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As one of the most common pathological processes in the clinic, wound healing has always been an important topic in medical research. Improving the wound healing environment, shortening the healing time and promoting fast and effective wound healing are hot and challenging issues in clinical practice. The nuclear factor‐erythroid–related factor 2 (NFE2L2 or NRF2) signalling pathway reduces oxidative damage and participates in the regulation of anti‐oxidative gene expression in the process of oxidative stress and thus improves the cell protection. Activation of the NRF2 signalling pathway increases the resistance of the cell to chemical carcinogens and inflammation. The signal transduction pathway regulates anti‐inflammatory and antioxidant effects by regulating calcium ions, mitochondrial oxidative stress, autophagy, ferroptosis, pyroptosis and apoptosis. In this article, the role of the NRF2 signalling pathway in wound healing and its research progress in recent years are reviewed. In short, the NRF2 signalling pathway has crucial clinical significance in wound healing and is worthy of further study.

Thumb duplication is one of common anomalies of the hand. Among of Wassel type IV subtypes, type IV-D duplication with a zigzag deformity is most challenging for reconstructing. Several factors may affect the surgical outcomes. This study aimed to present an opening wedge osteotomy at proximal phalangeal neck for treating type IV-D duplication. Data from 14 patients are presented in this study. Eight patients had duplication of the right thumb, and six left thumb. After removal of radial supernumerary thumb, a snug collateral ligament was repaired to correct angular deformity of metacarpophalangeal joint (MCP). Angular deformity of the interphalangeal (IP) joint was corrected by an opening wedge osteotomy at the proximal phalangeal neck. A wedge bone from ablated thumb was grafted to correct the malalignment. IP joint was further stabilized by plication of the ulnar capsule. The relocation of radial part of FPL to the center of distal phalangeal base by use of pull-out suture technique RESULTS: After surgery, the angulations of the IP joints and the MCP joints were improved. Bone union was observed in all patients. According to the Japanese Society for Surgery of the Hand evaluation form, twelve cases were rated good, 2 cases fair. Stability of IP and MCP joints was good in all cases. The active ROM of IP was less in residual thumb than in normal thumb. Small nails were observed in some patients. Although the reconstructed thumbs were smaller than normal counterparts, they were aligned and with stable joints. The opening wedge osteotomy at proximal phalangeal neck could improve realignment of IP joint and prevent reoccurrence of deformity over time. Der Doppeldaumen zählt zu den häufigsten Anomalien der Hand. Von den Subtypen des Typs IV nach Wassel stellt die Duplikation vom Typ IV-D mit Zickzack-Deformität die größte Herausforderung an die Rekonstruktion dar. Mehrere Faktoren können die chirurgischen Ergebnisse beeinflussen. Ziel dieser Studie war es, eine Opening-Wedge-Osteotomie am Hals der proximalen Phalanx zur Behandlung der Duplikation vom Typ IV-D vorzustellen. In dieser Studie werden die Daten von 14 Patienten präsentiert. Bei acht Patienten war der rechte Daumen dupliziert, bei sechs Patienten der linke. Nach Entfernung des radialen überzähligen Daumens wurde zur Korrektur der Winkeldeformität des Metacarpophalangealgelenks (MCP) eine straffe Rekonstruktion des Seitenbandes durchgeführt. Die Winkeldeformität des Interphalangeal(IP)-Gelenks wurde durch eine Opening-Wedge-Osteotomie am Hals der proximalen Phalanx korrigiert. Zur Korrektur der Fehlstellung wurde ein Knochenkeil aus dem abladierten Daumen transplantiert. Das IP-Gelenk wurde durch Raffung der ulnaren Kapsel weiter stabilisiert. Mithilfe der „Pull-Out“-Nahttechnik wurde der radiale Anteil der Sehne des M. flexor pollicis longus zur Mitte der Basis der distalen Phalanx verlagert. Nach der Operation zeigte sich eine Verbesserung der Winkelstellung in den IP-Gelenken und den MCP-Gelenken. Bei allen Patienten wurde eine knöcherne Durchbauung erreicht. Gemäß dem Auswertebogen der Japanischen Gesellschaft für Handchirurgie wurden zwölf Fälle als „gut“ und zwei als „befriedigend“ eingestuft. Die Stabilität der IP- und MCP-Gelenke war bei allen Patienten gut. Der aktive Bewegungsumfang des IP-Gelenks war im verbleibenden Daumen geringer als bei normalen Daumen. Bei einigen Patienten fanden sich verkürzte Nägel. Obwohl die rekonstruierten Daumen kleiner waren als ihre normalen Pendants, zeigten sie eine regelrechte Ausrichtung und stabile Gelenke. Die Opening-Wedge-Osteotomie am Hals der proximalen Phalanx könnte die Neuausrichtung des IP-Gelenks verbessern und rezidivierende Deformitäten im weiteren Verlauf verhindern.

