percentage of fully normal-appearing nails or nails with ≤5% abnormal appearance, and the mycological clearance rate (MCR) was assessed from the percentage of nails with negative fungal microscopy. RESULTS: The CER was evaluated at 3 time points: at the end of treatment (58.9%), at 1 month after the last treatment (63.5%), and at 3 months after the last treatment (68.5%). The MCRs at 1 month and 3 months after the last treatment were 77.4 and 74.2%, respectively. The evaluation of influencing factors showed significantly higher CER (p < 0.05) in nails of participants with age <50 years, distal lateral subungual onychomycosis (DLSO), superficial white onychomycosis (SWO), nail thickness <2 mm, affected first-to-fourth finger/toenails, Trichophyton rubrum, and Trichophyton mentagrophytes. All participants experienced tolerable mild burning sensation during laser treatment, but there were no other adverse reactions reported. CONCLUSIONS: Fractional CO2 laser treatment combined with terbinafine cream for 6 months was an effective and safe method for the treatment of onychomycosis. There were 5 factors that positively influenced the treatment outcome: age, clinical type of onychomycosis, nail thickness, involved nail, and species of fungus.

The efficacy of fractional carbon dioxide (CO2) laser combined with luliconazole 1% cream for the treatment of onychomycosis: A randomized, controlled trial.

BACKGROUND: To evaluate the efficacy of fractional carbon dioxide (CO2) laser combined with luliconazole 1% cream for the treatment of onychomycosis and to compare it with that of fractional CO2 laser alone. METHODS: This was a randomized, parallel group, 2-arm, positive-controlled, single-center, superiority trial with a 1:2 allocation ratio. Sixty patients with clinical and mycological diagnosis of onychomycosis were enrolled from the Dermatology Department of the First Affiliated Hospital of Nanjing Medical University in Nanjing, China from March 2015 to May 2015. Patients were randomized following simple randomization procedures (computerized random number generator) into 2 groups; L group only received 12 sessions of laser treatment at 2-week interval for 6 months, while L + D group received 12 sessions of laser treatment at 2-week interval combined with luliconazole 1% cream once daily for 6 months. This was not a blind trial. The main outcome measures were the clinical efficacy rate (CER) assessed from the percentage of fully and >60% normal-appearing nails and the mycological clearance rate (MCR) assessed from the percentage of nails with negative fungal microscopy. There were no changes to trial outcome measures after the trial commenced. RESULTS: A total of 60 patients (N = 233 nails) completed treatments and follow-up, and were randomized and divided into 2 groups: L group (31 patients, N = 108 nails) and L + D group (29 patients, N = 115 nails). The CER and MCR of L + D group were 69.6% and 57.4%, respectively. L + D group showed significantly higher CER (69.6% vs 50.9%; χ = 8.1, P = 0.004) and MCR (57.4% vs 38.9%; χ = 7.6, P = 0.006) compared with those in L group. Some patients experienced mild pain during laser treatment, but there was no bleeding or oozing during or after treatment. There were no adverse effects reported during the observation period. CONCLUSION: Fractional CO2 laser treatment combined with 1% luliconazole cream for 6 months was an effective and safe method for the treatment of onychomycosis, and had a higher efficacy than fractional CO2 laser treatment alone.

Protective Effects of Soy Oligopeptides in Ultraviolet B-Induced Acute Photodamage of Human Skin.

Aim. We explored the effects of soy oligopeptides (SOP) in ultraviolet B- (UVB-) induced acute photodamage of human skin in vivo and foreskin ex vivo. Methods. We irradiated the forearm with 1.5 minimal erythemal dose (MED) of UVB for 3 consecutive days, establishing acute photodamage of skin, and topically applied SOP. Erythema index (EI), melanin index, stratum corneum hydration, and transepidermal water loss were measured by using Multiprobe Adapter 9 device. We irradiated foreskin ex vivo with the same dose of UVB (180 mJ/cm(2)) for 3 consecutive days and topically applied SOP. Sunburn cells were detected by using hematoxylin and eosin staining. Apoptotic cells were detected by using terminal deoxynucleotidyl transferase dUTP nick end labeling assay. Cyclobutane pyrimidine dimers (CPDs), p53 protein, Bax protein, and Bcl-2 protein were detected by using immunohistochemical staining. Results. Compared with UVB group, UVB-irradiated skin with topically applied SOP showed significantly decreased EI. Compared with UVB group, topical SOP significantly increased Bcl-2 protein expression and decreased CPDs-positive cells, sunburn cells, apoptotic cells, p53 protein expression, and Bax protein expressions in the epidermis of UVB-irradiated foreskin. Conclusion. Our study demonstrated that topical SOP can protect human skin against UVB-induced photodamage.

