Refracture-related bone transport of tibia: technical notes and preliminary clinical results in nineteen cases.

PURPOSE: Refracture is one of the main complications of bone transport, which brings additional physical and mental burden to surgeries and patients. We aimed to raise a new classification system of refracture-related bone transport based on the Simpson classification and to present our experience on treatment. METHODS: This retrospective analysis included 19 patients with refracture-related bone transport (average age of 37.7 years; 18 men). We developed a modified Simpson classification system to assist decision-making (conservative versus surgical). The ASAMI criteria were used to assess the outcomes at last follow-up. RESULTS: The mean follow-up was 12.3 ± 3.2 months. Complete union was achieved in all patients, with no reinfection. Based on the modified Simpson classification, refracture was Ia type (within regeneration area) in three cases, Ib (collapsed fracture at the regeneration area) in one case, Ic (stress fracture) in three cases, II (at the junction between the regenerate and original bone) in one case, III (at the docking site) in nine cases, and V (at distant site) in two cases. Refracture was managed conservatively in six cases and surgically in 13 cases. Average time to bone union was 2.8 ± 1.2 months in the conservative group versus 4.4 ± 1.4 months in the surgery group. Assessment at the final follow-up using the ASAMI criteria revealed excellent bone result in all patients, excellent functional results in six patients (31.6%), and good functional results in 13 patients. CONCLUSIONS: The modified Simpson classification could include refracture at the docking site and stress fracture in the regeneration zone and provide some guidance in determining the appropriate treatment strategy.

Visible-Light-Driven Semiconductor-Metal Transition in Electron Gas at the (100) Surface of KTaO3.

Two-dimensional electron gas (2DEG) at the (100) KTaO3(KTO) surface and interfaces has attracted extensive interest because of its abundant physical properties. Here, light illumination-induced semiconductor-metal transition in the 2DEG at the KTO surface was investigated. 2DEG was formed at the surface of KTO by argon ion bombardment. The 2DEG prepared with a shorter bombardment time (300 s) exhibits semiconducting behavior in the range of 20~300 K in the dark. However, it shows a different resistance behavior, namely, a metallic state above ~55 K and a semiconducting state below ~55 K when exposed to visible light (405 nm) with a giant conductivity increase of about eight orders of magnitude at 20 K. The suppression of the semiconducting behavior is found to be more pronounced with increasing light power. After removing the illumination, the resistance cannot recover quickly, exhibiting persistent photoconductivity. More interestingly, the photoresponse of the 2DEG below 50 K was almost independent of the laser wavelength, although the photon energy is lower than the band gap of KTO. The present results provide experimental support for tuning oxide 2DEG by photoexcitation, suggesting promising applications of KTO-based 2DEG in future electronic and optoelectronic devices.

Phase II, Open-Label Study of Ciltacabtagene Autoleucel, an Anti-B-Cell Maturation Antigen Chimeric Antigen Receptor-T-Cell Therapy, in Chinese Patients With Relapsed/Refractory Multiple Myeloma (CARTIFAN-1).

PURPOSE: CARTIFAN-1 aimed to evaluate the efficacy and safety of ciltacabtagene autoleucel (cilta-cel), a B-cell maturation antigen-targeting chimeric antigen receptor T-cell therapy, in Chinese patients with relapsed/refractory multiple myeloma (RRMM). METHODS: This pivotal phase II, open-label study (ClinicalTrials.gov identifier: NCT03758417), conducted across eight sites in China, enrolled adult patients with RRMM who had received ≥ 3 lines of prior therapy, including a proteasome inhibitor and immunomodulatory drug. Patients received a single infusion of cilta-cel (target dose 0.75 × 106 chimeric antigen receptor-positive viable T cells/kg). The primary end point was overall response rate. Secondary end points included progression-free survival (PFS), overall survival (OS), and incidence and severity of adverse events (AEs). RESULTS: As of the clinical cutoff of July 19, 2021, 48 patients received a cilta-cel infusion. At an 18-month median follow-up, the overall response rate was 89.6% (95% CI, 77.3 to 96.5), with a median time to first response of approximately 1 month; 77.1% of patients (95% CI, 62.7 to 88.0) achieved complete response or better. Medians for duration of response, PFS, and OS were not reached. The 18-month PFS and OS rates were 66.8% (95% CI, 49.4 to 79.4) and 78.7% (95% CI, 64.0 to 88.0), respectively. Hematologic AEs were common, including anemia (100%), neutropenia (97.9%), lymphopenia (95.8%), and thrombocytopenia (87.5%). Cytokine release syndrome occurred in 97.9% of patients (35.4% grade 3/4); the median time to onset was 7 days, and the median duration was 5 days. Infections occurred in 85.4% of patients (37.5% grade 3/4). Ten deaths occurred after cilta-cel infusion, eight of which were due to treatment-related AEs. CONCLUSION: These data demonstrate a favorable risk-benefit profile for a single infusion of cilta-cel, resulting in early, deep, and durable responses in heavily pretreated patients with RRMM in China.

