Surgical efficacy analysis of tarsal tunnel syndrome: a retrospective study of 107 patients.

Tarsal tunnel syndrome (TTS) is an entrapment neuropathy of the posterior tibial nerve or its terminal branches compressed by its fibro-osseous tunnel beneath the flexor retinaculum on the medial side of the ankle. The current study was a retrospective study of 107 cases of patients with TTS, in which the onset characteristics were summarized, the factors that might affect the surgical treatment effects of TTS were discussed and analyzed. The syndrome diagnoses and treatment experiences of TTS were extracted and analyzed. In our cohort, TTS was more often found in middle-aged and older women. And the medial plantar nerve bundle was the most frequently affected nerve structure. The efficacy of surgical treatment were correlated to the causes of the disease, involved nerve bundles, methods of operation, and whether neurolysis of the epineurium was performed. Neurolysis of the epineurium is was recommended for patients with an enlarged tibial nerve due to impingement. The Singh method was recommended to release the tibial nerve and its branches. Patients with negative preoperative EMG results should carefully be cautious when considering their decision to undergo surgical treatment.

Role of N6-methyl-adenosine modification in mammalian embryonic development.

N6-methyl-adenosine (m6A) methylation is one of the most common and abundant modifications of RNA molecules in eukaryotes. Although various biological roles of m6A methylation have been elucidated, its role in embryonic development is still unclear. In this review, we focused on the function and expression patterns of m6A-related genes in mammalian embryonic development and the role of m6A modification in the embryonic epigenetic reprogramming process. The modification of m6A is regulated by the combined activities of methyltransferases, demethylases, and m6A-binding proteins. m6A-related genes act synergistically to form a dynamic, reversible m6A pattern, which exists in several physiological processes in various stages of embryonic development. The lack of one of these enzymes affects embryonic m6A levels, leading to abnormal embryonic development and even death. Moreover, m6A is a positive regulator of reprogramming to pluripotency and can affect embryo reprogramming by affecting activation of the maternal-to-zygotic transition. In conclusion, m6A is involved in the regulation of gene expression during embryonic development and the metabolic processes of RNA and plays an important role in the epigenetic modification of embryos.

Protective role of NRF2 in macrovascular complications of diabetes.

Macrovascular complications develop in over a half of the diabetic individuals, resulting in high morbidity and mortality. This poses a severe threat to public health and a heavy burden to social economy. It is therefore important to develop effective approaches to prevent or slow down the pathogenesis and progression of macrovascular complications of diabetes (MCD). Oxidative stress is a major contributor to MCD. Nuclear factor (erythroid-derived 2)-like 2 (NRF2) governs cellular antioxidant defence system by activating the transcription of various antioxidant genes, combating diabetes-induced oxidative stress. Accumulating experimental evidence has demonstrated that NRF2 activation protects against MCD. Structural inhibition of Kelch-like ECH-associated protein 1 (KEAP1) is a canonical way to activate NRF2. More recently, novel approaches, such as activation of the Nfe2l2 gene transcription, decreasing KEAP1 protein level by microRNA-induced degradation of Keap1 mRNA, prevention of proteasomal degradation of NRF2 protein and modulation of other upstream regulators of NRF2, have emerged in prevention of MCD. This review provides a brief introduction of the pathophysiology of MCD and the role of oxidative stress in the pathogenesis of MCD. By reviewing previous work on the activation of NRF2 in MCD, we summarize strategies to activate NRF2, providing clues for future intervention of MCD. Controversies over NRF2 activation and future perspectives are also provided in this review.

Inhibition of P53/miR-34a improves diabetic endothelial dysfunction via activation of SIRT1.

Endothelial dysfunction contributes to diabetic macrovascular complications, resulting in high mortality. Recent findings demonstrate a pathogenic role of P53 in endothelial dysfunction, encouraging the investigation of the effect of P53 inhibition on diabetic endothelial dysfunction. Thus, high glucose (HG)-treated endothelial cells (ECs) were subjected to pifithrin-α (PFT-α)-a specific inhibitor of P53, or P53-small interfering RNA (siRNA), both of which attenuated the HG-induced endothelial inflammation and oxidative stress. Moreover, inhibition of P53 by PFT-α or P53-siRNA prohibited P53 acetylation, decreased microRNA-34a (miR-34a) level, leading to a dramatic increase in sirtuin 1 (SIRT1) protein level. Interestingly, the miR-34a inhibitor (miR-34a-I) and PFT-α increased SIRT1 protein level and alleviated the HG-induced endothelial inflammation and oxidative stress to a similar extent; however, these effects of PFT-α were completely abrogated by the miR-34a mimic. In addition, SIRT1 inhibition by EX-527 or Sirt1-siRNA completely abolished miR-34a-I's protection against HG-induced endothelial inflammation and oxidative stress. Furthermore, in the aortas of streptozotocin-induced diabetic mice, both PFT-α and miR-34a-I rescued the inflammation, oxidative stress and endothelial dysfunction caused by hyperglycaemia. Hence, the present study has uncovered a P53/miR-34a/SIRT1 pathway that leads to endothelial dysfunction, suggesting that P53/miR-34a inhibition could be a viable strategy in the management of diabetic macrovascular diseases.

