Mesenchymal stem cells (MSCs) have regenerative properties in acute kidney injury (AKI). However, the potential function of MSCs in chronic kidney disease remains elusive. Renal fibrosis is the common endpoint of chronic progressive kidney diseases and causes a considerable health burden worldwide. In this study, the protective effects of bone marrow mesenchymal stem cells (BM-MSCs) were assessed in repeated administration of low-dose cisplatin-induced renal fibrosis mouse model in vivo as well as a TGF-β1-induced fibrotic model in vitro. Differentially expressed miRNAs in mouse renal tubular epithelial cells (mRTECs) regulated by BM-MSCs were screened by high-throughput sequencing. We found microRNA (miR)-146a-5p was the most significant up-regulated miRNA in mRTECs. In addition, the gene Tfdp2 was identified as one target gene of miR-146a-5p by bioinformatics analysis. The expression of Tfdp2 in the treatment of BM-MSCs on cisplatin-induced renal injury was evaluated by immunohistochemistry analysis. Our results indicate that BM-MSC attenuates cisplatin-induced renal fibrosis by regulating the miR-146a-5p/Tfdp2 axis in mRTECs.

Inflammation, an adaptive reaction to harmful stimuli, is a necessary immune system response and can be either acute or chronic. Since acute inflammation tends to eliminate harmful stimuli and restore equilibrium, it is generally advantageous to the organism. Chronic inflammation, however, is caused by either increased inflammatory signaling or decreased pro-anti-inflammatory signaling. According to current studies, inflammation is thought to be a major factor in a number of chronic diseases, including diabetes, cancer, arthritis, inflammatory bowel disease, and obesity. Consequently, reducing inflammation is essential for both preventing and delaying diseases. The application of biomaterials in the treatment of inflammatory illnesses has grown in recent years. A variety of biomaterials can be implanted either by themselves or in conjunction with other bioactive ingredients and therapeutic agents. The mechanisms of action and therapeutic applications of well-known anti-inflammatory biomaterials are the main topics of this article.

Ubiquitin C-terminal hydrolases (UCHs), a subfamily of deubiquitinating enzymes (DUBs), have been found in a variety of tumor entities and play distinct roles in the pathogenesis and development of various cancers including head and neck cancer (HNC). HNC is a heterogeneous disease arising from the mucosal epithelia of the upper aerodigestive tract, including different anatomic sites, distinct histopathologic types, as well as human papillomavirus (HPV)-positive and negative subgroups. Despite advances in multi-disciplinary treatment for HNC, the long-term survival rate of patients with HNC remains low. Emerging evidence has revealed the members of UCHs are associated with the pathogenesis and clinical prognosis of HNC, which highlights the prognostic and therapeutic implications of UCHs for patients with HNC. In this review, we summarize the physiological and pathological functions of the UCHs family, which provides enlightenment of potential mechanisms of UCHs family in HNC pathogenesis and highlights the potential consideration of UCHs as attractive drug targets.

Soft tissue sarcomas (STS), including rhabdomyosarcoma (RMS), exhibit significant heterogeneity and limited responsiveness to immune checkpoint blockade (ICB). Unsupervised tumor immune phenotype based on multi-omics expression profiling of STS has been less studied. To reveal the tumor immune phenotype of STS and identify promising therapeutic targets, multi-omics expression profiling across various subtypes of STS was investigated. Here, we established a novel molecular classifier based on immune cell subsets related to TGFβ1 and IFNγ to identify distinct immune phenotypes with higher or lower cytotoxic contents. Immune-high clusters demonstrated enriched immune cell infiltration, elevated IFNγ-related signatures, and favorable clinical outcomes. In contrast, immune-low clusters were enriched for immunosuppressive cell types and exhibited poor survival. CHEK1 emerged as a key node associated with immunosuppressive phenotypes and was significantly overexpressed in immune-low tumors. In situ analysis of independent validation cohorts revealed the significant correlation between CHEK1 and tumor-infiltrating immune cells. Collectively, our findings establish a novel risk assessment strategy for RMS and STS patients, and highlight the potential of CHEK1 as a promising therapeutic target in combination with immune checkpoint inhibitor therapy.

Persistent high-risk HPV infection drives tumorigenesis in various human malignancies, including cervical, oropharyngeal, anal, and vulvar carcinomas. Although HPV-related tumors arise in several different sites, they share many common genetic and epigenetic events. Complex and heterogeneous genomic aberrations and mutations induced by high-risk HPV contribute to the initiation and progression of cervical cancer (CC). However, the associations between high-risk HPV infection and DNA methylation have not been clearly investigated. In the present study, HPV-related gene promoter methylation signature was comprehensively analyzed using multiple interactive platforms. CC patients were successfully classified into high-risk and low-risk groups with significant differences in clinical outcomes based on the HPV-related gene promoter methylation signature. Moreover, the protein levels of ALDH1A2 and clinical prognostic value were confirmed in the CC patients cohort. In summary, our study provides compelling evidence that HPV-related gene promoter methylation signature serves as a strong prognostic signature for CC patients. Clinical investigations in large CC patient cohorts are greatly needed to pave the way to implement epigenetic biomarkers into better clinical management.

Background: Medical devices are used in almost all orthopedic surgical subspecialties, and the frequency of adverse events is increasing, which should not be ignored. To provide suggestions on how to avoid implant recalls from the perspective of manufacturers, medical institutions and supervisions, as well as how to respond promptly to adverse events. Methods: The research extracted recalls of osteosynthesis implants and joint replacement implants from January 1, 2011, to June 30, 2021, in the CNMPA, FDA, HC and ATGA websites and collected the information on device name, recall time, recall class, recall manufacturer, device classification and affected areas. Moreover, the McKinsey 7S model and fishbone diagram were used to analyze recall reasons. Results: A total of 315 cases of osteosynthesis implants and 286 cases of joint replacement implants were reported in China, the USA, Canada and Australia. The recalls number from 2016 to 2021 was more than that from 2011 to 2015 for osteosynthesis implant (p = 0.012) and joint replacement implant (p = 0.002), and both mainly focused on class II (76.19% and 78.32%). There were statistical differences in the four countries for both implants (p = 0.000), especially osteosynthesis implant between China and the USA (p = 0.000), China and Canada (p = 0.001), the USA and Australia (p = 0.002), and joint replacement implant between China and Australia (p = 0.000). Conclusions: To avoid the recalls of such implants, manufacturers should strictly select implant materials and components, develop detailed labels and instructions, severely control the packaging process and establish the integrity of medical device data. Medical institutions should standardize procurement procedures, use qualified equipment and train medical workers. It also requires supervisions to conduct premarket safety assessments. In addition, regulators should strengthen supervision and establish reporting systems to deal with the occurrence of adverse events promptly.