ALA-PDT elicits oxidative damage and apoptosis in UVB-induced premature senescence of human skin fibroblasts.

BACKGROUND: 5-Aminolevulinic acid photodynamic therapy (ALA-PDT) has been used for the treatment of skin photoaging. It can significantly improve the appearance of fine lines, dotted pigmentation, and roughness of photoaged skin. However, the mechanisms by which ALA-PDT yields rejuvenating effects on photoaged skin have not been well elucidated. Thus, in this study we explored the effects of ALA-PDT in photoaged fibroblasts. METHODS: We established a stress-induced premature senescence (SIPS) model by repeated exposures of human dermal fibroblasts (HDFs) to ultraviolet B (UVB) irradiation. Cells were irradiated by red light laser at 635nm wavelength (50mW/cm(2)). Intracellular protoporphyrin IX (PpIX) was detected by confocal microscopy. Intracellular reactive oxygen species (ROS) level and mitochondrial membrane potential (MMP) change were detected by fluorescence microscopy and flow cytometry. Morphological changes were observed by optical microscopy. Proliferative activity was measured by a cell counting kit-8 (CCK-8). Cell apoptosis was detected by fluorescence microscopy using Hoechst staining and flow cytometry using annexin V/propidium Iodide double staining. RESULTS: Intracellular PpIX fluorescence in UVB-induced premature senescent HDFs (UVB-SIPS-HDFs) reached the highest intensity after incubation with 1.00mmol/L ALA for 6h (P<0.05). Compared with control group, intracellular ROS level, MMP, and apoptotic rate were increased (P<0.05) and proliferative activity was decreased (P<0.05) in UVB-SIPS-HDFs treated with ALA-PDT, which were positively correlated to ALA incubation time and red light laser dose. CONCLUSION: Our study demonstrated that ALA-PDT elicits oxidative damage and apoptosis in photoaged fibroblasts in vitro, which may be the basis for the rejuvenating effects on photoaged skin.

The efficacy of conditioned media of adipose-derived stem cells combined with ablative carbon dioxide fractional resurfacing for atrophic acne scars and skin rejuvenation.

OBJECTIVE: To evaluate the effects of conditioned medium of adipose-derived stem cells (ADSC-CM) on efficacy and side effects after fractional carbon dioxide laser resurfacing (FxCR) when treating subjects with facial atrophic acne scars or with skin rejuvenation needs. MATERIALS AND METHODS: Twenty-two subjects were enrolled in the study and divided into two groups. Nine subjects were included in skin rejuvenation group and thirteen subjects were included in acne scar group, and all subjects underwent three sessions of FxCR. ADSC-CM was applied on FxCR site of one randomly selected face side. Evaluations were done at baseline, 1 week after first treatment, and 1 month after each treatment. The outcome assessments included subjective satisfaction scale; blinded clinical assessment; and the biophysical parameters of roughness, elasticity, skin hydration, transepidermal water loss (TEWL), and the erythema and melanin index. Biopsies taken from one subject in skin rejuvenation group were analyzed using hematoxylin and eosin, Masson's Trichrome, and Gomori's aldehyde fuchsin staining. RESULTS: ADSC-CM combined with FxCR increased subject satisfaction, elasticity, skin hydration, and skin elasticity and decreased TEWL, roughness, and the melanin index in both acne scars and skin rejuvenation groups. Histologic analysis showed that ADSC-CM increased dermal collagen density, elastin density, and arranged them in order. CONCLUSION: ADSC-CM with FxCR is a good combination therapy for treating atrophic acne scars and skin rejuvenation. TRIAL REGISTRATION: JSPH2012-082 - Registered 14 Feb 2012.

The protective effect of baicalin against UVB irradiation induced photoaging: an in vitro and in vivo study.