Background aims Tissue engineering technology is a promising therapeutic strategy in peripheral nerve injury. Schwann cells (SCs) are deemed to be a vital component of cell-based nerve regeneration therapies. Many methods for producing SC-like cells derived from adipose-derived stromal cells (ADSCs) have been explored, but their phenotypic and functional characteristics remain unsatisfactory. Methods We investigated whether human ADSCs can be induced to differentiate into mature and stable SC-like cells with the addition of insulin, progestero``ne and glucocorticoids. The phenotypic and functional characteristics of new differentiated ADSCs (modified SC-like cells) were evaluated by real-time quantitative polymerase chain reaction, enzyme-linked immunosorbent assay and immunocytochemistry in vitro. Cells loaded into collagen sponge biomaterials were implanted around transected sciatic nerves with a 10-mm gap in vivo. The axon regrowth and functional recovery of the regenerated nerves were assessed by immunohistochemistry and Walking footprint analysis. Results After differentiation induction, the modified SC-like cells showed significantly up-regulated levels of S100B and P0 and enhanced proliferative and migratory capacities. In addition, the modified SC-like cells showed increased secretion of neurotrophic factors, and their functional characteristics were maintained for more than 3 weeks after removing the induction reagents. The modified SC-like cells exhibited significantly enhanced axon regrowth, myelination and functional recovery after sciatic nerve injury. Conclusions Overall, the results suggest that this modified induction method can induce human ADSCs to differentiate into cells with the molecular and functional properties of mature SCs and increase the promotion of peripheral nerve regeneration.

Diabetic peripheral neuropathy (DPN) is considered to be the most frequent neuropathic complication of diabetes, and severely affects the quality of life of patients. Long noncoding RNAs (lncRNAs) participate in various pathophysiological processes and associate with many diseases. However, the exact impact of lncRNAs on DPN remains obscure. To discover a potential connection, a microarray study was conducted to analyze the expression profiling of lncRNAs and messenger RNAs (mRNAs) in dorsal root ganglia (DRG) from streptozotocin-induced diabetic rats with DPN. As a result, 983 lncRNAs and 1357 mRNAs were aberrantly expressed compared with control samples. Using bioinformatics analyses, we identified 558 Gene Ontology terms and 94 Kyoto Encyclopedia of Genes and Genomes pathways to be significantly enriched. Additionally, the signal-net analysis indicated that integrin receptors, including Itgb3, Itgb1, Itgb8, and Itga6, might be important players in network regulation. Furthermore, the lncRNA-mRNA network analysis showed dynamic interactions between the dysregulated lncRNAs and mRNAs. This is the first study to present an overview of lncRNA and mRNA expressions in DRG tissues from DPN rats. Our results indicate that these differentially expressed lncRNAs may have crucial roles in pathological processes of DPN by regulating their coexpressed mRNAs. The data may provide novel targets for future studies, which should focus on validating their roles in the progression of DPN.