Internal fixation with Kirschner wires is as efficient as rigid screw fixation in scaphoid fracture: long-term functional outcome.

This study aimed to compare the long-term efficacy of Kirschner wires and Herbert screw internal fixation in scaphoid fracture. A retrospective chart with radiographic review and functional follow-up was conducted for patients with the scaphoid fracture. 65 patients (40 for K-wire fixation and 25 for Herbert screw) were enrolled. The nonunion rate for K-wire fixation and screw method were indifferent comprehensively and for iliac graft subgroup. Less bone necrosis was found with K-wire fixation (2.5% vs 16%, P=0.049). There's no difference between groups in Mayo scores, post-operation pain and grid strength. Patients with K-wire fixation have larger range of motion on radial/ulnar deviation (35.25±11.32 vs 28.00±8.66, P=0.007). The results support the use of Kirschner wires in the treatment of scaphoid fractures. Advantages such as high union rates and good function recovery of wrist could be expected from minimal invasion, multi-axial stable fixation.

Comparison of perioperative complications of pedicled island flap in reconstruction of extremities.

PURPOSE: The aim of this study was to analyze the differences in perioperative complications for pedicled island flaps in the reconstruction of extremities and to identify the factors contributing to pedicled island flap necrosis. Furthermore, the flap indications based on these outcomes are summarized. METHODS: Based on the inclusion criteria, 228 skin flaps were included in this study. Univariate and multivariate analyses were used to identify the risk factors for pedicled island flap necrosis. Differences in perioperative complications between upper and lower extremities were analyzed using the chi-square test or Fisher's exact test. RESULTS: The average age of the patients was 38 years. The overall complication rate was 21.93%, including partial flap necrosis (10.09%) and total flap necrosis (5.70%). The overall complication rate and flap necrosis rate in upper extremity reconstruction were significantly lower than the rates in lower extremity reconstruction. Flap area and postoperative wound infection were statistically significant risk factors for pedicled island flap necrosis in extremity reconstruction. Preoperative contamination of the wound bed was a statistically significant risk factor for postoperative wound infection. CONCLUSIONS: The flap area and postoperative wound infection were both independent risk factors for pedicled island flap necrosis in extremity reconstruction. The causes contributing to the differences in perioperative complications between upper and lower extremities reconstruction included preoperative contamination of the wound bed, postoperative wound infection, and the flap area but were also related to anatomical factors of the skin flap. Pedicled island flaps are more suitable for small- and medium-sized soft tissue defects.

Clinical Application and the Free Posterior Thigh Perforator Flap.

OBJECTIVE: The posterior thigh region has been neglected as a donor site for free perforator flaps, likely due to difficulties in positioning the patient during surgery. This study describes the clinical application of the posterior thigh perforator flap based on the third perforating artery of the profunda femoris artery (PFA). METHODS: The free posterior thigh perforator flap based on the third perforating artery of the PFA was used for reconstruction of soft tissue defects in nine patients between February 2010 and May 2014. RESULTS: Flap sizes ranged from 12 × 7 cm to 20 × 13 cm. The length of the vascular pedicle averaged 10.28 cm, and the mean diameters of the third perforating artery and venae comitantes were 1.68 and 1.14 mm, respectively. All of the perforators originated from the PFA. Of the 9 free flaps used in 9 patients, 7 flaps survived completely. There were no early complications in these flaps. During the follow-up period, no patient experienced cold intolerance, scar contracture, or scar pain. There were no functional impairments at the donor or recipient sites. CONCLUSIONS: The posterior thigh flap based on the third perforating artery of the PFA is an excellent option for reconstructing soft tissue defects. The anatomical location of the third perforating artery is relatively consistent. The vascular pedicle is relatively longer and has large caliber vessels. The scar at the donor site can be well concealed with low morbidity. The skin color and texture of this flap show satisfactory results.