OBJECTIVE: This study was aimed to evaluate the anti-photoaging effects of baicalin on Ultraviolet B (UVB)-induced photoaging in the dorsal skin of hairless mice and premature senescence in human dermal fibroblasts. METHODS: We established in vivo and in vitro photoaging models by repeated exposures to UVB irradiation. By HE staining, masson staining, immunohistostaing and real-time RT-PCR, we analyzed epidermal thickness, collagen expression and the mRNA and protein levels of type I collagen, type III collagen, interstitial collagenase (MMP-1 and MMP-3) in UVB exposed dorsal mice skin. The aging condition in human dermal fibroblasts was determined by senescence-associated ß-galactosidase (SA-ß-gal) staining. Cell viability was determined using the Cell Counting Kit-8 (CCK-8). The G1 phase cell growth arrest was analyzed by flow cytometry. The senescence-related protein levels of p16INK-4a, p21WAF-1, and p53 and protein levels of phosphorylated histone H2AX were estimated by Western blotting. RESULTS: Topically application of baicalin treatment reduced UVB-induced epidermal thickening of mouse skin and also result in an increase in the production of collagen I and III, and a decrease in the expression of MMP-1 and MMP-3. Compared with the UVB-irradiated group, we found that the irradiated fibroblasts additionally treated with baicalin demonstrated a decrease in the expression of SA-ß-gal, a increase in the cell viability, a decrease in the G1 phase cell proportion, a downregulation in the level of senescence-associated and γ-H2AX proteins. However, Baicalin had no difference in the normal fibroblasts without UVB irradiation and long-term Baicalin incubation of UVB-SIPS fibroblasts gave no effects on the cell proliferation. CONCLUSIONS: Taken together, these results suggest that baicalin significantly antagonizes photoaging induced by UVB in vivo and in vitro, indicating the potential of baicalin application for anti-photoaging treatment.

Anti-photoaging potential of Botulinum Toxin Type A in UVB-induced premature senescence of human dermal fibroblasts in vitro through decreasing senescence-related proteins.

This study was aimed to evaluate the anti-photoaging effects of Botulinum Toxin Type A (BoNTA) in Ultraviolet B-induced premature senescence (UVB-SIPS) of human dermal fibroblasts (HDFs) in vitro and the underlying mechanism. We established a stress-induced premature senescence model by repeated subcytotoxic exposures to Ultraviolet B (UVB) irradiation. The aging condition was determined by cytochemical staining of senescence-associated ß-galactosidase (SA-ß-gal). The tumor suppressor and senescence-associated protein levels of p16(INK-4a), p21(WAF-1), and p53 were estimated by Western blotting. The G1 phase cell growth arrest was analyzed by flow cytometry. The mRNA expressions of p16, p21, p53, COL1a1, COL3a1, MMP1, and MMP3 were determined by real-time PCR. The level of Col-1, Col-3, MMP-1, and MMP-3 were determined by ELISA. Compared with the UVB-irradiated group, we found that the irradiated fibroblasts additionally treated with BoNTA demonstrated a decrease in the expression of SA-ß-gal, a decrease in the level of tumor suppressor and senescence-associated proteins, a decrease in the G1 phase cell proportion, an increase in the production of Col-1 and Col-3, and a decrease in the secretion of MMP-1 and MMP-3, in a dose-dependent manner. Taken together, these results indicate that BoNTA significantly antagonizes premature senescence induced by UVB in HDFs in vitro, therefore potential of intradermal BoNTA injection as anti-photoaging treatment still remains a question.

Palmitic acid induces production of proinflammatory cytokines interleukin-6, interleukin-1ß, and tumor necrosis factor-α via a NF-κB-dependent mechanism in HaCaT keratinocytes.

To investigate whether palmitic acid can be responsible for the induction of inflammatory processes, HaCaT keratinocytes were treated with palmitic acid at pathophysiologically relevant concentrations. Secretion levels of interleukin-6 (IL-6), tumor necrosis factor- α (TNF- α), interleukin-1 ß (IL-1 ß), NF- κ B nuclear translocation, NF- κ B activation, Stat3 phosphorylation, and peroxisome proliferator-activated receptor alpha (PPAR α) mRNA and protein levels, as well as the cell proliferation ability were measured at the end of the treatment and after 24 hours of recovery. Pyrrolidine dithiocarbamate (PDTC, a selective chemical inhibitor of NF- κ B) and goat anti-human IL-6 polyclonal neutralizing antibody were used to inhibit NF- κ B activation and IL-6 production, respectively. Our results showed that palmitic acid induced an upregulation of IL-6, TNF- α , IL-1 ß secretions, accompanied by NF- κ B nuclear translocation and activation. Moreover, the effect of palmitic acid was accompanied by PPAR α activation and Stat3 phosphorylation. Palmitic acid-induced IL-6, TNF- α , IL-1 ß productions were attenuated by NF- κ B inhibitor PDTC. Palmitic acid was administered in amounts able to elicit significant hyperproliferation and can be attenuated by IL-6 blockage. These data demonstrate for the first time that palmitic acid can stimulate IL-6, TNF- α , IL-1 ß productions in HaCaT keratinocytes and cell proliferation, thereby potentially contributing to acne inflammation and pilosebaceous duct hyperkeratinization.

Epidermal barrier: Adverse and beneficial changes induced by ultraviolet B irradiation depending on the exposure dose and time (Review).