The Relationship between the Injury Mechanism and the Incidence of ACL Avulsions in Schatzker Type IV Tibial Plateau Fractures: A 3D Quantitative Analysis Based on Mimics Software.

INTRODUCTION: Tibial plateau fractures are often accompanied with ligamental and meniscal injuries. Among which, the combined existence of Schatzker type IV fracture with anterior cruciate ligament (ACL) avulsion has been reported rarely. The purpose of this study was to determine the injury mechanism of Schatzker type IV fracture with ACL avulsion based on Mimics software. METHODS: Ninety-nine Schatzker type IV tibial plateau fractures were retrospectively analyzed by quantitative three-dimensional measurements. ACL avulsions were diagnosed through the data of computed tomography and magnetic resonance imaging. We simulated the knee posture when an injury occurred and defined different injury patterns. The chi-square test was used for determining the main mechanism which causes Schatzker type IV fractures associated with ACL avulsions. RESULTS: There were more ACL avulsions and more displaced ACL avulsions associated with the knee in flexion in the setting of Schatzker type IV fracture (p < 0.05). More ACL avulsions were found in the injury pattern of flexion-valgus than the other injury patterns of the same level (p < 0.05). The rotation of the tibial showed no significant difference in producing ACL avulsion fractures. CONCLUSION: This study found that a flexed knee at the occurrence of a Schatzker type IV tibial plateau fracture is a high-risk factor for causing associated ACL avulsion and producing more displaced avulsions. Flexion-valgus pattern was the main cause of Schatzker type IV fractures associated with ACL avulsions. The findings will help orthopedists understand the injury mechanism and enhance their awareness of such injuries to avoid unfavorable prognosis.

Rational Design, Synthesis, and Biological Evaluation of Novel S1PR2 Antagonists for Reversing 5-FU-Resistance in Colorectal Cancer.

Resistance to 5-FU reduces its clinical efficacy for the treatment of colorectal cancer. Sphingosine-1-phosphate receptor 2 (S1PR2) has emerged as a potential target to reverse 5-FU-resistance by inhibiting the expression of dihydropyrimidine dehydrogenase (DPD). In this study, 38 novel S1PR2 antagonists based on aryl urea structure were designed and synthesized, and the structure-activity relationship was investigated based on the S1PR2 binding assay. Representative compound 43 potently interacts with S1PR2 with a KD value of 0.73 nM. It displays potent 5-FU resensitizing activity in multiple 5-FU-resistant tumor cell lines, particularly in SW620/5-FU (EC50 = 1.99 ± 0.03 µM) but shows no cytotoxicity in the normal colon cell line NCM460 up to 1000 µM. Moreover, 43 significantly enhances the antitumor efficacy of 5-FU in the SW620/5-FU animal model. These data suggest that 43 could be a novel lead compound for developing a 5-FU resensitizing agent.

N6-Methyladenosine Modification of CDH1 mRNA Promotes PM2.5-Induced Pulmonary Fibrosis via Mediating Epithelial Mesenchymal Transition.