CRISPR technology in human diseases.

Gene editing is a growing gene engineering technique that allows accurate editing of a broad spectrum of gene-regulated diseases to achieve curative treatment and also has the potential to be used as an adjunct to the conventional treatment of diseases. Gene editing technology, mainly based on clustered regularly interspaced palindromic repeats (CRISPR)-CRISPR-associated protein systems, which is capable of generating genetic modifications in somatic cells, provides a promising new strategy for gene therapy for a wide range of human diseases. Currently, gene editing technology shows great application prospects in a variety of human diseases, not only in therapeutic potential but also in the construction of animal models of human diseases. This paper describes the application of gene editing technology in hematological diseases, solid tumors, immune disorders, ophthalmological diseases, and metabolic diseases; focuses on the therapeutic strategies of gene editing technology in sickle cell disease; provides an overview of the role of gene editing technology in the construction of animal models of human diseases; and discusses the limitations of gene editing technology in the treatment of diseases, which is intended to provide an important reference for the applications of gene editing technology in the human disease.

Triple synergistic sterilization of Prussian blue nanoparticle-doped chitosan/gelatin packaging film for enhanced food preservation.

To mitigate food spoilage caused by microbial contamination and extend the shelf life of food, antibacterial and eco-friendly biological packaging materials as an alternative to petroleum-based plastics is encouraged. Herein, an innovative and green composite film with triple antibacterial activity has been fabricated by introducing prussian blue nanoparticles (PBNPs) into chitosan (CS)-based films blended with gelatin (Gel) for the preservation of food, named CS/Gel/PB film. Due to the incorporation of PBNPs, CS/Gel/PB film exhibits enhanced mechanical, barrier and water resistance, and thermal abilities. The inherent bacterial trapping and killing capabilities of CS (contact killing), photothermal/photodynamic killing based on the excellent photothermal property of PBNPs under NIR irradiation synergistically facilitate the sterilization against Escherichia coli and Staphylococcus aureus (antibacterial ratio = 99.99 %). The film exhibits outstanding preservation capability in product storage, significantly extending the shelf life of strawberry and pork to 15 and 7 days, respectively. Meanwhile, the cytotoxicity assessment of CS/Gel/PB against HepG2 cells ascertains a cell viability exceeding 96 %, indicating a negligible toxicity level. Additionally, this film also exhibits superior biodegradability (preliminary degradation on the 10th day and completion on the 40th day) compared with PE film. Overall, these properties demonstrate great potential of CS/Gel/PB film as a novel packaging material.

Study of charge transfer contribution in Surface-Enhanced Raman scattering (SERS) based on indium oxide nanoparticle substrates.

Surface-enhanced Raman scattering (SERS) has outstanding merits in biochemical molecular analysis, and the development of new SERS substrates is the focus of research. Herein, In2O3 nanoparticles (NPs) were synthesized by a high temperature pyrolysis method with cubic phase and small particle size at 10 nm. The structures and properties of In2O3 NPs were characterized by X-ray powder diffraction (XRD), transmission electron microscope (TEM) and other characterization methods. Additionally, the SERS spectra of In2O3-MBA with the enhancement factor (EF) up to 1.22 × 104 is discussed. The results demonstrate that there is a charge transfer (CT) effect revealed between the adsorbed molecules of 4-mercaptobenzoic acid (4-MBA) and the substrates of In2O3 NPs, and it could be excited by long wavelength energy. Based on the In2O3 NPs, the study is beneficial to develop more potential semiconductor SERS substrates.

Compounds purified from edible fungi fight against chronic inflammation through oxidative stress regulation.

Chronic inflammation is associated with various chronic diseases, including cardiovascular disease, neurodegenerative disease, and cancer, which severely affect the health and quality of life of people. Oxidative stress induced by unbalanced production and elimination of reactive oxygen species (ROS) is one of the essential risk factors for chronic inflammation. Recent studies, including the studies of mushrooms, which have received considerable attention, report that the antioxidant effects of natural compounds have more advantages than synthetic antioxidants. Mushrooms have been consumed by humans as precious nourishment for 3,000 years, and so far, more than 350 types have been identified in China. Mushrooms are rich in polysaccharides, peptides, polyphenols, alkaloids, and terpenoids and are associated with several healthy biological functions, especially antioxidant properties. As such, the extracts purified from mushrooms could activate the expression of antioxidant enzymes through the Keap1/Nrf2/ARE pathway to neutralize excessive ROS and inhibit ROS-induced chronic inflammation through the NF-κB pathway. Recently, the antioxidant properties of mushrooms have been successfully applied to treating cardiovascular disease (CAD), neurodegenerative diseases, diabetes mellitus, and cancer. The present review summarizes the antioxidant properties and the mechanism of compounds purified from mushrooms, emphasizing the oxidative stress regulation of mushrooms to fight against chronic inflammation.