Background Epidemiological and clinical features of patients with COVID‐19 have been reported, but none of them focused on medical staff, and few predictors of the duration of viral shedding have been reported. It is urgent to help healthcare workers prevent and recover quickly from the coronavirus disease 2019 (COVID‐19). Methods We enrolled 140 medical workers with COVID‐19 in Wuhan. Epidemiological, demographic, clinical, laboratory, radiological, treatment and clinical outcome data were collected, and predictors of the duration of viral shedding were explored through multivariable linear regression analysis. Results The medical staff with COVID‐19 presented mild clinical symptoms and showed a low frequency of abnormal laboratory indicators. All the medical staff were cured and discharged, of whom 96 (68.6%) were female, 39 (27.9%) had underlying diseases, the median age was 36.0 years, and 104 (74.3%) were infected whilst working in hospital. The median duration of viral shedding was 25.0 days (IQR:20.0–30.0). Multivariable linear regression analysis showed reducing viral shedding duration was associated with receiving recombinant human interferon alpha (rIFN‐α) treatment, whilst the prolonged duration of viral shedding correlated with the use of glucocorticoid treatment, the durations from the first symptom to hospital admission and the improvement in chest computed tomography (CT) evidence. Moreover, infected healthcare workers with lymphocytes less than 1.1 × 109/L on admission had prolonged viral shedding. Conclusion Medical staff with timely medical interventions shows milder clinical features. Glucocorticoid treatment and lymphocytes less than 1.1 × 109/L are associated with prolonged viral shedding. Early admission and rIFN‐α treatment help shorten the duration of viral shedding.

Aim We aim to study the anti-apoptotic effect of microRNA-21-5p (miR-21-5p) in the oxidative stress-induced apoptosis of Schwann cells and the relevant mechanism in this research, laying a foundation for the treatment of peripheral neuropathy (PNP). Methods and materials The oxidative stress model was established by using hydrogen peroxide (H2O2). ROS level were detected by DCFH-DA (2,7-Dichlorodi-hydrofluorescein diacetate). Western blot and fluorescence staining were used to detect the apoptosis and autophagy level. The miR-21-5p overexpression model was established by transfection of miR-21-5p mimics into RSC96 cells. Five groups of control group, H2O2 group, H2O2 + chloroquine (CQ) group, H2O2 + miR-21-5p mimics group, and H2O2 + miR-21-5p mimics+rapamycin (RAPA) group were included in our experiment. Key findings Compared with control group, miR-21-5p was decreased in H2O2-treated RSC96 cells, while autophagy and apoptosis were both promoted. The result revealed that apoptosis was probably triggered by activation of autophagy in H2O2-treated group. In order to verify the relationship between autophagy and apoptosis more accurately, we used CQ to inhibit autophagy. Compared with H2O2-treated group, autophagy and apoptosis were both weakened in H2O2 + CQ group. Subsequently, we found the antiapoptotic effect of miR-21-5p in this model, overexpression of miR-21-5p prevented cells from being damaged by oxidative stress, it induced the decrease of PTEN and the level of autophagy, leading to decreased level of apoptosis. Significance The identified relationship between miR-21-5p, apoptosis, and autophagy promotes us to find a new mechanism to improve the treatment for PNP.