The association between ambient airborne fine particulate matter (PM2.5) exposure and respiratory diseases has been investigated in epidemiological studies. To explore the potential mechanism of PM2.5-induced pulmonary fibrosis, 60 mice were divided into 3 groups to expose to different levels of PM2.5 for 8 and 16 weeks: filtered air, unfiltered air, and concentrated PM2.5 air, respectively. BEAS-2B cells were treated with 0, 25, 50, and 100 µg/ml PM2.5 for 24 h. The biomarkers of pulmonary fibrosis, epithelial-mesenchymal transition, N6-methyladenosine (m6A) modification, and metabolism of mRNAs were detected to characterize the effect of PM2.5 exposure. The results illustrated that PM2.5 exposure induced pathological alteration and pulmonary fibrosis in mice. The expression of E-cadherin was decreased whereas vimentin and N-cadherin expression were increased in a dose- and time-dependent manner after PM2.5 exposure. Mechanistically, PM2.5 exposure increased the levels of METTL3-mediated m6A modification of CDH1 mRNA. As a target gene of miR-494-3p, YTHDF2 was upregulated by miR-494-3p down-regulation and then recognized m6A-modified CDH1 mRNA to inhibit the E-cad expression, consequently induced the EMT progression after PM2.5 exposure. Our study indicated that PM2.5 exposure triggered EMT progression to promote the pulmonary fibrosis via miR-494-3p/YTHDF2 recognized and METTL3 mediated m6A modification.

Design, synthesis and biological evaluation of sphingosine-1-phosphate receptor 2 antagonists as potent 5-FU-resistance reversal agents for the treatment of colorectal cancer.

5-Fluorouracil (5-FU) and its prodrugs are the essential clinical drugs for colorectal cancer (CRC) treatment. However, the drug resistance of 5-FU has caused high mortality of CRC patients. Thus, it is urgent to develop reversal agents of 5-FU resistance. Sphingosine-1-phosphate receptor 2 (S1PR2) was proved to be a potential target for reversing 5-FU resistance, but the activity of known S1PR2 antagonists JTE-013 were weak in 5-FU-resistant cell lines. To develop more potent S1PR2 antagonists to treat 5-FU-resistant cancer, a series of JTE-013 derivatives were designed and synthesized. The most promising compound 40 could markedly reverse the resistance in 5-FU-resistant HCT116 cells and 5-FU-resistant SW620 cells via inhibiting the expression of dihydropyrimidine dehydrogenase (DPD). The key was that compound 40 with improved pharmacokinetic properties significantly increased the inhibitory rate of 5-FU in the SW620/5-FU cells xenograft model with no observable toxicity by inhibiting the expression of DPD in tumor and liver tissues. Altogether, these results suggest that compound 40 may be a promising drug candidate to reverse 5-FU resistance in the treatment of CRC.

Overlapping motifs on the herpes viral proteins ICP27 and ORF57 mediate interactions with the mRNA export adaptors ALYREF and UIF.

The TREX complex mediates the passage of bulk cellular mRNA export to the nuclear export factor TAP/NXF1 via the export adaptors ALYREF or UIF, which appear to act in a redundant manner. TREX complex recruitment to nascent RNA is coupled with 5' capping, splicing and polyadenylation. Therefore to facilitate expression from their intronless genes, herpes viruses have evolved a mechanism to circumvent these cellular controls. Central to this process is a protein from the conserved ICP27 family, which binds viral transcripts and cellular TREX complex components including ALYREF. Here we have identified a novel interaction between HSV-1 ICP27 and an N-terminal domain of UIF in vivo, and used NMR spectroscopy to locate the UIF binding site within an intrinsically disordered region of ICP27. We also characterized the interaction sites of the ICP27 homolog ORF57 from KSHV with UIF and ALYREF using NMR, revealing previously unidentified binding motifs. In both ORF57 and ICP27 the interaction sites for ALYREF and UIF partially overlap, suggestive of mutually exclusive binding. The data provide a map of the binding sites responsible for promoting herpes virus mRNA export, enabling future studies to accurately probe these interactions and reveal the functional consequences for UIF and ALYREF redundancy.

Protective effects of allicin on 1,3-DCP-induced lipid metabolism disorder in HepG2 cells.

Allicin (2-propene-1-sulfinothioic acid S-2-propenyl ester), with quite a good range of hepatoprotective and antineoplastic properties, is a functional substance from garlic (Allium sativum L.) The purpose of this study was to provide evidence that allicin could protect 1,3-DCP-induced lipid metabolism disorder in HepG2 cells. Allicin reduced the accumulation of triglycerides (TG) and total cholesterol (TC) in 1,3-DCP-induced HepG2 cells. Allicin significantly increased the phosphorylation of AMP-activated protein kinase (AMPK) and down-regulated the levels of sterol regulatory element binding protein-1 (SREBP-1) and sterol regulatory element binding protein-2 (SREBP-2) in 1,3-DCP-induced HepG2 cells. Additionally, allicin had obvious recovery influence on the phosphorylation level of PKA and CREB in 1,3-DCP-induced HepG2 cells. These observations indicated that allicin alleviated lipid metabolism disorder induced by 1,3-DCP in HepG2 cells by regulating AMPK-SREBPs and PKA-CREB signaling pathways.