Exposure of the skin to ultraviolet (UV) radiation induces various harmful effects in the tissues, particularly disruption of the epidermal barrier. However, ultraviolet B (UVB) irradiation has been applied in the treatment of atopic dermatitis, a skin disease in which the epidermal barrier is defective. We reviewed the homeostasis of the epidermal barrier and several studies investigating the adverse and beneficial effects caused by different doses of UVB irradiation in the epidermal barrier. It may be concluded that, despite the harmful effects of UVB irradiation on the skin, UVB irradiation is able to exert beneficial effects in the epidermal barrier when administered in suberythemal doses and over a relatively short period of time, with no clinically evident inflammation or barrier disruption. This may be a useful therapeutic strategy for the use of UVB irradiation in the treatment of skin diseases with a disrupted epidermal barrier, such as atopic dermatitis, while reducing or avoiding the side-effects.

Elevated miR-34c-5p mediates dermal fibroblast senescence by ultraviolet irradiation.

Previous studies showed that several miRNAs can regulate pathways involved in UVB-induced premature senescence and response to ultraviolet irradiation. It has also been reported that miR-34c-5p may be involved in senescence-related mechanisms. We propose that miR-34c-5p may play a crucial role in senescence of normal human primary dermal fibroblasts. Here, we explored the roles of miR-34c-5p in UVB-induced premature senescence on dermal fibroblasts. MiR-34c-5p expression was increased in dermal fibroblasts after repeated subcytotoxic UVB treatments. Underexpression of miR-34c-5p in dermal fibroblasts led to a marked delay of many senescent phenotypes induced by repeated UVB treatments. Furthermore, underexpression of miR-34c-5p in dermal fibroblasts can antagonize the alteration of G1-arrested fibroblasts. Moreover, E2F3, which can inactivate p53 pathway and play a role in cell cycle progression, is a down-stream target of miR-34c-5p. Forced down-expression of miR-34c-5p decreased the expression of UVB-SIPS induced P21 and P53 at both mRNA and protein levels. Our data demonstrated that down-regulation of miR-34c-5p can protect human primary dermal fibroblasts from UVB-induced premature senescence via regulations of some senescence-related molecules.

MiR-23a regulates DNA damage repair and apoptosis in UVB-irradiated HaCaT cells.

BACKGROUND: MiRNAs remain at a constant level under physiological conditions. However, how the expression of miRNAs is regulated and what are the roles of miRNAs in response to UVB damage to skin cells is still not fully understood. In our preliminary study, we observed that miR-23a was upregulated following a treatment with a DNA repair agent and UVB exposure. OBJECTIVE: To investigate the regulation and function of miR-23a in response to UVB-induced injury in human keratinocyte cell line (HaCaT) cells. METHODS: The changes in expression of miR-23a after UVB irradiation of HaCaT cells were measured by qRT-PCR. The level of miR-23a expression was also modulated by transfecting with a miR-23a mimic or an inhibitor. Cell viability was assessed by the CCK-8 assay. Immunofluorescence staining and Southwestern dot blotting were used to detect the levels of cyclobutane pyrimidine dimers (CPDs). Flow cytometry, Hoechst staining, and measurements of caspase-3 activity were employed to measure the incidence of apoptosis. The mRNA and protein expression levels of genes related to DNA reparation and apoptosis, such as topoisomerase-1, caspase-7, and STK4, were analyzed by qRT-PCR and Western blotting, respectively. RESULTS: MiR-23a expression was remarkably up-regulated at 4 h and 24 h after the UVB irradiation of HaCaT cells. UVB-induced apoptosis was increased by down-regulation of miR-23a. UVB-induced removal of CPDs was accelerated by miR-23a up-regulation and delayed by miR-23a down-regulation. Forced over-expression of miR-23a decreased the expression of UVB-induced topoisomerase-1\caspase7\STK4 at both the mRNA and protein levels, and these effects were reversed by down-regulation of miR-23a. CONCLUSION: The protection of HaCaT cells against UVB damage is afforded by miR-23a through regulation of topoisomerase-1\caspase7\STK4, and this miRNA may be a novel therapeutic target in skin diseases related to UVB radiation.

The effect of conditioned media of adipose-derived stem cells on wound healing after ablative fractional carbon dioxide laser resurfacing.