Corrigendum: Compounds purified from edible fungi fight against chronic inflammation through oxidative stress regulation.

[This corrects the article DOI: 10.3389/fphar.2022.974794.].

Modulation of immunosuppressive cells and noncoding RNAs as immunotherapy in osteosarcoma.

The most common bone cancer is osteosarcoma (OS), which mostly affects children and teenagers. Early surgical resection combined with chemotherapy significantly improves the prognosis of patients with OS. Existing chemotherapies have poor efficacy in individuals with distant metastases or inoperable resection, and these patients may respond better to novel immunotherapies. Immune escape, which is mediated by immunosuppressive cells in the tumour microenvironment (TME), is a major cause of poor OS prognosis and a primary target of immunotherapy. Myeloid-derived suppressor cells, regulatory T cells, and tumour-associated macrophages are the main immunosuppressor cells, which can regulate tumorigenesis and growth on a variety of levels through the interaction in the TME. The proliferation, migration, invasion, and epithelial-mesenchymal transition of OS cells can all be impacted by the expression of non-coding RNAs (ncRNAs), which can also influence how immunosuppressive cells work and support immune suppression in TME. Interferon, checkpoint inhibitors, cancer vaccines, and engineered chimeric antigen receptor (CAR-T) T cells for OS have all been developed using information from studies on the metabolic properties of immunosuppressive cells in TME and ncRNAs in OS cells. This review summarizes the regulatory effect of ncRNAs on OS cells as well as the metabolic heterogeneity of immunosuppressive cells in the context of OS immunotherapies.

Flavonoids Inhibit Cancer by Regulating the Competing Endogenous RNA Network.

Flavonoids are present in a wide range of plants. They have been used in the treatment of cancer, but the mechanism underlying this activity is unclear. In recent years, microRNA (miRNA) and long non-coding RNA (lncRNA) levels have been observed to differ between normal tissues and cancer cells, and both types of RNA have been shown to have a role in tumor treatment. In addition, flavonoids have been proven to regulate miRNAs and LncRNAs in the treatment of cancer. The competing endogenous RNA (ceRNA) network is a complex post-transcriptional regulatory mechanism in cells, in which coding and non-coding RNAs competitively bind miRNAs to regulate messenger RNAs (mRNAs). This review focused on the role of the ceRNA network in the treatment of cancer by flavonoids.

The application of collagen in the repair of peripheral nerve defect.

Collagen is a natural polymer expressed in the extracellular matrix of the peripheral nervous system. It has become increasingly crucial in peripheral nerve reconstruction as it was involved in regulating Schwann cell behaviors, maintaining peripheral nerve functions during peripheral nerve development, and being strongly upregulated after nerve injury to promote peripheral nerve regeneration. Moreover, its biological properties, such as low immunogenicity, excellent biocompatibility, and biodegradability make it a suitable biomaterial for peripheral nerve repair. Collagen provides a suitable microenvironment to support Schwann cells' growth, proliferation, and migration, thereby improving the regeneration and functional recovery of peripheral nerves. This review aims to summarize the characteristics of collagen as a biomaterial, analyze its role in peripheral nerve regeneration, and provide a detailed overview of the recent advances concerning the optimization of collagen nerve conduits in terms of physical properties and structure, as well as the application of the combination with the bioactive component in peripheral nerve regeneration.

Advances of hydrogel combined with stem cells in promoting chronic wound healing.

Wounds can be divided into two categories, acute and chronic. Acute wounds heal through the normal wound healing process. However, chronic wounds take longer to heal, leading to inflammation, pain, serious complications, and an economic burden of treatment costs. In addition, diabetes and burns are common causes of chronic wounds that are difficult to treat. The rapid and thorough treatment of chronic wounds, including diabetes wounds and burns, represents a significant unmet medical need. Wound dressings play an essential role in chronic wound treatment. Various biomaterials for wound healing have been developed. Among these, hydrogels are widely used as wound care materials due to their good biocompatibility, moisturizing effect, adhesion, and ductility. Wound healing is a complex process influenced by multiple factors and regulatory mechanisms in which stem cells play an important role. With the deepening of stem cell and regenerative medicine research, chronic wound treatment using stem cells has become an important field in medical research. More importantly, the combination of stem cells and stem cell derivatives with hydrogel is an attractive research topic in hydrogel preparation that offers great potential in chronic wound treatment. This review will illustrate the development and application of advanced stem cell therapy-based hydrogels in chronic wound healing, especially in diabetic wounds and burns.

