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Objective Methods Results Conclusion To investigate the effect of retaining the vessels around the orbicularis oculi muscle on reducing local swelling after blepharoplasty.A total of 309 patients undergoing blepharoplasty (total incision) were observed and randomly assigned to three groups; (A) conventional operation; (B) preservation of deep vessels; (C) preservation of anterior vessels of orbicularis oculi muscle. The groups were compared based on intraoperative blood loss, operation time, swelling, satisfaction, and complications.Among the 309 patients, 39 were lost to follow‐up. c Additionally, A had the shortest operation time, followed by C with slightly longer duration. On the 7th day, 15th day, and 1 month after surgery, both B and C demonstrated significantly lower levels of swelling compared to A. Moreover, patient satisfaction was higher in B and C than in A.Retaining either superficial or deep veins of the orbicularis oculi muscle can effectively reduce short‐term postoperative swelling. However, when retaining the superficial central group of this muscle during surgery, it is crucial to strictly control the amount of surrounding tissue around vessels. [ABSTRACT FROM AUTHOR]

Background: SPRY1 is associated with the invasiveness and prognosis of various tumors, and TET3 affects aging by regulating gene expression. Aims: We investigated the roles of SPRY1 and TET3 in natural skin aging, replicative aging, and photoaging, along with the effect of UVA on genome‐wide DNA methylation in HaCaT cells. Methods: TET3 and SPRY1 expression were measured in the skin of patients of different age groups, as well as in vitro human skin, HaCaT cell replicative senescence, and HaCaT and HaCaT‐siTET3 cell photoaging models. Senescence was verified using β‐galactosidase staining, and DNA damage was detected using immunofluorescence staining for γ‐H2A.X. 5‐Methyl cytosine (5‐mC) content in the genome was determined using ELISA. Results: SPRY1 expression increased with age, whereas TET3 expression decreased. Similarly, SPRY1 was upregulated and TET3 was downregulated with increasing cell passages. TET3‐siRNA upregulated SPRY1 expression in HaCaT cells. UVA irradiation promoted HaCaT cell senescence and induced cellular DNA damage. SPRY1 was upregulated and TET3 was downregulated upon UVA irradiation. Genome‐wide 5‐mC content increased upon TET3 silencing and UVA irradiation, indicating a surge in overall methylation. Conclusions: SPRY1 and TET3 are natural skin aging‐related genes that counteract to regulate replicative aging and UVA‐induced photoaging in HaCaT cells. The cell photoaging model may limit experimental bias caused by different exposure times of skin model samples. [ABSTRACT FROM AUTHOR]

Purpose: Due to poor prognosis and immunotherapy failure of skin cutaneous melanoma (SKCM), this study sought to find necroptosis-related biomarkers to predict prognosis and improve the situation with predicted immunotherapy drugs. Experimental Design: The Cancer Genome Atlas (TCGA) and The Genotype-Tissue Expression Program (GTEx) database were utilized to recognize the differential necroptosis-related genes (NRGs). Univariate Cox (uni-Cox) and least absolute shrinkage and selection operator (LASSO) Cox analysis were utilized for prognostic signature establishment. The signature was verified in the internal cohort. To assess the signature's prediction performance, the area under the curve (AUC) of receiver operating characteristic (ROC) curves, Kaplan-Meier (K-M) analyses, multivariate Cox (multi-Cox) regression, nomogram, and calibration curves were performed. The molecular and immunological aspects were also reviewed using single-sample gene set enrichment analysis (ssGSEA). Cluster analysis was performed to identify the different types of SKCM. Finally, the expression of the signature gene was verified by immunohistochemical staining. Results: On basis of the 67 NRGs, 4 necroptosis-related genes (FASLG, PLK1, EGFR, and TNFRSF21) were constructed to predict SKCM prognosis. The area's 1-, 3-, and 5-year OS under the AUC curve was 0.673, 0.649, and 0.677, respectively. High-risk individuals had significantly lower overall survival (OS) compared to low-risk patients. Immunological status and tumor cell infiltration in high-risk groups were significantly lower, indicating an immune system that was suppressed. In addition, hot and cold tumors could be obtained by cluster analysis, which is helpful for accurate treatment. Cluster 1 was considered a hot tumor and more susceptible to immunotherapy. Immunohistochemical results were consistent with positive and negative regulation of coefficients in signature. Conclusion: The results of this finding supported that NRGs could predict prognosis and help make a distinction between the cold and hot tumors for improving personalized therapy for SKCM. [ABSTRACT FROM AUTHOR]