OBJECTIVE: To evaluate the benefits of conditioned medium of Adipose-derived stem cells (ADSC-CM) on wound healing after fractional carbon dioxide laser resurfacing (FxCR) on human skin. MATERIALS AND METHODS: Nineteen subjects were treated with FxCR on the bilateral inner arms. ADSC-CM was applied on FxCR site of one randomly selected arm. Transepidermal water loss (TEWL), skin color, and gross-elasticity of FxCR site on both arms were measured. Skin samples were taken by biopsy from three subjects 3 weeks after treatment for histopathological manifestations and mRNA expressions of procollagen types I and III, elastin genes were noted. RESULTS: The index of erythema, melanin, and TEWL of the ADSC-CM-treated skin were significantly lower than those of the control side. The mRNA expression of type III procollagen in ADSC-CM-treated group at 3 weeks posttreatment was 2.6 times of that of the control group. CONCLUSION: Application of allograft ADSC-CM is an effective method for enhancing wound healing after FxCR, by reducing transient adverse effects such as erythema, hyperpigmentation, and increased TEWL.

Tanshinone IIA inhibits the dihydrotestosterone-induced secretion of lipids and activation of sterol regulatory element binding protein-1 in HaCaT cells.

To study the effects and mechanisms of Tanshinone IIA (Tan IIA) on the dihydrotestosterone (DHT)-induced expression of sterol regulatory element binding protein-1 (SREBP-1), the synthesis and secretion of lipids in HaCaT cells were examined. HaCaT cells were treated with DHT and Tan IIA at different concentrations. Real-time PCR was used to detect the expression of SREBP-1c, fatty acid synthase (FAS), acyl-CoA synthetase (ACS), stearoyl-CoA desaturase (SCD) and HMG-CoA reductase (HMGCR) mRNA in HaCaT cells. Western blotting was used to analyze the protein expression of SREBP-1 and phosphorylation of Akt. Flow cytometry and Nile red staining were used to detect the synthesis and secretion of lipids in HaCaT cells. We observed that Tan IIA inhibited the DHT-induced expression of SREBP-1 and p-AKT in HaCaT cells, which produced an effect similar to that of LY294002. Tan IIA significantly inhibited the transcription of lipid synthesis-related genes and decreased lipid secretion in HaCaT cells. In conclusion, Tan IIA downregulates the expression of lipid synthesis-related genes and decreases lipid secretion in HaCaT cells, which is correlated with the inhibitory effect on the DHT-induced mRNA and protein expression of SREBP-1 in HaCaT cells.

Baicalin protects human skin fibroblasts from ultraviolet A radiation-induced oxidative damage and apoptosis.

Reactive oxygen species (ROS) are an important factor in the development of skin photodamage after ultraviolet A (UVA) radiation. A flavonoid antioxidant, baicalin, can selectively neutralize super-oxide anion (O(2)(-)) while having no significant effect on (•)OH. Fibroblasts are a key component of skin dermis. In the present study, we investigated the protective effects of baicalin on human skin fibroblasts (HSFs) under UVA induced oxidative stress. Fluorescence microscopy and flow cytometry were used to assay the intracellular O(2)(-), NO, ROS concentrations and the mitochondrial membrane potential. Cell viability was determined using the Cell Counting Kit-8 (CCK-8). The concentrations of cellular MDA, SOD, GSH, T-AOC, and 8-oxo-dG were also measured. Cellular apoptosis was measured by flow cytometry and caspase-3 detection. The results revealed that UVA radiation could cause oxidative stress and apoptosis in HSFs. Interestingly, the use of baicalin after UVA radiation significantly reduced the level of intracellular O(2)(-), NO, and ROS, stabilized the mitochondrial membrane potential, and attenuated production of MDA and 8-oxo-dG. These efficiently enhanced the antioxidative defense system and protected the HSFs from subsequent oxidative stress damage and apoptosis. In other words, baicalin decreased the excessive generation of intracellular ROS and NO, and elevated the cellular antioxidative defense, which eventually mitigate the UVA-induced apoptosis. Based on our results, baicalin may have applications in the treatment of skin photodamage caused by UVA irradiation.

Characterization of the miRNA profile in UVB-irradiated normal human keratinocytes.

The aim of this study was to assess the effects of ultraviolet B (UVB) irradiation on microRNA (miRNA) expression in normal human keratinocytes. Global miRNA expression profiles of primary cultures of normal human keratinocytes 4 and 24 h postirradiation were studied using miRNA microarray with further confirmation by real-time PCR. We found that upon 30 or 60 mJ/cm(2) of UVB radiation, the expression of 44 miRNAs was up- or downregulated more than twofold compared with non-irradiated keratinocytes. MiRNAs were either up- or downregulated after 4 h and then either returned to normal levels or remained affected after 24 h, resulting in four distinct patterns of miRNA expression change. It appears that acute exposure of keratinocytes to UVB radiation results in several specific patterns of miRNA response.