The W-Plasty Serial Excision Method for Treating Medium Congenital Melanocytic Nevi: A Retrospective Analytical Study.

BACKGROUND: Serial excision remains the most commonly used surgical procedure for treating congenital melanocytic nevus (CMN). It is critical to remove as much of the lesion as possible with each procedure to reduce the number of procedures and to shorten the treatment duration. OBJECTIVE: To investigate the clinical efficacy of W-plasty serial excision for the repair of postoperative CMN defects. METHODS: A retrospective analysis of patients with medium CMN was conducted from April 2018 to March 2022. Treatment options were divided into elliptical serial excision (10 cases) and W-plasty serial excision (10 cases). RESULTS: Follow-up occurred over 6 months. The number of elliptical excision procedures was 2 to 4 (mean 2.9). The scar-to-lesion length ratio was 1.5 to 2.0 (mean 1.7). The mean Vancouver Scar Scale (VSS) score was 5.40 ± 0.42. The number of W-plasty excision procedures was 2 to 3 (mean 2.2). The scar-to-lesion length ratio was 1.2 to 1.5 (mean 1.4). The mean VSS score was 2.70 ± 0.26. W-plasty excision was superior to elliptical excision regarding the number of procedures and the effect on postoperative scars. CONCLUSION: W-plasty serial excision can be considered a suitable option for the excision of medium CMN, leading to excellent results.

The Combination of the Mini-Punch Technique and Photodynamic Therapy for the Treatment of Mandibular Keloids and Hypertrophic Scars.

BACKGROUND: Mandibular keloids and hypertrophic scars can exert significant effects on the appearance of a patient. However, current treatments are not effective in all cases. Consequently, it is vital to identify a safe and effective treatment method. OBJECTIVE: To investigate the therapeutic effect of the mini-punch technique combined with photodynamic therapy (PDT) on mandibular keloids and hypertrophic scars. PATIENTS AND METHODS: Twenty patients with mandibular keloids and hypertrophic scars were enrolled, including 5 cases of keloids and 15 cases of hypertrophic scars, with a total of 40 lesions. The mini-punch technique was performed first, and then, PDT was conducted, once a week on 3 occasions in total. RESULTS: After 12 months of follow-up, 30 lesions had improved by more than 50%, thus achieving a good therapeutic effect. The Vancouver Scar Scale score of patients ranged between 8 and 12 points with a mean of 9.60 ± 1.09 points before surgery and between 2 and 9 points with a mean of 4.15 ± 2.05 points at 12 months after surgery. The mean Vancouver Scar Scale score after treatment was significantly lower than that before treatment (t = 11.80, p < .001). CONCLUSION: A combination of the mini-punch technique and PDT is an effective treatment for mandibular keloids and hypertrophic scars.

Melanocyte activation and skin barrier disruption induced in melasma patients after 1064 nm Nd:YAG laser treatment.

Melasma is a frequently acquired hyperpigmentary skin disorder, for which several therapies are available. Among them, 1064 nm QS Nd:YAG laser therapy is an effective method, but the recurrence rate of laser treatment is still high. The aim of the present study was to elucidate the mechanism of the high relapse rate of melasma after 1064 nm Nd:YAG laser treatment. Twenty-five female melasma patients were treated with 1064 nm Nd:YAG laser for 10 times. The lesional skin and non-lesional skin were evaluated by means of a reflectance confocal laser scanning microscope before and after laser treatment. Melanin content and transepidermal water loss (TEWL) were measured by an MPA9 skin multifunction tester accordingly. The melanin index value was significantly decreased in the lesional skin after laser treatment, while the non-lesional skin had no difference. The dendritic cells were observed at the level of the dermal-epidermal junction (DEJ) in the lesions of 8 patients before laser treatment, while after laser treatment, the dendritic cells were observed in all 25 subjects. Moreover, there was significant difference between the TEWL value of the lesions before and after laser treatment. Furthermore, the TEWL value was higher in lesions of the 8 subjects which had dendritic cells compared with other 17 subjects which had no dendritic cells, no matter before or after laser treatment. The relapse patients of melasma had higher TEWL value compared with the non-relapse patients. Melanocyte activation and skin barrier disruption may be related to the high relapse rate of melasma after laser treatment.

Structure-guided peptide engineering of a positive allosteric modulator targeting the outer pore of TRPV1 for long-lasting analgesia.

