A novel method of assessing intraoperative surgical margins in patients with dermatofibrosarcoma protuberans: A specimen radiography system.

Background Dermatofibrosarcoma protuberans (DFSP) is one of the most challenging cutaneous cancers in surgical clinic practice. Excision with negative margins is essential for effective disease control. However, wide surgical margins and maximal tissue conservation are mutually exclusive. Mohs micrographic surgery conserves tissue but is time-consuming. Thus, we developed a novel specimen radiography system that can be used intraoperatively. Aims To introduce a specimen radiography system for evaluating intraoperative surgical margins in patients with dermatofibrosarcoma protuberans. Methods Since September 2017, we have treated seven biopsy-proven cases of local DFSPs via local excision with surgical margins of 2-4 cm. During operations, the operative specimens were screened using the specimen radiography system. All surgical specimens were pathologically examined intraoperatively. Results Five patients were men and two were women, of median age 36 years. The mean radiographic screening time was 9.7 ± 2.3 min. Radiographically negative margins were confirmed intraoperatively. The minimal margin width ranged from 5.0 to 35.4 mm (mean width 16.9 ± 10.4 mm). The intraoperatively negative radiographic margins were consistent with those revealed by postoperative pathology. The minimal pathological margin width ranged from 4.0 to 34.5 mm (mean 16.6 ± 10.1 mm) and was not significantly different from the intraoperative data. Limitations The sample size was small and positive or negative predictive values were not calculated. Conclusions We introduce a novel method of intraoperative surgical margin assessment for DFSP patients. It may find broad clinical and research applications during oncoplastic surgery.

Antiphotoaging Effect of Micronized Fat in Ultraviolet B-Induced Human Dermal Fibroblasts.

BACKGROUND: Adipose-derived stromal vascular fraction (SVF) and mesenchymal stem cells have been proven to reduce the effects of skin photoaging. However, there is no standardized protocol for their preparation. This study aimed to investigate the skin rejuvenation potential of micronized fat, obtained using a novel device attached with a trifoliate blade, in the ultraviolet B (UV-B)-induced human dermal fibroblast model. METHODS: Micronized fat was prepared to obtain adipose-derived SVF, and the adipose-derived mesenchymal stem cell-to-SVF ratio was determined by flow cytometry. The UV-B-induced human dermal fibroblasts model was constructed to identify the characteristics of the human dermal fibroblasts using vimentin and S-100 immunostaining, observe their morphology, and measure the levels of photoaging-related factors. After the previous steps were completed, different cell groups were co-cultured with UV-B-induced human dermal fibroblasts, and the extent of improvement of photoaging was evaluated. RESULTS: Micronized fat had a higher adipose-derived mesenchymal stem cell-to-SVF ratio than the control fat preparations. The UV-B-induced human dermal fibroblasts model showed lowered levels of type I collagen and transforming growth factor-ß and increased expression of matrix metalloproteinases (MMPs), which are the characteristics of photoaging in normal human dermal fibroblasts. Compared with different cell groups co-cultured with UV-B-induced human dermal fibroblasts, micronized fat could lower the expression of MMPs and increase the level of type I collagen but lower the level of transforming growth factor-ß. CONCLUSIONS: Obtaining micronized fat is more effortless and clinically safer. Micronized fat has an antiphotoaging effect by inhibiting the expression of MMPs by means of the mitogen-activated protein kinases signaling pathway. CLINICAL RELEVANCE STATEMENT: The authors' work has potential clinical applications in fat grafting for facial rejuvenation.

Waterjet in Bacterial Clearance of Diabetic Lower Extremity Contaminated Wounds: A Retrospective Cohort Study.