Investigation of Microsurgical Technique Combined With Skin Flap Expansion for Ear Reconstruction in Treating Hunter Type III Congenital Microtia.

OBJECTIVE: This study aims to observe the efficacies of microsurgical technique combined with the Zhuang's skin soft tissue expander in treating Hunter type III congenital microtia. METHODS: Fifty-eight patients (61 ears) were enrolled from 2003 to 2012; the skin tissue expander was embedded subepidermally in the first stage via the intrahairline longitudinal incision in the postauricular mastoid area, the diseased-side rib cartilage was then taken for preparing the ear bracket in the second stage, and the tragus was surgically reconstructed in the third stage. RESULTS: The mean follow-up lasted 6 months to 10 years, the results were satisfactory for 54 ears and acceptable for 5 ears, and 2 ears (in two patients) appeared with complications, including 1 case of ear flap expansion rupture and 1 case of postoperative lateral helix flap necrosis. CONCLUSIONS: The combination of microsurgical technique, Zhuang's skin soft tissue expander, and autogenous rib cartilage graft could achieve satisfactory results in treating Hunter type III congenital microtia, and the complications were less, so it was worthy of clinical applications.

Application of circulating tumor cells scope technique on circulating tumor cell research.

Circulating tumor cells (CTCs) are becoming promising biomarkers in several cancers, such as colon, prostate, and breast carcinomas. Independent research groups have reported a correlation between CTC numbers and patient prognosis. Even more, the development of personalized medicine gives physicians impetus to utilize the advancement of molecular characterization of CTCs. This review introduces a new technique, CTCscope, and compares it with the current methods of CTCs detection, with particular emphasis on cancer research, and discusses the future application of this new method from bench to bed-side.

[Correction of secondary lip whistle deformities and nasal base depression after bilateral cleft lip repair with lip subdermal soft tissue flap].

OBJECTIVE: To explore a new method to correct secondary lip whistle deformities and nasal base depression after bilateral complete cleft lip (BCCL) repair with lip subdermal soft tissue flap. METHODS: Bilateral subdermal soft tissue "C" flaps and "lambda" flap were designed to repair secondary deformities of nasal base and reconstruct vermilion tubercle in patients after BCCL repair. RESULTS: Good results were achieved in all the patients with primary healing. No flap necrosis happened. The result was satisfactory. CONCLUSIONS: With bilateral subdermal soft tissue "C" flaps and " lambda" flap, nasal base depression deformities and lip whistle deformities can be corrected. It is an ideal method for correction of deformities after BCCL repair.

Hepatitis B virus (HBV) surface antigen interacts with and promotes cyclophilin a secretion: possible link to pathogenesis of HBV infection.

Cyclophilin A (CypA), predominantly located intracellularly, is a multifunctional protein. We previously reported decreased CypA levels in hepatocytes of transgenic mice expressing hepatitis B virus (HBV) surface antigen (HBsAg). In this study, we found that expression of HBV small surface protein (SHBs) in human hepatoma cell lines specifically triggered CypA secretion, whereas SHBs added extracellularly to culture medium did not. Moreover, CypA secretion was not promoted by the expression of a secretion deficient SHBs mutant, suggesting a close association between secretion of CypA and SHBs. Interaction between CypA and SHBs was observed by using coimmunoprecipitation and glutathione S-transferase pull-down assays. Hydrodynamic injection of the SHBs expression construct into C57BL/6J mice resulted in increased serum CypA levels and ALT/AST levels, as well as the infiltration of inflammatory cells surrounding SHBs-positive hepatocytes. The inflammatory response and serum ALT/AST level were reduced when the chemotactic effect of CypA was inhibited by cyclosporine and anti-CD147 antibody. Furthermore, higher serum CypA levels were detected in chronic hepatitis B patients than in healthy individuals. In HBV patients who had received liver transplantation, serum CypA levels declined dramatically after the loss of HBsAg as a consequence of liver transplantation. Taken together, these results indicate that expression and secretion of SHBs can promote CypA secretion, which may contribute to the pathogenesis of HBV infection.

