Management of deep sacral and ischial pressure injuries with free-style local perforator flaps: A D+P+DPD model.

BACKGROUND: Previous reports on the treatment of sacral and ischial pressure injuries have not provided clear algorithms for surgical therapies. The objective of this study was to establish a reconstruction algorithm to guide the selection of an ideal free-style perforator flap that can be tailored to the defect in question. METHODS: We used 23 perforator flaps to reconstruct 14 sacral and 8 ischial defects in 22 patients over 5 years. A reconstruction algorithm system was developed based on the anatomical features of the perforator vessels (diameter, D; pulsatility [++∼+++], P) and their position in the skin island (DPD) (ie, D+P+DPD). A perforator-based propeller flap was applied as the first-line choice; if this plan was not feasible, we applied an altered V-Y advancement model or another second-choice technique. RESULTS: All flaps survived, and only 1 patient experienced partial wound dehiscence, which healed by secondary intention. After an average follow-up period of 11.2 months, no patient experienced recurrence or infection. CONCLUSIONS: Free-style perforator flap selection is determined by pressure injury and the desired advantage of a specific approach. The use of free-style perforator-based propeller flaps allows a surgeon to transfer healthy tissue into the defect, shifts the suture line away from the bony prominence, and preserves additional future donor sites. In cases where unexpected variations are encountered, the V-Y advancement model or another technique can be used. The simplified surgical algorithm (D+P+DPD) can provide versatility and reliability, achieve a durable, natural esthetic outcome, and minimize injuries to future donor sites.

A modified perforator-based stepladder V-Y advancement flap in the Achilles tendon area for coverage of larger posterior heel defects.

BACKGROUND: Posterior heel defect coverage is challenging because of the paucity of suitable flaps. The traditional local stepladder V-Y advancement flap is recommended only for small defects because of the lack of an axial pedicle. This study reports our experience of using the perforator-based stepladder V-Y advancement flaps in a larger posterior heel defect repair. METHODS: Twenty-two patients with posterior heel defects were treated with modified perforator-based stepladder V-Y advancement flaps in the Achilles tendon area for 11 years. Sixteen males and six females aged 3-74 years underwent surgery. The defect size, perforator characteristics, flap size, flap movement, sural nerve, lesser saphenous vein, deep fascia, flap survival, and outcome quality were analyzed. RESULTS: The perforators were found to predominate within two 2-cm intervals: 0-2 cm and 4-6 cm proximal to the tip of the lateral malleolus. Twenty-one perforator-based flaps healed uneventfully, and only one developed tip necrosis on the lower edge, which healed by secondary intention. The maximum distance of distal movement was 5.0 cm for the modified flap in contrast to 2.5 cm for the traditional flap. All flaps allowed adequate and durable reconstruction to be achieved, with excellent contouring after 2-28 months of follow-up. CONCLUSIONS: The perforator-based stepladder V-Y advancement flap resulted in good outcomes for larger posterior heel defects compared with conventional transfer methods. The flap is a reliable, well-vascularized, sensate, and pliable local flap option that uses similar tissue from adjacent skin for defect repair and creates an internal gliding surface for the Achilles tendon.

Flap failure prediction in microvascular tissue reconstruction using machine learning algorithms.

BACKGROUND: Microvascular tissue reconstruction is a well-established, commonly used technique for a wide variety of the tissue defects. However, flap failure is associated with an additional hospital stay, medical cost burden, and mental stress. Therefore, understanding of the risk factors associated with this event is of utmost importance. AIM: To develop machine learning-based predictive models for flap failure to identify the potential factors and screen out high-risk patients. METHODS: Using the data set of 946 consecutive patients, who underwent microvascular tissue reconstruction of free flap reconstruction for head and neck, breast, back, and extremity, we established three machine learning models including random forest classifier, support vector machine, and gradient boosting. Model performances were evaluated by the indicators such as area under the curve of receiver operating characteristic curve, accuracy, precision, recall, and F1 score. A multivariable regression analysis was performed for the most critical variables in the random forest model. RESULTS: Post-surgery, the flap failure event occurred in 34 patients (3.6%). The machine learning models based on various preoperative and intraoperative variables were successfully developed. Among them, the random forest classifier reached the best performance in receiver operating characteristic curve, with an area under the curve score of 0.770 in the test set. The top 10 variables in the random forest were age, body mass index, ischemia time, smoking, diabetes, experience, prior chemotherapy, hypertension, insulin, and obesity. Interestingly, only age, body mass index, and ischemic time were statistically associated with the outcomes. CONCLUSION: Machine learning-based algorithms, especially the random forest classifier, were very important in categorizing patients at high risk of flap failure. The occurrence of flap failure was a multifactor-driven event and was identified with numerous factors that warrant further investigation. Importantly, the successful application of machine learning models may help the clinician in decision-making, understanding the underlying pathologic mechanisms of the disease, and improving the long-term outcome of patients.