Objective: The purpose of this article is to investigate whether the percutaneous delivery of compound lidocaine cream by roller microneedles can shorten the minimal effective onset time of anesthesia, enhance the intensity of anesthesia and prolong the analgesic time, so as to provide a theoretical basis for exploring a comfortable, safe and effective anesthesia method for photoelectric cosmetic surgery. Methods: A total of 90 healthy volunteers, including 18 male and 72 female, met the criteria and were enrolled in the study from December 2020 to September 2021 in Department of Plastic and Burn Surgery of the First Affiliated Hospital of Chongqing Medical University. This study adopted a two‐factor randomized block design of 3 (anesthesia time on the test side: 30, 45, 60 min) × 2 (the test side: the left and right side), and the subjects were divided into group A (n = 30), group B (n = 30), and group C (n = 30). On the test side, the compound lidocaine cream was used for topic anesthesia for 10 min, then the roller microneedle was used to roll on the treatment area, compound lidocaine cream was appropriately supplemented, and the topic anesthesia was kept continued for 20 min (group A), 35 min (group B), and 50 min (group C), respectively. The mirrorsymmetrical area of the test side of the three groups was the control side, and the compound lidocaine cream was used for topic anesthesia for 60 min. Photoelectric therapy was performed after anesthesia was completed. The analgesic effect of the subjects on both sides was comprehensively compared; the scores were obtained using the Kuttner Facial Expression Scale, the Frankl Treatment Compliance Scale, the Houpt Behavior Scale, and the Visual Analog Scale (VAS); the satisfaction with anesthesia was investigated. Before and after treatment the skin temperature, color and adverse reactions of the subjects were recorded. Results: Comparing both sides of the same group, there was no significant difference in terms of the comprehensive evaluation, intraoperative comfort, tolerance, cooperation, pain or satisfaction between the 30‐min test side and the routine anesthesia side in group A; the comprehensive evaluation, intraoperative tolerance, cooperation degree, pain degree and satisfaction evaluation of the subjects on the 45‐min test side in group B were significantly better than those on the control side; the comprehensive evaluation, intraoperative comfort, tolerance, cooperation, pain and satisfaction of the subjects on the 60‐min test side in group C were significantly better than those on the control side. Comparing groups on the control side, there was no significant difference in the comprehensive evaluation, intraoperative comfort, tolerance, cooperation, pain or satisfaction between the three groups of subjects on the control side. Comparing the three groups on the test side, with the prolongation of compound lidocaine cream indwelling time, the subjects' comprehensive evaluation, comfort and pain degree were significantly improved. There was no significant difference in postoperative bruising, swelling, pain, discoloration, redness, or tenderness between the test side and the control side. Conclusion: The percutaneous delivery of compound lidocaine cream by roller microneedles can not only shorten the effective time of anesthesia, but also has a good analgesic effect without obvious adverse reactions. [ABSTRACT FROM AUTHOR]

Wound healing is a complex but well-orchestrated tissue repair process composed of a series of molecular and cellular events conducted by various types of cells and extracellular matrix. Despite a variety of therapeutic strategies proposed to accelerate the healing of acute and/or chronic wounds over the past few decades, effective treatment of chronic nonhealing wounds still remains a challenge. Due to the recent advances in stem cell research, a dramatic enthusiasm has been drawn to the application of stem cells in regenerative medicine. Both embryonic and adult stem cells have prolonged self-renewal capacity and are able to differentiate into various tissue types. Nevertheless, use of embryonic stem cells is limited, owing to ethical concerns and legal restrictions. Adult stem cells, which could be isolated from bone marrow, umbilical cord blood, adipose tissue, skin and hair follicles,are being explored extensively to facilitate the healing of both acute and chronic wounds. The current article summarizes recent research on various types of stem cell-based strategies applied to improve wound healing. In addition, future directions of stem cell-based therapy in wound healing have also been discussed. Finally, despite its apparent advantages, limitations and challenges of stem cell therapy are discussed. [ABSTRACT FROM AUTHOR]

To explore the relationship between methylated binding protein 2 (MeCP2) and mothers against decapentaplegic homolog 7 (Smad7) in the pathogenesis and development of pathological scars. Immunohistochemistry, Western blot and real-time polymerase chain reaction (RT-PCR) were used to detect the expression of MeCP2 in different types of human scars and hypertrophic scars at different growth times. The methylation status of Smad7 gene promoter in different scar tissues was determined by methylation-specific PCR. After transfection with MeCP2-siRNA (small interfering RNA) in human keloid fibroblasts, MTT assay was used to assess the proliferation activity of keloid fibroblasts, while RT-PCR and Western blot assays were used to detect the expression levels of MeCP2, transforming growth factor-β1 (TGF-β1), α-smooth muscle actin (α-SMA), phospho-Smad2 (p-Smad2) and Smad7. MeCP2 was mainly expressed in the nucleus of fibroblasts. The mRNA and protein levels of MeCP2 were significantly higher in keloids than in hypertrophic scars, normal scars and normal skin (p<.05). The expression level of MeCP2 in hypertrophic scars during the growth period of <6 months was markedly higher than that of >6 months (p<.05). The methylation level of Smad7 was significantly higher in keloids compared to normal skin. After MeCP2 silencing, the proliferation rate of human keloid fibroblasts was decreased, the mRNA and protein levels of Smad7 were increased, and the expression levels of TGF-β1, α-SMA and p-Smad2 were decreased (p<.05). MeCP2 and Smad7 play an important role in formation of pathological scars. During keloid formation, MeCP2 weakens the inhibitory effect of Smad7 on p-Smad2/3 by downregulating the expression of Smad7, which in turn promotes fibrosis and scar hyperplasia. [ABSTRACT FROM AUTHOR]