Proteomic analysis of cell lines expressing small hepatitis B surface antigen revealed decreased glucose-regulated protein 78 kDa expression in association with higher susceptibility to apoptosis.

Accumulating evidence suggests a key role of hepatocyte apoptosis in the pathogenesis of viral hepatitis B. It was found in this study that stable expression of small hepatitis B surface antigen (SHBs) in HepG2 and Huh7 cells increased susceptibility to apoptosis. Proteomic analysis of SHBs expressing HepG2 cells revealed 43 down-regulated and 38 up-regulated proteins. Some have been implicated in apoptosis, including glucose-regulated protein 78 kDa (GRP78), heterogeneous nuclear ribonucleoprotein H3 (hnRNP H), Rho GDP dissociation inhibitor (GDI), cystatin B, far upstream element-binding protein (FUSEbp), and TNF receptor-associated protein 1 (TRAP1). Differential expression of GRP78 and several other proteins was confirmed by Western blot analysis. Replenishing GRP78 improved cellular resistance to apoptosis, whereas reduction of GRP78 by siRNA increased susceptibility even in the absence of SHBs. Taken together, these results suggest that HBsAg plays a pro-apoptotic role through down-regulation of GRP78.

Role of hepatitis B surface antigen in the development of hepatocellular carcinoma: regulation of lymphoid enhancer-binding factor 1.

BACKGROUND: There are around 350 million of hepatitis B surface antigen (HBsAg) carriers worldwide, and among them, high risk of developing hepatocellular carcinoma (HCC) has been identified by epidemiological studies. To date, the molecular role of HBsAg in HCC development has not been fully studied. We have previously reported that in cell cultures, HBsAg up-regulated the expression of lymphoid enhancer-binding factor 1 (LEF-1), a key component of the Wnt pathway. In this study we aimed to study this effect of HBsAg on LEF-1 in the development of HCC. METHODS: Expression of HBsAg, LEF-1 and its downstream effector genes were compared among 30 HCCs, their peritumor tissue counterparts and 9 normal control liver tissues by quantitative real-time PCR. In addition, immunohistochemical staining studies on HBsAg and LEF-1 expression were conducted among these samples. RESULTS: The expression of LEF-1 was compared between 13 HBsAg positive HCC tissues and 17 HBsAg negative HCC tissues. Simultaneous detection of LEF-1 and HBsAg was observed in HBsAg positive HCC tissues and, additionally, the simultaneous detection of HBsAg and LEF-1 was more pronounced in peritumor tissues, compared to that in the tumor tissues. The distribution of cellular LEF-1 in peritumor tissues was predominantly in the cytoplasm; while LEF-1 in the tumor tissues was located either exclusively in the nucleus or both in the nucleus and cytoplasm. By real-time PCR, the expression levels of LEF-1 downstream effector genes cyclin D1 and c-myc were higher in peritumor cells compared to that of the tumor cells. However, a 38 kDa truncated isoform of LEF-1, rather than the 55 kDa wild-type LEF-1, was significantly elevated in the HBsAg positive tumor cells. CONCLUSION: Data indicate that deregulation of the Wnt pathway by HBsAg occurred in HBV-associated HCCs, but was more pronounced in the peritumor cells. It is speculated that HBsAg could stimulate proliferation and functional modification of hepatocytes via LEF-1 through the Wnt pathway at the pre-malignant stage.

A double-spliced defective hepatitis B virus genome derived from hepatocellular carcinoma tissue enhanced replication of full-length virus.

In hepatitis B virus (HBV) replication cycle, pregenomic RNA undergoes splicing and the reverse transcribed defective genomes can be packaged and released. Various types of spliced defective HBV genomes have been isolated from the sera and liver tissues of viral hepatitis B patients. To explore the functions of a 2.2 kb double spliced HBV variant, a 3.2 kb full-length HBV isolate (#97-34) and its 2.2 kb double-spliced HBV variant (#AP-12) from the tumor tissue of a patient with hepatocellular carcinoma (HCC) were amplified and cloned. Sequencing results showed that #AP12 had deletions in pre-S2, part of pre-S1, S genes, part of the spacer, and part of the reverse transcriptase gene, while the X gene was intact. When this defective double-spliced genome and its full-length counterpart genome were co-transfected into HepG2 cells, the former was shown to enhance the replication of the latter, both by real-time PCR and Southern blotting. When a replication incompetent clone 97-34G1881A was used to co-transfect with #AP12, #AP12 DNA was increased, indicating that replication of the wild-type virus was not the only factor involved in this observation. However, the replication enhancing competency of #AP12 was shown to require an intact HBV X expression cassette. The double-spliced defective variant might contribute to persistent HBV replication in a subpopulation of HCC patients.