Ginkgo biloba Extract Inhibited Cell Proliferation and Invasion by Stimulating TET2 Expression Through miR-29a in Colorectal Carcinoma Cells.

Ginkgo biloba extract (GBE) has antitumor and antioxidant properties, which play a role in regulating gene and protein expression. The ten-eleven translocation (TET) proteins have the ability to regulate epigenetic modifications. However, the abnormal expression of TET2 protein has also been demonstrated in cancer development. In the present study, we analyzed the effects of GBE administration on TET2 expression in human colorectal cancer (CRC). The Cancer Genome Atlas database suggested that the expression of TET2 was lost in CRC. To investigate the expression profiles of TET2, GBE was used to treat CRC cells. The results showed that GBE could increase the expression of TET2 and 5-hydroxymethylcytosine (5hmC). In addition, GBE inhibited cell growth and invasion in SW480 cells. Moreover, to confirm whether TET2 expression affected cell proliferation, apoptosis, migration, and invasion, TET2 was knocked down and a TET2-overexpressing vector was constructed in human CRC cells. The results showed that overexpression of TET2 induced cell proliferation and invasion. Bioinformatic analyses showed that TET2 is a target gene of microRNA-29a (miR-29a). Moreover, reduced expression of miR-29a and increased TET2 expression in CRC cells. GBE was also used to treat a tumor model in nude mice. Compared to the control group, tumor growth was inhibited, and there was increased expression of TET2 in the GBE-treatment group in vivo. In conclusion, these results indicated that GBE inhibited cell proliferation and invasion through TET2 protein expression regulated by miR-29a in the development of CRC.

Observation of tunable surface plasmon resonances and surface enhanced infrared absorption (SEIRA) based on indium tin oxide (ITO) nanoparticle substrates.

The application of surface enhanced infrared absorption (SEIRA) is severely restricted in many fields due to the SEIRA substrates are constructed mainly from expensive noble metals. Therefore, the development of new SEIRA substrates other than the noble metallic ones is very valuable. Here we introduced a new semiconductor SEIRA substrate, the indium tin oxide (ITO) nanoparticles (NPs), to study the SEIRA property. The results demonstrate that the ITO NPs show the SEIRA property and the enhancement is dependent to the doping ratio of the heteroatoms of tin. The ITO NPs with the 5% atomic doping ratio show the highest SEIRA enhancement factor (EF), which is about 24. The limit of detection (LOD) of the 1,1'-dicarboxyferrocene (dcFc) molecule was as low as 10-5 mol/L. The present study proves that the tin-doped indium oxide can be used as a new and inexpensive semiconductor SEIRA substrate. It also proves that the doped semiconductor NPs have strong potentials for being used as emerging SEIRA substrates.

Corrigendum: Applications of chitosan and its derivatives in skin and soft tissue diseases.

[This corrects the article DOI: 10.3389/fbioe.2022.894667.].

Interferon and interferon-stimulated genes in HBV treatment.

Human hepatitis B virus (HBV) is a small enveloped DNA virus with a complex life cycle. It is the causative agent of acute and chronic hepatitis. HBV can resist immune system responses and often causes persistent chronic infections. HBV is the leading cause of liver cancer and cirrhosis. Interferons (IFNs) are cytokines with antiviral, immunomodulatory, and antitumor properties. IFNs are glycoproteins with a strong antiviral activity that plays an important role in adaptive and innate immune responses. They are classified into three categories (type I, II, and III) based on the structure of their cell-surface receptors. As an effective drug for controlling chronic viral infections, Type I IFNs are approved to be clinically used for the treatment of HBV infection. The therapeutic effect of interferon will be enhanced when combined with other drugs. IFNs play a biological function by inducing the expression of hundreds of IFN-stimulated genes (ISGs) in the host cells, which are responsible for the inhibiting of HBV replication, transcription, and other important processes. Animal models of HBV, such as chimpanzees, are also important tools for studying IFN treatment and ISG regulation. In the present review, we summarized the recent progress in IFN-HBV treatment and focused on its mechanism through the interaction between HBV and ISGs.