Background Diabetes mellitus is a worldwide disease with high incidence. Diabetic peripheral neuropathy (DPN) is one of the most common but often ignored complications of diabetes mellitus that cause numbness and pain, even paralysis. Recent studies demonstrate that Schwann cells (SCs) in the peripheral nervous system play an essential role in the pathogenesis of DPN. Furthermore, various transcriptome analyses constructed by RNA-seq or microarray have provided a comprehensive understanding of molecular mechanisms and regulatory interaction networks involved in many diseases. However, the detailed mechanisms and competing endogenous RNA (ceRNA) network of SCs in DPN remain largely unknown. Methods Whole-transcriptome sequencing technology was applied to systematically analyze the differentially expressed mRNAs, lncRNAs and miRNAs in SCs from DPN rats and control rats. Gene ontology (GO) and KEGG pathway enrichment analyses were used to investigate the potential functions of the differentially expressed genes. Following this, lncRNA-mRNA co-expression network and ceRNA regulatory network were constructed by bioinformatics analysis methods. Results The results showed that 2925 mRNAs, 164 lncRNAs and 49 miRNAs were significantly differently expressed in SCs from DPN rats compared with control rats. 13 mRNAs, 7 lncRNAs and 7 miRNAs were validated by qRT-PCR and consistent with the RNA-seq data. Functional and pathway analyses revealed that many enriched biological processes of GO terms and pathways were highly correlated with the function of SCs and the pathogenesis of DPN. Furthermore, a global lncRNA-miRNA-mRNA ceRNA regulatory network in DPN model was constructed and miR-212-5p and the significantly correlated lncRNAs with high degree were identified as key mediators in the pathophysiological processes of SCs in DPN. These RNAs would contribute to the diagnosis and treatment of DPN. Conclusion Our study has shown that differentially expressed RNAs have complex interactions among them. They also play critical roles in regulating functions of SCs involved in the pathogenesis of DPN. The novel competitive endogenous RNA network provides new insight for exploring the underlying molecular mechanism of DPN and further investigation may have clinical application value.

Schwannoma, which is also known as neurilemmoma, is a type of tumor that arises from the peripheral nerve sheaths. Cases of schwannomas located in different regions have been reported. Some schwannomas present as asymptomatic masses, while others cause discomfort, such as pain and numbness. Magnetic resonance imaging (MRI) is a valuable diagnostic tool. A 23-year-old woman presented to our hospital with a mass in the left axilla that was misdiagnosed as mammae erraticae. The patient also considered the condition to be mammae erraticae for approximately 14 months because of a lack of symptoms. MRI was recommended by a surgeon from the galactophore department. A giant schwannoma was found. The mass was surgically excised, while preserving the continuity of the long thoracic nerve. Routine histopathological analysis confirmed the presence of a benign schwannoma. Schwannomas located in the axilla are rare and may be easily misdiagnosed as mammae erraticae or enlarged lymph nodes. Early investigation is necessary to make the diagnosis, and surgical excision is usually curative.

Neuroactive steroids such as progesterone, testosterone, and their derivatives have been widely studied for their neuroprotective roles in the nervous system. Autologous nerve transplantation is considered as the gold standard repair technique when primary suture is impossible; nevertheless, this method is far from ideal. In this study, we aimed to explore the impact of dihydrotestosterone (DHT), a 5α-reduced derivative of testosterone, on the recovery of peripheral nerve injury treated with autologous nerve transplantation. Sprague-Dawley rats were subjected to a 10-mm right side sciatic nerve reversed autologous nerve transplantation and randomly divided into groups that received DHT or DHT + flutamide (an androgen receptor blocker) daily for 8 weeks after operation. Our results demonstrated that DHT could speed up the rate of axonal regeneration and increase the expression of myelin protein zero (P0) in autograft reversal sciatic nerves. Thus, our study provided new insights into improving the prognosis of patients with long gap peripheral nerve defects.

