Identification of novel potential biomarkers in infantile hemangioma via weighted gene co-expression network analysis.

BACKGROUND: Infantile hemangioma (IH) is the most common benign tumor in children and is characterized by endothelial cells proliferation and angiogenesis. Some hub genes may play a critical role in angiogenesis. This study aimed to identify the hub genes and analyze their biological functions in IH. METHODS: Differentially expressed genes (DEGs) in hemangioma tissues, regardless of different stages, were identified by microarray analysis. The hub genes were selected through integrated weighted gene co-expression network analysis (WGCNA) and protein-protein interaction (PPI) network. Subsequently, detailed bioinformatics analysis of the hub genes was performed by gene set enrichment analysis (GSEA). Finally, quantitative real-time polymerase chain reaction (qRT-PCR) analysis was conducted to validate the hub genes expression in hemangioma-derived endothelial cells (HemECs) and human umbilical vein endothelial cells (HUVECs). RESULTS: In total, 1115 DEGs were identified between the hemangiomas and normal samples, including 754 upregulated genes and 361 downregulated genes. Two co-expression modules were identified by WGCNA and green module eigengenes were highly correlated with hemangioma (correlation coefficient = 0.87). Using module membership (MM) > 0.8 and gene significance (GS) > 0.8 as the cut-off criteria, 108 candidate genes were selected and put into the PPI network, and three most correlated genes (APLN, APLNR, TMEM132A) were identified as the hub genes. GSEA predicted that the hub genes would regulate endothelial cell proliferation and angiogenesis. The differential expression of these genes was validated by qRT-PCR. CONCLUSIONS: This research suggested that the identified hub genes may be associated with the angiogenesis of IH. These genes may improve our understanding of the mechanism of IH and represent potential anti-angiogenesis therapeutic targets for IH.

Retraction notice to: Minimal Scar Dissection for Partial Parotidectomy via a Modified Cosmetic Incision and an Advanced Wound Closure Method [YJOMS 77 (2019) 1317.E1-1317.E9].

This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/our-business/policies/article-withdrawal). This article has been retracted at the request of the Editor-in-Chief. The authors have duplicated an image that previously appeared in: J Clin Otorhinolaryngol Head Neck Surg (China) 2018 https://doi.org/10.13201/j.issn.1001-1781.2018.16.011 One of the conditions of submission of a paper for publication is that authors declare explicitly that their work is original and has not appeared in a publication elsewhere. Re-use of any data should be appropriately cited. As such this article represents a severe abuse of the scientific publishing system. The scientific community takes a very strong view on this matter and apologies are offered to readers of JOMS that this was not detected during the submission process.

A competing risk nomogram for predicting cancer-specific death of patients with buccal mucosa cancer.

OBJECTIVES: Our aim was to develop and validate a competing risk nomogram to determine the probability of cancer-specific death in buccal mucosa cancer (BMC) patients. MATERIALS AND METHODS: We examined the records of BMC patients in the Surveillance, Epidemiology, and End Results (SEER) Program and First Affiliated Hospital of Nanchang University (China). We adopted the cumulative incidence function and Fine-Gray proportional hazards model based on univariate and multivariate analyses by R-software to identify the risk factors associated with cancer-specific death. Subsequently, a nomogram was developed and validated to predict the 3- and 5-year probability of cancer-specific death. RESULTS: In 1,286 BMC patients identified from SEER database, cumulative incidences of cancer-specific death after diagnosis were 33.4% and 35.5% for 3 and 5 years, respectively. In the training cohort (n = 902) from SEER database, the Fine-Gray model indicated that age, Tumor Node Metastasis (TNM) stages, grade, surgery, and histological type were independent risk factors associated with cancer-specific death, based on which a prognostic nomogram was developed. In the internal validation cohort from SEER database (n = 384) and the external validation cohort from our medical center (n = 174), the nomogram was well calibrated and showed remarkable prediction performance. CONCLUSION: The nomogram created herein may prove to be a good assistant tool for assessing the prognosis of BMC patients.

Minimal Scar Dissection for Partial Parotidectomy via a Modified Cosmetic Incision and an Advanced Wound Closure Method.