Transient receptor potential vanilloid 1 (TRPV1) ion channel is a classic analgesic target, but antagonists of TRPV1 failed in clinical trials due to their side effects like hyperthermia. Here we rationally engineer a peptide s-RhTx as a positive allosteric modulator (PAM) of TRPV1. Patch-clamp recordings demonstrate s-RhTx selectively potentiated TRPV1 activation. s-RhTx also slows down capsaicin-induced desensitization of TRPV1 in the presence of calcium to cause more calcium influx in TRPV1-expressing cells. In addition, our thermodynamic mutant cycle analysis shows that E652 in TRPV1 outer pore specifically interacts with R12 and K22 in s-RhTx. Furthermore, we demonstrate in vivo that s-RhTx exhibits long-lasting analgesic effects in noxious heat hyperalgesia and CFA-induced chronic inflammatory pain by promoting the reversible degeneration of intra-epidermal nerve fiber (IENF) expressing TRPV1 channels in mice, while their body temperature remains unaffected. Our results suggest s-RhTx is an analgesic agent as a PAM of TRPV1.

[Cross-talk between nuclear factor-kappaB and P53 signal pathway in keratinocytes after ultraviolet B irradiation].

OBJECTIVE: To investigate the cross-talk between nuclear factor kappaB (NF-kappaB) and P53 signal pathways in human epidermal keratinocytes (NHEKs) after ultraviolet B (UVB) irradiation. METHODS: Normal NHEKs harboring wild p53 gene and immortal human keratinocytes of the line HaCaT harboring mutant p53 gene were cultured at 37 degrees C in an atmosphere containing 5% CO(2) and then underwent irradiation of UVB of the dose of 60 mJ/cm(2). Part of the NHEKs and HaCaT cells were pretreated with BAY11-7082, NF-kappaB inhibitor inhibiting IkB-a phosphorylation, of the final concentration of 5 micromol/L. Western blotting was used to detect the protein expression of NF-kappaB, P53, and P21. The transcriptional activity of NF-kappaB was analyzed by electrophoretic mobility shift assay (EMSA). RESULTS: UVB irradiation increased the protein expression of NF-kappaB, P53, and P21 and triggered the transcriptional activity of NF-kappaB. BAY11-7082 significantly inhibited the NF-kappaB protein expression induced by UVB irradiation in the NHEKs and HaCaT cells. The P53 protein expression of the NHEKs undergoing pretreatment of BAY11-7082 and UVB irradiation was 0.08 +/- 0.07, significantly lower than that of the NHEKs undergoing only UVB irradiation (0.78 +/- 0.32, P < 0.01). The P21 protein expression of the NHEKs undergoing pretreatment of BAY11-7082 and UVB irradiation was 0.65 +/- 0.22, significantly lower than that of the NHEKs undergoing only UVB irradiation (1.58 +/- 0.77, P < 0.05). However, the P53 and the P21 protein expression of the HaCaT cells undergoing pretreatment of BAY11-7082 and UVB irradiation was not significantly different from that of the HaCaT cells undergoing only UVB irradiation. CONCLUSION: There exists a UVB-induced cross-talk between NF-kappaB and P53 signal pathways in human epidermal keratinocytes. This cross-talk is correlated with P53 functional condition.

[Effects of antisense epidermal growth factor receptor oligodeoxynucleotides on ultraviolet-induced c-jun activity of keratinocytes].

OBJECTIVE: To explore the effects of antisense epidermal growth factor receptor (EGF-R) oligodeoxynucleotides on ultraviolet-induced c-jun activity of keratinocytes after EGF-R oligodeoxynucleotides transfect to HaCaT in vitro. METHODS: c-jun DNA binding activity after ultraviolet-B (UVB) irradiation and EGF-R oligodeoxynucleotides transfection were determined with a highly sensitive and specific colorimetric method. After EGF-R oligodeoxynucleotides transfection, the mRNA level of EGF-R was detected by reverse transcription polymerase chain reaction method. RESULTS: Compared with control groups, c-jun activity increased significantly in UVB (10, 20, 30 mJ/cm2) irradiation groups (P < 0.05). EGF-R mRNA and c-jun activities induced by UVB were inhibited after the keratinocytes were transfected with EGF-R antisense oligodeoxynucleotides at 2, 4 and 8 microg/ml concentrations (P < 0.01). CONCLUSION: The ultraviolet-induced c-jun activity of keratinocytes can be mediated by EGF-R and inhibited by EGF-R antisense oligodeoxynucleotides, which is transfected to keratinocytes and mediated by lipofectamine.

Green tea polyphenol epigallocatechin-3-gallate inhibits the expression of nitric oxide synthase and generation of nitric oxide induced by ultraviolet B in HaCaT cells.