Rationale: Peripheral nerve injury is common in clinic, which leads to severe atrophy and dysfunction of the denervated muscles, but the underlying mechanism is not fully understood. Recent studies advanced the causative role of mitochondrial dysfunction in muscle atrophy, while the upstream triggers remained unclear. Methods: In the present study, Atrophy of gastrocnemius and tibialis anterior (TA) were evaluated in mice sciatic nerve transection model. Transmission electron microscopy (TEM) was then used to observe the microstructure of atrophic gastrocnemius and mitochondria. Subsequently, small RNA sequencing, luciferase reporter assay and Electrophoretic Mobility Shift (EMSA) were performed to explore the potential signaling pathway involved in skeletal muscle atrophy. The effects of the corresponding pathway on mitochondrial function, mitophagy, apoptosis and muscle atrophy were further determined in C2C12 cells and denervated gastrocnemius. Results: Gastrocnemius and TA atrophied rapidly after denervation. Obvious decrease of mitochondria number and activation of mitophagy was further observed in atrophic gastrocnemius. Further, miR-142a-5p/ mitofusin-1 (MFN1) axis was confirmed to be activated in denervated gastrocnemius, which disrupted the tubular mitochondrial network, and induced mitochondrial dysfunction, mitophagy and apoptosis. Furthermore, the atrophy of gastrocnemius induced by denervation was relieved through targeting miR-142a-5p/MFN1 axis. Conclusions: Collectively, our data revealed that miR-142a-5p was able to function as an important regulator of denervation-induced skeletal muscle atrophy by inducing mitochondrial dysfunction, mitophagy, and apoptosis via targeting MFN1. Our findings provide new insights into the mechanism of skeletal muscle atrophy following denervation and propose a viable target for therapeutic intervention in individuals suffering from muscle atrophy after peripheral nerve injury.

Human adipose-derived stem cells (ASCs) have a potential for the treatment of peripheral nerve injury. Recent studies demonstrated that stem cells can mediate therapeutic effect by secreting exosomes. We aimed to investigate the effect of human ASCs derived exosomes (ASC-Exos) on peripheral nerve regeneration in vitro and in vivo. Our results showed after being internalized by Schwann cells (SCs), ASC-Exos significantly promoted SC proliferation, migration, myelination, and secretion of neurotrophic factors by upregulating corresponding genes in vitro. We next evaluated the efficacy of ASC-Exo therapy in a rat sciatic nerve transection model with a 10-mm gap. Axon regeneration, myelination, and restoration of denervation muscle atrophy in ASC-Exos treated group was significantly improved compared to vehicle control. This study demonstrates that ASC-Exos effectively promote peripheral nerve regeneration via optimizing SC function and thereby represent a novel therapeutic strategy for regenerative medicine and nerve tissue engineering.

Background Human adipose stem cells (ASCs) have emerged as a promising treatment paradigm for skin wounds. Recent works demonstrate that the therapeutic effect of stem cells is partially mediated by extracellular vesicles, which comprise exosomes and microvesicles. In this study, we investigate the regenerative effects of isolated microvesicles from ASCs and evaluate the mechanisms how ASC microvesicles promote wound healing. Methods Adipose stem cell-derived microvesicles (ASC-MVs) were isolated by differential ultracentrifugation, stained by PKH26, and characterized by electron microscopy and dynamic light scattering (DLS). We examined ASC-MV effects on proliferation, migration, and angiogenesis of keratinocytes, fibroblasts, and endothelial cells both in vitro and in vivo. Next, we explored the underlying mechanisms by gene expression analysis and the activation levels of AKT and ERK signaling pathways in all three kinds of cells after ASC-MV stimulation. We then assessed the effect of ASC-MVs on collagen deposition, neovascularization, and re-epithelialization in an in vivo skin injury model. Results ASC-MVs could be readily internalized by human umbilical vein endothelial cells (HUVECs), HaCAT, and fibroblasts and significantly promoted the proliferation, migration, and angiogenesis of these cells both in vitro and in vivo. The gene expression of proliferative markers (cyclin D1, cyclin D2, cyclin A1, cyclin A2) and growth factors (VEGFA, PDGFA, EGF, FGF2) was significantly upregulated after ASC-MV treatment. Importantly, ASC-MVs stimulated the activation of AKT and ERK signaling pathways in those cells. The local injection of ASC-MVs at wound sites significantly increased the re-epithelialization, collagen deposition, and neovascularization and led to accelerated wound closure. Conclusions Our data suggest that ASC-MVs can stimulate HUVEC, HaCAT, and fibroblast functions. ASC-MV therapy significantly accelerates wound healing, and the benefits of ASC-MVs may due to the involvement of AKT and ERK signaling pathways. This illustrates the therapeutic potential of ASC-MVs which may become a novel treatment paradigm for cutaneous wound healing. Electronic supplementary material The online version of this article (10.1186/s13287-019-1152-x) contains supplementary material, which is available to authorized users.