Objective. Myofibroblast transformation has been shown to be associated with the reactive oxygen species- (ROS-) producing enzyme NADPH oxidase (Nox4). Inhibition of transient receptor potential channel canonical type 3 (TRPC3) attenuates mitochondrial calcium handling and ROS production in the vasculature of hypertensive rats. However, it remains elusive whether TRPC3 regulates mitochondrial calcium and ROS production and participates in myofibroblast transdifferentiation during wound healing. Methods and Results. In this study, we demonstrated that activation of TRPC3 by transforming growth factor β (TGFβ1) elevated myofibroblast transdifferentiation by upregulating the myofibroblast marker alpha smooth muscle actin (αSMA). Inhibition of TRPC3 with its specific inhibitor, Pyr3, significantly decreased TGFβ1-induced αSMA expression, as demonstrated by immunofluorescence. Real-time PCR and immunohistochemistry revealed higher TRPC3 and TGFβ1 mRNA expression levels in fibroblasts from hypertrophic scar (HTS) tissue than in those from normal skin tissue. TGFβ1 treatment increased TRPC3-mediated mitochondrial calcium uptake and ROS production but decreased ATP content in human fibroblasts, whereas inhibition of TRPC3 significantly reversed these effects. The beneficial effects were associated with improvements in mitochondrial respiratory function mediated by recovery of the activity of pyruvate dehydrogenase (PDH). In vivo, Trpc3-/- mice exhibited significantly attenuated myofibroblast transdifferentiation, as demonstrated by decreased αSMA, TGFβ1, fibronectin, and collagen-1 (Col1a1) protein expression in wound granulation tissues. Furthermore, TGFβ1-induced store-operated calcium entry (SOCE) was significantly decreased in fibroblasts from Trpc3-/- mice compared with those from Trpc3+/+ mice. In addition, Trpc3-/- mice exhibited significantly decreased Nox4 and phosphorylated Smad2/3 protein expression in wound granulation tissues. Conclusions. Our data indicate that TGFβ1-mediated activation of TRPC3 enhances mitochondrial calcium and ROS production, which promotes myofibroblast transdifferentiation and HTS formation. Inhibition of the TRPC3-mediated Nox4/pSmad2/3 pathway may be a useful strategy to limit HTS formation after injury. [ABSTRACT FROM AUTHOR]

A correction to the article "Role of Ran-regulated nuclear-cytoplasmic trafficking of pVHL in the regulation of microtubular stability-mediated HIF-1α in hypoxic cardiomyocytes" that was published in the March 17, 2015 is presented.

Our previous study suggested that microtubule network alteration affects the process of glycolysis in cardiomyocytes (CMs) via the regulation of hypoxia-inducible factor (HIF)-1α during the early stages of hypoxia. However, little is known regarding the underlying mechanisms of microtubule network alteration-induced changes of HIF-1α. The von Hippel-Lindau tumor suppressor protein (pVHL) has been shown to mediate the ubiquitination of HIF-1α in the nuclear compartment prior to HIF-1α exportation to the cytoplasm, and pVHL dynamic nuclear-cytoplasmic trafficking is indicated to be involved in the process of HIF-1α degradation. In this study, by administering different microtubule-stabilizing and -depolymerizing interventions, we demonstrated that microtubule stabilization promoted pVHL nuclear export and drove the translocation of pVHL to the cytoplasm, while microtubule disruption prevented pVHL nuclear export in hypoxic CMs. Moreover, the ratio between nuclear and cytoplasmic pVHL was associated with HIF-1α regulation. Importantly, microtubule network alteration also affected the subcellular localization of Ran, which was involved in the regulation of pVHL nuclear-cytoplasmic trafficking. The above results suggest that the subcellular translocation of pVHL plays an important role in microtubular structure alteration-induced HIF-1α regulation. Interestingly, Ran is involved in the process of pVHL nuclear-cytoplasmic trafficking following microtubule network alteration in hypoxic CMs. [ABSTRACT FROM AUTHOR]