[Preliminary study on the phenomenon of epidermal stem cell ectopy in expanded skin].

OBJECTIVE: To observe the differentiation and distribution of epidermal stem cell (ESC) after skin soft tissue expansion, and to initially probe into the growth mechanism of expanded skin tissue. METHODS: Samples of normal skin and expanded skin (mean effusion period 45 days) were harvested from head and cervical region in 15 patients who underwent II stage surgery after skin expansion. Samples were divided into scalp adjacent to the center of expander group (expanded scalp, 3 cm from the vertical axis of the expander), scalp from lateral part of the expander group (expanded scalp, 5 - 7 cm lateral to the vertical axis of the expander), cervical skin expansion group, un-expanded scalp control group, and un-expanded cervical skin control group, according to the position of skin harvested. The tissue structure of skin in each group was observed with HE staining, and the differentiation and distribution characteristics of cytokeratin 19 (CK19) positive cells were observed with immunohistochemical staining. RESULTS: Compared with those in the un-expanded control groups, uneven, relatively thickened and obviously folded epidermis with more cell layers and cells with obvious aggregation close to the basal layer were observed in the expanded groups, but those cells were not well-arranged and the transition of polarity was not obvious. The continuity of CK19 positive cells in the basal layer of skin was observed in each of the expanded group with immunohistochemical staining, and positive cells increased obviously and arranged in multilayer in certain parts of basal layer. Clustered or dispersed CK19 positive cells were also observed outside the basal layer. No above-mentioned phenomenon was observed in the un-expanded control group. CONCLUSIONS: The proliferation and differentiation of ESC with ectopic distribution may enhance the repair process after skin soft tissue expansion.

Gene-expression profiles of a hepatitis B small surface antigen-secreting cell line reveal upregulation of lymphoid enhancer-binding factor 1.

The genome of hepatitis B virus (HBV) consists of four open reading frames, encoding the envelope proteins (Pre-S/S), the core proteins (Pre-C/C), the polymerase (P) and the transactivating X protein (X). In the sera of HBV-infected patients, hepatitis B surface antigen (HBsAg) particles without the viral genome can outnumber virions by more than 1000-fold. To analyse the interactions between HBsAg and host cells, global gene-expression profiles of a small HBsAg (SHBs)-secreting stable cell line (HepG2-S-G2) and its counterpart control cell line (HepG2-Neo-F4) were compared. Marked upregulation of lymphoid enhancer-binding factor 1 (LEF-1), a transcription factor in the Wnt pathway, was found in SHBs-expressing cells and was confirmed by interference experiments with small interfering RNA. However, compared with the control cells, HepG2-S-G2 did not show higher proliferative competence in culture or increased tumorigenesis in nude mice. A possible mechanism to explain the discrepancy between the upregulation of LEF-1 and the lack of increased tumorigenesis is SHBs expression resulting in altered expression and distribution of LEF-1 protein in cell compartments and upregulation of LEF-1 isoforms that could suppress, rather than enhance, the Wnt pathway.

[The applications of the repetitive sub-platysmal expansion in repair the defects of skin and soft tissue in face and neck].

OBJECTIVE: To study a new effective approach which repairs large defects of skin and soft tissue in neck and face. METHOD: This procedure accomplishes repetitive sub-platysmal expansion to form large musculocutaneous flap with underlying pedicel. The surgeon slides it toward neck and face to repair the defects of skin and soft tissue. RESULT: Eleven patients, who had such defects in neck, face, cheek, chin or submental skin and soft tissue, underwent this treatment. All the flaps survive with no complications of blood supply deficiency or necrosis. The short-term and long-term results are both satisfying. CONCLUSION: This method, making repetitive sub-platysmal expansion to form musculocutaneous flap and then slide it toward neck/face to repair large defects of skin and soft tissue, proves to be safe and reliable. And appropriate cases and strict operations are important.