Background Transforming growth factor beta 1 (TGF-β1) is a classical modulator of skeletal muscle and regulates several processes, such as myogenesis, regeneration and muscle function in skeletal muscle diseases. Skeletal muscle atrophy, characterized by the loss of muscle strength and mass, is one of the pathological conditions regulated by TGF-β1, but the underlying mechanism involved in the atrophic effects of TGF-β1 is not fully understood. Methods Mice sciatic nerve transection model was created and gastrocnemius were analysed by western blot, immunofluorescence staining and fibre diameter quantification after 2 weeks. Exogenous TGF-β1 was administrated and high-mobility group box-1 (HMGB1), autophagy were blocked by siRNA and chloroquine (CQ) respectively to explore the mechanism of the atrophic effect of TGF-β1 in denervated muscle. Similar methods were performed in C2C12 cells. Results We found that TGF-β1 was induced in denervated muscle and it could promote atrophy of skeletal muscle both in vivo and in vitro, up-regulated HMGB1 and increased autophagy activity were also detected in denervated muscle and were further promoted by exogenous TGF-β1. The atrophic effect of TGF-β1 could be inhibited when HMGB1/autophagy pathway was blocked. Conclusions Thus, our data revealed that TGF-β1 is a vital regulatory factor in denervated skeletal muscle in which HMGB1/ autophagy pathway mediates the atrophic effect of TGF-β1. Our findings confirmed a new pathway in denervation-induced skeletal muscle atrophy and it may be a novel therapeutic target for patients with muscle atrophy after peripheral nerve injury. Electronic supplementary material The online version of this article (10.1186/s12964-018-0310-6) contains supplementary material, which is available to authorized users.

Marrow stromal cells (MSCs) can be induced to differentiate into Schwann-like cells under classical induction conditions. However, cells derived from this method are unstable, exhibiting a low neurotrophin expression level after the induction conditions are removed. In Schwann cell (SC) culture, progesterone (PROG) enhances neurotrophic synthesis and myelination, specifically regulating the expression of the myelin protein zero (P0)- and peripheral myelin protein 22 (PMP22)-encoding genes by acting in concert or in synergy with insulin and glucocorticoids (GLUCs). In the present study, we investigated whether combined PROG, GLUC, and insulin therapy induced MSCs to differentiate into modified SC-like cells with phenotypes similar to those of mature SCs. After being cultured for 2 weeks in modified differentiation medium, the modified SC-like cells showed increased expression of P0 and PMP22. In addition, morphological and phenotypic characterizations were conducted over a period of over 2 weeks, and functional characteristics persisted for more than 3 weeks after the induction reagents were withdrawn. The transplantation of green fluorescent protein-labeled, modified SC-like cells into transected sciatic nerves with a 10-mm gap significantly increased the proliferation of the original SCs and improved axon regeneration and myelination compared with original BM-SCs. Immunostaining for P0 revealed that more of the transplanted modified SC-like cells retained the phenotypic characteristics of SCs. Taken together, these results reveal that the combined application of PROG, GLUC, and insulin induces MSCs to differentiate into cells with phenotypic, molecular, and functional properties of mature SCs.

The calcium channel blocker, verapamil, has been shown to reduce scar formation by inhibiting fibroblast adhesion and proliferation in vitro. It was not clear whether topical application of verapamil after surgical repair of the nerve in vivo could inhibit the formation of excessive scar tissue. In this study, the right sciatic nerve of adult Sprague-Dawley rats was transected and sutured with No. 10-0 suture. The stoma was wrapped with gelfoam soaked with verapamil solution for 4 weeks. Compared with the control group (stoma wrapped with gelfoam soaked with physiological saline), the verapamil application inhibited the secretion of extracellular matrix from fibroblasts in vivo, suppressed type I and III collagen secretion and increased the total number of axons and the number of myelinated axons. These findings suggest that verapamil could reduce the formation of scar tissue and promote axon growth after peripheral nerve repair.