Plastic surgical repair of ulcer wounds of diabetic foot patients through systemic treatment and local infection control.

BACKGROUND: This study was to investigate the efficacy of plastic surgery in patients with diabetic foot (DF) ulcer who had systemic treatment and local infection control. METHODS: A total of 112 patients with DF were randomly divided into surgery group and drug treatment group according to treatment methods. Firstly, the pathogenic bacteria were isolated and cultured to explore the specific factors causing glycosuria foot ulcer. Secondly, the wound recovery and average hospitalization of the patients were analyzed, and the effects of different treatment methods on the clinical cure rate and recovery rate of the patients were compared. RESULTS: The results showed that 53 patients were diagnosed with type 2 DF, accounting for 47.32%; 22 patients were diagnosed with DF disease complicated by infections, accounting for 19.64%; 25 patients were diagnosed with DF complicated by ulcers, accounting for 22.32%; and 12 patients (10.71%) were diagnosed with DF complicated by ulcer infection. Of the pathogens cultured, Enterococcus faecalis accounted for the highest proportion (19.35%). Statistical analysis was conducted on Wagner grading. It was found that with the increase of the grade, the wound recovery time of patients gradually increased, with the longest recovery time for grade V and the shortest recovery time for grade I. Additionally, with the extension of hospital stay, the area of the ulcer wound gradually decreased. In the analysis of induced factors, there were 17 cases of nail cutting, accounting for 15.18%. CONCLUSIONS: The operation of repairing DF ulcer wound under the guidance of plastic surgery principle had good efficacy, safety, and reliability, and was worthy of clinical promotion.

Identification and validation of an epithelial mesenchymal transition-related gene pairs signature for prediction of overall survival in patients with skin cutaneous melanoma.

BACKGROUND: We aimed to construct a novel epithelial-mesenchymal transition (EMT)-related gene pairs (ERGPs) signature to predict overall survival (OS) in skin cutaneous melanoma (CM) patients. METHODS: Expression data of the relevant genes, corresponding clinicopathological parameters, and follow-up data were obtained from The Cancer Genome Atlas database. Univariate Cox regression analysis was utilized to identify ERGPs significantly associated with OS, and LASSO analysis was used to identify the genes used for the construction of the ERGPs signature. The optimal cutoff value determined by the receiver operating characteristic curve was used to classify patients into high-risk and low-risk groups. Survival curves were generated using the Kaplan-Meier method, and differences between the two groups were estimated using the log-rank test. The independent external datasets GSE65904 and GSE19234 were used to verify the performance of the ERGPs signature using the area under the curve (AUC) values. In addition, we also integrated clinicopathological parameters and risk scores to develop a nomogram that can individually predict the prognosis of patients with CM. RESULTS: A total of 104 ERGPs related to OS were obtained, of which 21 ERGPs were selected for the construction of the signature. All CM patients were stratified into high-and low-risk groups based on an optimal risk score cutoff value of 0.281. According to the Kaplan-Meier analysis, the mortality rate in the low-risk group was lower than that in the high-risk group in the TCGA cohort (P < 0.001), GSE65904 cohort (P = 0.006), and GSE19234 cohort (P = 0.002). Multivariate Cox regression analysis indicated that our ERGP signature was an independent risk factor for OS in CM patients in the three cohorts (for TCGA: HR, 2.560; 95% CI [1.907-3.436]; P < 0.001; for GSE65904: HR = 2.235, 95% CI [1.492-3.347], P < 0.001; for GSE19234: HR = 2.458, 95% CI [1.065-5.669], P = 0.035). The AUC value for predicting the 5-year survival rate of patients with CM of our developed model was higher than that of two previously established prognostic signatures. Both the calibration curve and the C-index (0.752, 95% CI [0.678-0.826]) indicated that the developed nomogram was highly accurate. Most importantly, the decision curve analysis results showed that the nomogram had a higher net benefit than that of the American Joint Committee on Cancer stage system. CONCLUSION: Our study established an ERGPs signature that could be potentially used in a clinical setting as a genetic biomarker for risk stratification of CM patients. In addition, the ERGPs signature could also predict which CM patients will benefit from PD-1 and PD-L1 inhibitors.