BACKGROUND: Nitic oxide (NO) has been implicated in the pathogenesis of various inflammatory diseases, including sunburn and pigmentation induced by ultraviolet irradiation. Epigallocatechin-3-gallate (EGCG) is the major effective component in green tea and can protect skin from ultraviolet-induced damage. The purpose of this study was to investigate the protective mechanisms of EGCG on inducible nitric oxide synthase (iNOS) expression and NO generation by ultraviolet B (UVB) irradiation in HaCaT cells. METHODS: HaCaT cells were irradiated with UVB 30 mJ/cm 2 and pretreated with EGCG at varying concentrations. The iNOS mRNA was detected by reverse transcriptase polymerase chain reaction (RT-PCR) and NO production was quantified by spectrophotometric method. The expression of NF-kappaB P65 was measured by immunofluorescence cytochemistry staining. RESULTS: The expression of iNOS mRNA and generation of NO in HaCaT cells were increased by UVB irradiation. EGCG down regulated the UVB-induced iNOS mRNA synthesis and NO generation in a dose dependent manner. The UVB-induced ctivation and translocation of NF-kappaB were also down regulated by EGCG treatment in HaCaT cells (P < 0.01). CONCLUSIONS: Green tea derived-EGCG can inhibit and down regulate the UVB-induced activation and translocation of NF-kappaB, expression of iNOS mRNA and generation of NO respectively, indicating EGCG may play a protective role from UVB-induced skin damage.

Effects of (-)-epigallocatechin-3-gallate on expression of matrix metalloproteinase-1 and tissue inhibitor of metalloproteinase-1 in fibroblasts irradiated with ultraviolet A.

BACKGROUND: It is known that ultraviolet irradiation can affect cellular function through a number of signaling pathways. (-)-epigallocatechin-3-gallate (EGCG) is the major effective component in green tea and can offer protection from ultraviolet-induced damage. In this study, we investigated the protective mechanism of EGCG on human dermal fibroblasts damaged by ultraviolet A (UVA) in vitro. METHODS: Transcription factor Jun protein levels were measured by Western blot. Matrix metalloproteinase 1 (MMP-1) and tissue inhibitor of metalloproteinase-1 (TIMP-1) mRNA were studied by reverse transcription-polymerase chain reaction (RT-PCR) analysis in conjunction with computer-assisted image analysis. MMP-1 and TIMP-1 proteins were quantified by enzyme-linked immunosorbent assay (ELISA). RESULTS: EGCG decreased transcription activity of Jun protein after induction by UVA. Both the mRNA and protein levels of MMP-1 were increased by UVA irradiation, while no significant changes were observed in TIMP-1 levels. The ratio of MMP-1 to TIMP-1 showed statistically significant differences compared with the control. EGCG decreased the ratio of MMP-1 to TIMP-1 by inhibiting UVA-induced MMP-1 expression (P < 0.05). CONCLUSION: EGCG can protect human fibroblasts against UVA damage by downregulating the transcription activity of Jun protein and the expression of MMP-1. The ratio of MMP-1 to TIMP-1, rather than the levels of MMP-1 or TIMP-1 alone, may play a significant role in human skin photodamage.

Clinical, pathologic, and ultrastructural studies of progressive macular hypomelanosis.

BACKGROUND: Progressive macular hypomelanosis (PMH), a condition of uncertain etiology, is characterized by asymptomatic hypopigmented macules, predominantly located on the trunk. To date, the study of this disease has been sporadic and there are still no clinical diagnostic criteria. The aim of this study was to investigate the histopathologic and ultrastructural characteristics of PMH, and propose the clinical diagnostic criteria of PMH. METHODS: The Wood's lamp and Confocal Laser Scanning Microscopy were used to observe the lesions' features. Skin biopsies were used for hematoxylin and eosin staining, melanin staining, antibodies staining of S-100 protein, tyrosinase-related protein-1(TRP-1) and tyrosinase (T311), and also for ultra-structural study. Melanocytes were isolated and cultured from the lesions. RESULTS: Under Wood's lamp examination, the lesions of PMH showed punctiform red fluorescence. Confocal Laser Scanning Microscopy observation of the lesion showed that its "pigmented ring" around the dermal papillae was intact, but its melanin content was decreased compared with the surrounding normal skin. Ferrous sulfate staining showed that melanin content in the lesion of PMH was significantly decreased compared with the normal skin (P < 0.05). S-100 staining showed that the number of positive cells in the basal layer had no statistical significance (P > 0.05) between the lesion areas (8.25 ± 0.96) and the surrounding normal skin (8.75 ± 1.71). TRP-1 staining showed no significant difference between lesion areas (4.25 ± 0.96) and the surrounding normal skin (4.50 ± 1.29) (P > 0.05), and T311 staining also showed no difference between lesion areas (4.01 ± 0.87) and the surrounding normal skin (4.30 ± 1.05) (P > 0.05). Ultra-structural studies revealed a large reduction in the number of mature melanosome from PMH lesions. There were many membrane-bound groups in PMH lesions with normal appearance the margin, which contained a number of smaller type II-IV melanosomes, which were distributed in clusters. No degradation of melanosomes was present in the lysosomal compartments of PMH lesions. When melanocytes from the PMH lesions were cultured in vitro, the morphology of those melanocytes showed no difference compared with normal melanocytes. CONCLUSION: As a result of the above findings, we discussed and summarized the PMH's clinical diagnostic criteria.