Foot degloving injuries are frequently encountered by reconstructive surgeons as there are more and more vehicles on the road. The separation between the deep facia and the superficial skin often damage the blood supply of the cutaneous tissue, resulting skin defect and digit necrosis. In order to manage these challenging situations, reconstructive surgeons have explored various types of techniques. Our team have managed to cure one such patient through bilateral anterolateral thigh flaps, in which the two flaps cover the dorsal and plantar side respectively. The flaps survived uneventfully and second stage operation of defatting was consequently arranged. The patient obtained protective sensation and felt satisfied with the cosmetic outcome. With the development of microsurgery, bilateral anterolateral thigh flaps could be effectively adopted to manage foot degloving injuries.

Current animal models of chronic peripheral nerve compression are mainly silicone tube models. However, the cross section of the rat sciatic nerve is not a perfect circle, and there are differences in the diameter of the sciatic nerve due to individual differences. The use of a silicone tube with a uniform internal diameter may not provide a reliable and consistent model. We have established a chronic sciatic nerve compression model that can induce demyelination of the sciatic nerve and lead to atrophy of skeletal muscle. In 3-week-old pups and adult rats, the sciatic nerve of the right hind limb was exposed, and a piece of surgical latex glove was gently placed under the nerve. N-butyl-cyanoacrylate was then placed over the nerve, and after it had set, another piece of glove latex was placed on top of the target area and allowed to adhere to the first piece to form a sandwich-like complex. Thus, a chronic sciatic nerve compression model was produced. Control pups with latex or N-butyl-cyanoacrylate were also prepared. Functional changes to nerves were assessed using the hot plate test and electromyography. Immunofluorescence and electron microscopy analyses of the nerves were performed to quantify the degree of neuropathological change. Masson staining was conducted to assess the degree of fibrosis in the gastrocnemius and intrinsic paw muscles. The pup group rats subjected to nerve compression displayed thermal hypoesthesia and a gradual decrease in nerve conduction velocity at 2 weeks after surgery. Neuropathological studies demonstrated that the model caused nerve demyelination and axonal irregularities and triggered collagen deposition in the epineurium and perineurium of the affected nerve at 8 weeks after surgery. The degree of fibrosis in the gastrocnemius and intrinsic paw muscles was significantly increased at 20 weeks after surgery. In conclusion, our novel model can reproduce the functional and histological changes of chronic nerve compression injury that occurs in humans and it will be a useful new tool for investigating the mechanisms underlying chronic nerve compression.

A high matrix metalloproteinase–9/tissue inhibitor of metalloproteinase–1 (MMP9/TIMP1) ratio is associated with poor ulcer healing, yet how the ratio of MMP9/TIMP1 changes in diabetic foot ulcers (DFUs) with infection and how these changes may affect wound healing remain unclear. Therefore, the objective of this investigation was to explore relationships among the MMP9/TIMP1 ratio, infection, and DFUs. After being informed of the details of this study, 32 patients signed consent forms. Skin biopsies were performed for all patients. Wound tissues were obtained from all patients with wounds, and healthy skin samples were collected from patients without wounds during orthopedic surgery. Microbial cultures were obtained using the samples from diabetic patients with wounds. All patients were divided into 4 groups according to colony-forming units (CFUs) per gram of tissue (>1 × 106 or 6): group A (diabetic wounds with high quantities of bacteria), group B (diabetic wounds with low quantities of bacteria), group C (diabetic patients without wounds), and group D (nondiabetic patients with wounds). In addition, the biopsies were evaluated by both reverse transcription–quantitative polymerase chain reaction and Western blotting to assess the levels of MMP9, TIMP1, and vascular endothelial growth factor (VEGF). The results show that for both mRNA and protein, expression of MMP9 (fold change 1.14 ± 0.12 vs 0.60 ± 0.08 vs 0.39±0.09 vs 0.13 ± 0.06, P < .01) decreased, whereas that of TIMP1 (1.01 ± 0.09 vs 2.86 ± 0.85 vs 4.88 ± 0.83 vs 7.29 ± 1.55, P < .01) and VEGF (1.01 ± 0.22 vs 3.55 ± 0.97 vs 5.72 ± 0.55 vs 6.92 ± 1.55, P < .01) increased from group A to group D. These results suggest that an increase in the MMP9/TIMP1 ratio in infected DFUs may induce a decrease in VEGF expression.