The effect of inhibiting exosomes derived from adipose-derived stem cells via the TGF-ß1/Smad pathway on the fibrosis of keloid fibroblasts.

BACKGROUND: The main mechanism of keloid formation is that keloid fibroblasts (KFs) apoptosis is inhibited, leading to excessive proliferation. Transforming growth factor-ß1 (TGF-ß1) is a key signal molecule in the process of regulating cell fibrosis. This paper discusses the effect of adipose-derived stem cell exosomes (ADSCs-EXO) on the proliferation and apoptosis of KFS and its possible mechanism, in order to provide reference for the clinical intervention of hypertrophic scar. METHODS: ADSCs were isolated and cultured from human adipose tissue, the supernatant was collected, and the exosomes secreted by ADSCs-EXO were extracted by ultracentrifugation. At the same time, KFs were cultured from human keloid tissue to P3 generation, and then divided into four groups: control group, experimental group A, experimental group B and experimental group C. KFs were then cultured with four concentrations of ADSCs-EXO (0, 1, 10, and 100 µg/mL, respectively). After 24 hours, cells in each group were taken to detect the following: proliferation of cells in each group using the cell counting Kit 8 (CCK-8) method, cell migration ability via the Transwell test, cell apoptosis by flow cytometry, collagen synthesis using the hydroxyproline method, messenger ribonucleic acid (mRNA) expression of fibrosis-related genes in each group by real-time fluorescent polymerase chain amplification, and the expression of fibrosis-related proteins in the cells of each group by western blotting. RESULTS: Compared with the control group, the proliferation rate, migration rate, and collagen synthesis levels in the three experimental groups decreased with the increase of ADSCs-EXO concentration, while the apoptosis rate in the three experimental groups increased with the increase of ADSCs-EXO concentration, and the differences were statistically significant (P<0.05). Also, compared with the control group, the relative mRNA and protein expression of alpha-smooth muscle actin (α-SMA), TGF-ß1, and Smad3 in the three groups decreased significantly, while the expression of three kinds of mRNA and protein decreased with the increase of ADSCs-EXO concentration, and the differences were statistically significant (P<0.05). CONCLUSIONS: ADSCs-EXO may inhibit the proliferation and migration, and promote the apoptosis of KFs by inhibiting the expression of the TGF-ß1/Smad pathway.

Effect of lentivirus-mediated hIL-24 gene on proliferation, migration and invasion of keloid fibroblasts / 中华整形外科杂志

<p><b>OBJECTIVE</b>To investigate the effect of hIL-24 gene on proliferation, migration and invasion activity of human keloid fibroblasts (KFs).</p><p><b>METHODS</b>hIL-24 gene was cloned into lentivirus vector, then the lentivirus particles expressing hlL-24 were infected into KF cells. Real-time PCR and Western blot were performed to examine the expression of hIL-24 in lentivirus infected cells. The growth ability was detected by MTT assay. The cell cycle was analyzed by flow cytometry, The invasion and migration were detected by matrigel invasion assay and wound healing assay.</p><p><b>RESULTS</b>Comparing to controls group and KF-NC group, the expression levels of hIL-24 mRNA and protein were both significantly up-regulated after 4 days of hIL-24 lentivims infection. Comparing with the KF-NC group, MTT assay showed that the A490 of KF-hlL-24 group was down-regulated after lentivims infection ( P < 0. 05 ). Comparing with the KF-NC group, Cell cycle test revealed hlL-24 gene could block KF cells in G1 [(75. 40 ±2. 10)% ] , the proportion of KF cells was decreased in S phase [(4. 96 ± 1. 60)% ] and G2 phase [(0.01 ± 0.01)% ]. After KF cells were infected(P <0.01). Transfection of hlL-24 lentivirus inhibited the migration and invasion activity of KF cells.</p><p><b>CONCLUSION</b>Lentivirus-mediated hlL-24 gene efficiently inhibits proliferation, cell cycle progression, migration and invasion activity of KF cells.</p>