The use of fibular graft for the reconstruction of bone defects has been demonstrated to be a reliable method. The aim of this study was to assess the clinical outcome of graft union, functional outcome (hypertrophy of the graft bones) and complications of both non-vascularized and vascularized grafts. From 1981 to 2015, 10 patients were treated using non-vascularized fibular graft or free vascularized fibular graft. The outcomes were bony union time, graft hypertrophy and complications based on radiograph and functional outcomes according to the Musculoskeletal Tumor Society (MSTS) score. Mobility of the ankle at the donor site was evaluated using the Kofoed ankle score system. This study included 10 patients with an average follow-up of 6.8 years. The union rate for all patients was 100%. The mean union time was 21.3 weeks for vascularized fibular grafts and 30.5 weeks for non-vascularized fibular grafts (P = .310). There was a significant difference between the upper limbs and the lower limbs regarding hypertrophy of the grafts in 5 patients (P = .003). The mean MSTS score in 10 patients was 84% (range 53%–97%). Stress fracture of the graft occurred in 1 patient. Donor site complications, including valgus deformity and length discrepancy, between 2 legs occurred in 2 patients who were under 18 years of age at the time of operation (P = .114). The mean Kofoed score was 96.8 (range 88–100). A greater increase in hypertrophy of grafts was observed with reconstruction in the lower limbs. There was no difference in MSTS score between these 2 types of grafts. Children were more likely to experience the valgus deformity at the donor site after harvesting the fibula. Keeping at least the distal 1/4 of the fibula intact during the surgery is a valid means of ensuring ankle stability at the donor site, and children should be considered for prophylactic distal tibiofibular synostosis creation to prevent the valgus deformity of the ankle at the donor site.

HnRNP K is a heterogeneous nuclear ribonucleoprotein and has been identified as an oncogene in most solid tumors via regulating gene expression or alternative splicing of genes by binding both DNA and pre-mRNA. However, how hnRNP K affects tumorigenesis and regulates the gene expression in cervical cancer (CESC) remains to be elucidated. In these data, higher expression of hnRNP K was observed in CESC and was negatively correlated with the patient survival time. We then overexpressed hnRNP K (hnRNP K-OE) and found that its overexpression promoted cell proliferation in HeLa cells ( P = 0.0052). Next, global transcriptome sequencing (RNA-seq) experiments were conducted to explore gene expression and alternative splicing profiles regulated by hnRNP K. It is shown that upregulated genes by hnRNP K-OE were associated with inflammatory response and an apoptotic process of neuron cells, which involves in cancer. In addition, the alternative splicing of those genes regulated by hnRNP K-OE was associated with transcriptional regulation. Analysis of the binding features of dysregulated transcription factors (TFs) in the promoter region of the inflammatory response genes regulated by hnRNP K revealed that hnRNP K may modulate the expression level of genes related to inflammatory response by influencing the alternative splicing of TFs. Among these hnRNP K-TFs-inflammatory gene regulatory networks, quantitative reverse transcription polymerase chain reaction (RT-qPCR) experiments and gene silencing were conducted to verify the hnRNP K-IRF1-CCL5 axis. In conclusion, the hnRNP K-TFs-inflammatory gene regulatory axis provides a novel molecular mechanism for hnRNP K in promoting CESC and offers a new therapeutic target.

Objective To present the use of an intermediate dorsal neurocutaneous flap for the reconstruction of defects on the distal foot. Methods From September 2016 to October 2018, five patients (mean age at operation 33.8 years; range, 7–70 years; female/male = 2/3) with skin defects on one of their feet caused by road‐traffic accidents, electrical injury, and syndactyly correction were retrospectively reviewed. The size of the defects ranged from 2.0 cm × 1.0 cm to 5.0 cm × 3.5 cm. All patients had undergone a reconstruction surgery using intermediate dorsal neurocutaneous flap. One patient underwent a syndactyly correction, and four patients first experienced aggressive debridement. The sizes of the flaps were between 5.0 cm × 2.0 cm and 6.0 cm × 4.0 cm. The function, appearance, and pain of the injured foot were assessed using the Chinese Manchester Foot Pain and Disability Index and visual analogue scale. Results These five patients were systematically followed up for a mean of 15.8 months (range, 12–20 months). The donor sites were closed primarily in two cases, and skin grafts were performed in three cases. All the flaps survived with a success rate of 100%; the wounds healed well, and the color matches were excellent. Partial superficial flap necrosis occurred in one of five flaps, which was treated by dressing change using a hypertonic saline gauze. No significant problems were found at the donor site in any patient immediately afterwards or at follow‐up. There were no problems in any patients associated with wearing shoes. Based on the Chinese Manchester Foot Pain and Disability Index, four patients were strongly satisfied and one was satisfied with the recovery of physical function; all the patients were strongly satisfied with the appearance of the injured foot; all five patients had an excellent score of pain intensity subscale. Except for one patient who reported mild pain, all the other patients reported no pain based on the visual analogue scale. Two typical cases are presented in this paper. Conclusions The intermediate dorsal neurocutaneous flap is an alternative and effective technique that can reliably cover minor‐ to medium‐sized defects on the distal foot, toes, and web spaces. This surgical method leads to satisfactory functional recovery with minimal donor site morbidity, and no major vessels need to be sacrificed. This procedure offers an advisable option for orthopaedic surgeons to treat defects on the distal foot.

Chronic wounds represent a significant clinical challenge due to their impact on patient quality of life and healthcare costs, necessitating innovative therapeutic strategies. USP7 is an important member of the deubiquitinating enzyme family. Several studies have shown that USP7 promotes M1 polarization of macrophages and inhibits M2 polarization through various pathways in the tumour environment. However, it is unclear whether USP7 also promotes M1 polarization of macrophages in a wound inflammatory environment. This study aims to elucidate the role of Ubiquitin-specific peptidase 7 (USP7) in modulating M1 macrophage polarization and its underlying mechanisms in wound healing. Utilizing both in vitro and in vivo models, we investigated the effects of USP7 on M1 macrophage polarization and wound healing outcomes. Our findings indicate that USP7 inhibition significantly reduces M1 macrophage polarization, as evidenced by the levels of pro-inflammatory cytokines such as IL-1β, IL-6, and TNF-α being significantly lower than the control group when Usp7 is knockout (P < 0.05). Furthermore, we observed that Usp7-cKO in BMDM suppresses the NF-κB and MAPK signaling pathways, indicating a shift towards an anti-inflammatory phenotype. Additionally, Usp7-cKO has nearly doubled the migration and proliferation of fibroblasts in the inflammatory environment compared to the control group. Importantly, mice with Usp7-cKO in BMDM markedly improved wound healing efficiency in murine models and promoted angiogenesis. In conclusion, our study provides novel insights into the regulatory mechanisms of USP7 in M1 macrophage polarization and its potential therapeutic applications for wound management, paving the way for future research aimed at developing small molecule inhibitors targeting USP7 to improve tissue repair outcomes.