PURPOSE: To evaluate the usefulness of the modified cosmetic incision (MCI) and advanced wound closure method in partial parotidectomy by comparison with the modified Blair incision (MBI). PATIENTS AND METHODS: This study retrospectively enrolled 44 patients who underwent partial parotidectomy for benign parotid tumors. These patients were divided into 2 groups: MCI group and MBI group. The MCI surgical procedures were performed via a minimal facelift incision with no preauricular incision, postauricular and hairline incision, or extensive hairline incision and an advanced wound closure method, using continuous absorbable intradermal sutures and skin adhesive. The MBI surgical procedures were performed via a conventional MBI and standard transdermal, interrupted, nonabsorbable suturing approach. The operation variables and the cosmetic results of the patients in each group were compared. RESULTS: A total of 23 patients underwent the MCI and advanced wound closure approach and 21 patients underwent the MBI and standard wound closure approach. No significant differences were found in gender, mean age, tumor size, or tumor site between the 2 groups (P > .05). No differences between groups were seen in operative time and intraoperative blood loss volume (P > .05). Several postoperative complications, such as facial paralysis, Frey syndrome, salivary fistula, infection, or tumor recurrence, did not differ between the 2 groups (P > .05). However, postoperative drainage volume in the MCI group was significantly lower than that in the MBI group (P < .01). Moreover, the postoperative cosmetic satisfaction, skin numbness, and scar evaluation results in the MCI group were better than those in the MBI group (P < .001). CONCLUSIONS: MCI combined with continuous absorbable intradermal sutures and skin adhesive for partial parotidectomy is technically feasible and safe and could produce excellent cosmetic outcomes in selected patients with benign parotid tumors.

MicroRNA-125b suppresses the epithelial-mesenchymal transition and cell invasion by targeting ITGA9 in melanoma.

Increasing evidence has shown that aberrant miRNAs contribute to the development and progression of human melanoma. Previous studies have shown that miR-125b functions as a suppressor in malignant melanoma. However, the molecular function and mechanism by which miR-125b influences melanoma growth and invasion are still unclear. In this study, we aimed to investigate the role of miR-125b in melanoma progression and metastasis. We found that miR-125b expression is significantly downregulated in primary melanoma, and an even greater downregulation was observed in metastatic invasion. Restored expression of miR-125b in melanoma suppressed cell proliferation and invasion both in vitro and in vivo. Furthermore, our findings demonstrate that upregulating miR-125b significantly inhibits malignant phenotypes by repressing the expression of integrin alpha9 (ITGA9). Finally, our data reveal that upregulated expression of ITGA9 in melanoma tissues is inversely associated with miR-125b levels. Together, our results demonstrate that upregulation of ITGA9 in response to the decrease in miR-125b in metastatic melanoma is responsible for melanoma tumor cell migration and invasion.

Molecular mechanisms for tumour resistance to chemotherapy.

Chemotherapy is one of the prevailing methods used to treat malignant tumours, but the outcome and prognosis of tumour patients are not optimistic. Cancer cells gradually generate resistance to almost all chemotherapeutic drugs via a variety of distinct mechanisms and pathways. Chemotherapeutic resistance, either intrinsic or acquired, is caused and sustained by reduced drug accumulation and increased drug export, alterations in drug targets and signalling transduction molecules, increased repair of drug-induced DNA damage, and evasion of apoptosis. In order to better understand the mechanisms of chemoresistance, this review highlights our current knowledge of the role of altered drug metabolism and transport and deregulation of apoptosis and autophagy in the development of tumour chemoresistance. Reduced intracellular activation of prodrugs (e.g. thiotepa and tegafur) or enhanced drug inactivation by Phase I and II enzymes contributes to the development of chemoresistance. Both primary and acquired resistance can be caused by alterations in the transport of anticancer drugs which is mediated by a variety of drug transporters such as P-glycoprotein (P-gp), multidrug resistance associated proteins, and breast cancer resistance protein. Presently there is a line of evidence indicating that deregulation of programmed cell death including apoptosis and autophagy is also an important mechanism for tumour resistance to anticancer drugs. Reversal of chemoresistance is likely via pharmacological and biological approaches. Further studies are warranted to grasp the full picture of how each type of cancer cells develop resistance to anticancer drugs and to identify novel strategies to overcome it.