The waterjet debridement is now a standard practice in contaminated or infected diabetic lower extremity wounds. The bacterial clearance of the waterjet debridement remains an important parameter that should be predicted in this application. This study aimed to investigate the waterjet in reducing the diabetic lower extremity wound contaminants. A retrospective cohort study was conducted. Patients' etiology and pathogen diagnosis were established as diabetic lower extremity contaminated wound. The high-power waterjet (Versajet™, Smith-Nephew) was used in the treatment group and conventional surgical methods were used in the control group. The bacteriological swab samples were collected before and after the debridement. The results of bacterial culture were analyzed. A total of 74 patients were included in our study, 40 patients in the treatment group and 34 in the control group. Patient characteristics were well matched. The preoperative bacteriological swab samples of the 2 groups showed no significant difference between each other with a P value of .1022. The culture result of postoperative bacteriological swab samples in the treatment group was significantly lower than control with a P value of .0099. The odds of bacterial clearance were greater in the treatment group than in the control group (odds ratio, 5.139; 95% confidence interval, 1.386-18.41). As demonstrated by this retrospective research, waterjet debridement reduced the bacterial load in the diabetic lower extremity contaminated wounds.

Protein tyrosine phosphatase 1B regulates fibroblasts proliferation, motility and extracellular matrix synthesis via the MAPK/ERK signalling pathway in keloid.

Keloid is a fibroproliferative disorder resulting from trauma, characterized by abnormal activation of keloid fibroblasts and excessive deposition of extracellular matrix (ECM). It affects life quality of patients and lacks of effective therapeutic targets. Protein tyrosine phosphatase 1B (PTP1B) belongs to the protein tyrosine phosphatases and participates in many cellular processes such as metabolism, proliferation and motility. It has been reported that PTP1B negatively regulated diabetic wound healing and tumor progression. However, its effects in keloid remain unclear. Here, we aimed to evaluate the effects of PTP1B on keloid fibroblasts which play essential roles in keloids pathogenesis. Our results revealed that PTP1B expression was decreased both in keloid tissues and in keloid fibroblasts compared to healthy controls. Keloid fibroblasts (KFs) showed higher cell proliferation, motility, ECM production and ERK activity than normal fibroblasts (NFs). Overexpression of PTP1B in KFs and NFs inhibited cell proliferation, motility, ECM synthesis and the MAPK/ERK signalling pathway while knockdown of PTP1B showed converse effects. The rescue experiments with ERK inhibitor further verified that MAPK/ERK signalling pathway involved in PTP1B regulatory network. Taken together, our findings indicated that overexpression of PTP1B suppressed keloid fibroblasts bio-behaviours and promoted their phenotype switch to normal cells via inhibiting the MAPK/ERK signalling pathway, suggesting it may be a potential anti-keloid therapy.

Knockdown of DEAD-box RNA helicase 52 (DDX52) suppresses the proliferation of melanoma cells in vitro and of nude mouse xenografts by targeting c-Myc.

The ATP-dependent protein DEAD-box RNA helicase 52 (DDX52) is an important regulator in RNA biology and has been implicated in the development of prostate and lung cancer. However, its biological functions and clinical importance in malignant melanoma (MM) are still unclear. Understanding the potential mechanism underlying the regulation of MM progression by DDX52 might lead to novel therapeutic strategies. The aim of the present study was to investigate the role of DDX52 in the regulation of MM progression and its clinical relevance. DDX52 expression in normal and MM tissues was evaluated by GEO analysis and immunohistochemistry. The effects of DDX52 on cell growth were evaluated in MM cells with downregulated DDX52 expression. In this study, we found that DDX52 was markedly overexpressed in MM tissues compared with nontumor tissues and was associated with shorter overall survival in patients; therefore, DDX52 might be a prognostic marker in MM. Downregulation of DDX52 expression in the MM cell lines A2058 and MV3 markedly inhibited cell proliferation and colony formation. Additionally, knockdown of DDX52 in MM cells caused significant regression of established tumors in nude mice and delayed the onset time. Moreover, downregulation of DDX52 markedly suppressed c-Myc mRNA and protein expression, and an RNA immunoprecipitation assay confirmed the association between DDX52 and c-Myc. Restoration of c-Myc expression partly rescued the effects of DDX52 deficiency in MM cells. In conclusion, our study found that DDX52 mediated oncogenesis by promoting the transcriptional activity of c-Myc and could be a therapeutic target in MM.