This study aimed to investigate the reconstruction of the thumb and finger extension function in patients with middle and lower trunk root avulsion injuries of the brachial plexus. From April 2010 to January 2015, we enrolled in this study 4 patients diagnosed with middle and lower trunk root avulsion injuries of the brachial plexus via imaging tests, electrophysiological examinations, and clinical confirmation. Muscular branches of the radial nerve, which innervate the supinator in the forearm, were transposed to the posterior interosseous nerve to reconstruct the thumb and finger extension function. Electrophysiological findings and muscle strength of the extensor pollicis longus and extensor digitorum communis, as well as the distance between the thumb tip and index finger tip, were monitored. All patients were followed up for 24 to 30 months, with an average of 27.5 months. Motor unit potentials (MUP) of the extensor digitorum communis appeared at an average of 3.8 months, while MUP of the extensor pollicis longus appeared at an average of 7 months. Compound muscle action potential (CMAP) appeared at an average of 9 months in the extensor digitorum communis, and 12 months in the extensor pollicis longus. Furthermore, the muscle strength of the extensor pollicis longus and extensor digitorum communis both reached grade III at 21 months. Lastly, the average distance between the thumb tip and index finger tip was 8.8 cm at 21 months. In conclusion, for patients with middle and lower trunk injuries of the brachial plexus, transposition of the muscular branches of the radial nerve innervating the supinator to the posterior interosseous nerve for the reconstruction of thumb and finger extension function is practicable and feasible.

To investigate the effect of dihydrotestosterone (DHT) combined with Dezawa’s method on the differentiation of bone marrow stromal cells (BMSCs) into schwann-like cells. Compared to the Dezawa’s method, schwann-like cells obtained from our modified method were longer and thinner and exhibited a typical bipolar or tripolar shape. These cells had a higher mRNA expression of S100 and myelin protein zero (P0), about 1.7- and 2.5-fold respectively, while the glial fibrillary acidic protein (GFAP) mRNA level was decreased about 92 %. No significant difference in peripheral myelin protein 22 (PMP22) mRNA expression was found. Immunofluorescence and Western blot showed the similar results. DHT in combination with Dezawa’s method to induce a BMSCs to differentiate into schwann-like cells with higher expression of P0, which might be more effective in clinical application than previous method for nerve regeneration.

Introduction Percutaneous interventional sclerotherapy has been widely used to treat venous malformation. Satisfactory results have been reported, along with both mild and severe complications. Report A 1.5 year old girl was diagnosed as having a venous malformation of the right vulva and right inner thigh. The patient received sclerotherapy using polidocanol. After the surgery, the right foot and lower leg became pale, and then, a few days later, necrotic. Conclusion Accurate diagnosis and appropriate treatment are challenging for vascular malformations and should only be carried out in centers with ample expertise., Highlights • Interventional sclerotherapy has been widely used to treat venous malformations. • Satisfactory results have been reported along with both mild and severe complications. • There are no literature reports of limb necrosis, caused by sclerotherapy, requiring amputation. • Treatment of vascular malformations should only be carried out in expert centers with ample expertise.