Computational Identification of the Paralogs and Orthologs of Human Cytochrome P450 Superfamily and the Implication in Drug Discovery.

The human cytochrome P450 (CYP) superfamily consisting of 57 functional genes is the most important group of Phase I drug metabolizing enzymes that oxidize a large number of xenobiotics and endogenous compounds, including therapeutic drugs and environmental toxicants. The CYP superfamily has been shown to expand itself through gene duplication, and some of them become pseudogenes due to gene mutations. Orthologs and paralogs are homologous genes resulting from speciation or duplication, respectively. To explore the evolutionary and functional relationships of human CYPs, we conducted this bioinformatic study to identify their corresponding paralogs, homologs, and orthologs. The functional implications and implications in drug discovery and evolutionary biology were then discussed. GeneCards and Ensembl were used to identify the paralogs of human CYPs. We have used a panel of online databases to identify the orthologs of human CYP genes: NCBI, Ensembl Compara, GeneCards, OMA ("Orthologous MAtrix") Browser, PATHER, TreeFam, EggNOG, and Roundup. The results show that each human CYP has various numbers of paralogs and orthologs using GeneCards and Ensembl. For example, the paralogs of CYP2A6 include CYP2A7, 2A13, 2B6, 2C8, 2C9, 2C18, 2C19, 2D6, 2E1, 2F1, 2J2, 2R1, 2S1, 2U1, and 2W1; CYP11A1 has 6 paralogs including CYP11B1, 11B2, 24A1, 27A1, 27B1, and 27C1; CYP51A1 has only three paralogs: CYP26A1, 26B1, and 26C1; while CYP20A1 has no paralog. The majority of human CYPs are well conserved from plants, amphibians, fishes, or mammals to humans due to their important functions in physiology and xenobiotic disposition. The data from different approaches are also cross-validated and validated when experimental data are available. These findings facilitate our understanding of the evolutionary relationships and functional implications of the human CYP superfamily in drug discovery.

Overview of clinically approved oral antidiabetic agents for the treatment of type 2 diabetes mellitus.

Type 2 diabetes mellitus (T2DM) is caused by insulin resistance and characterized by progressive pancreatic ß-cell dysfunction. This articles reviews the application and limitations of currently approved oral drugs for the treatment of T2DM. Data were retrieved from the literature and well-recognized drug-related databases. Although lifestyle modifications and metformin are the cornerstones of the initial management of T2DM, there is an increasing array of second- and third-line pharmacological agents, including sulphonylureas, insulin, thiazolidinediones and glitazones, α-glucosidase inhibitors, glucagon-like peptide-1 agonists, dipeptidyl peptidase 4 inhibitors and the amylin receptor agonist pramlintide. Current T2DM treatment focuses on reducing blood glucose levels via different mechanisms, including nuclear hormone receptors, nucleic acid binding proteins, transcription factors, voltage-gated K(+) channels, glucosidase, G-protein-coupled receptors and non-receptor serine/threonine protein kinase. Extensive efforts are needed to address the pathogenesis of T2DM, which may facilitate the development of new therapies and the identification of new therapeutic targets to overcome the shortcomings of currently available drugs for T2DM and to achieve therapeutic goals.

Analysis of methylation-driven genes for predicting the prognosis of patients with oral squamous cell carcinoma.

Background: Oral squamous cell carcinoma (OSCC) is a highly aggressive malignancy that is characterized by early distant metastasis and poor prognosis. DNA methylation plays an important role in the etiology and pathogenesis of OSCC. This study aimed to identify methylation-driven genes through bioinformatics analysis as potential biomarkers for early diagnosis and prognostic assessment of OSCC. Methods: Methylation data, RNA sequencing (RNA-seq) data and clinical prognosis information of OSCC patients were retrieved from The Cancer Genome Atlas (TCGA) database. The R packages MethylMix were employed to analyze the correlation between methylation status and corresponding gene expression in tumor and normal tissues to obtain methylation-driven genes. Univariate Cox regression analysis was developed to further screen methylation-driven genes associated with the prognosis of OSCC patients. Subsequently, multivariate Cox regression analysis was utilized to construct a linear prognostic risk prediction model. Furthermore, a combined survival analysis integrating methylation and gene expression was performed to investigate the prognostic value. Results: A total of 374 differentially expressed methylation-driven genes were identified. Seven methylation-driven genes (BST2, KRT15, ZNF134, NT5E, GSTA7P, NAPRT, and GOLPH3L) were found to be significantly associated with patient prognosis. Additionally, four methylation-driven genes (BST2, KRT15, ZNF134 and NAPRT) were used to construct a linear prognostic risk prediction model for OSCC patients. Furthermore, a combined Kaplan-Meier survival analysis revealed that three methylation-driven genes (ZKSCAN7, MFF, ZNF134) alone can be used as independent prognostic markers or drug targets. Conclusions: Our findings facilitate a better understanding of molecular mechanisms of OSCC and provide potential biomarkers of early diagnosis, precision treatment and prognosis evaluation.

Botulinum toxin type A inhibits M1 macrophage polarization by deactivation of JAK2/STAT1 and IκB/NFκB pathway and contributes to scar alleviation in aseptic skin wound healing.

The non-neuronal and non-muscular effects of botulinum toxin type A (BTXA) on scar reduction has been discovered. This study was designed to investigate the effects of BTXA on macrophages polarization during the early stage of skin repair. A skin defect model was established on the dorsal skin of SD rats. BTXA was intracutaneous injected into the edge of wound immediately as the model was established. Histological examinations were performed on scar samples. Raw 264.7 was selected as the cell model of recruited circulating macrophages, and was induced for M1 polarization by LPS. Identify the signaling pathways that primarily regulated M1 polarization and respond to BTXA treatment. Application of BTXA at early stage of injury significantly reduced the scar diameter without delaying wound closure. BTXA treatment improved fiber proliferation and arrangement, and inhibited angiogenesis in scar granular tissue. The number of M1 macrophages and the levels of pro-inflammation were decreased after treated with BTXA in scar tissues. LPS activated JAK2/STAT1 and IκB/NFκB pathways were downregulated by BTXA, as well as LPS induced M1 polarization. At early stage of skin wound healing, injection of BTXA effectively reduced the number of M1 macrophages and the levels of pro-inflammatory mediators which contributes to scar alleviation. BTXA resisted the M1 polarization of macrophages induced by LPS via deactivating the JAK2/STAT1 and IκB/NFκB pathways.

Structural insights into the functional mechanism of the ubiquitin ligase E6AP.

E6AP dysfunction is associated with Angelman syndrome and Autism spectrum disorder. Additionally, the host E6AP is hijacked by the high-risk HPV E6 to aberrantly ubiquitinate the tumor suppressor p53, which is linked with development of multiple types of cancer, including most cervical cancers. Here we show that E6AP and the E6AP/E6 complex exist, respectively, as a monomer and a dimer of the E6AP/E6 protomer. The short α1-helix of E6AP transforms into a longer helical structure when in complex with E6. The extended α1-helices of the dimer intersect symmetrically and contribute to the dimerization. The two protomers sway around the crossed region of the two α1-helices to promote the attachment and detachment of substrates to the catalytic C-lobe of E6AP, thus facilitating ubiquitin transfer. These findings, complemented by mutagenesis analysis, suggest that the α1-helix, through conformational transformations, controls the transition between the inactive monomer and the active dimer of E6AP.

Plumbagin has an inhibitory effect on the growth of TSCC PDX model and it enhances the anticancer efficacy of cisplatin.

BACKGROUND: Head and neck squamous cell carcinomas are the sixth most common malignant tumors worldwide. Tongue squamous cell carcinoma is a common malignant tumor of this type, and it is associated with poor prognosis, a high rate of recurrence and a low survival rate. Plumbagin is derived from Plumbago zeylanica L, several studies report that plumbagin could inhibit cell, tumor metastasis, induce apoptosis in various cancer cells. Patient-derived xenograft (PDX) model can maintain the heterogeneity and microenvironment of human tumors, is a powerful research tool for developing potentially effective therapies for TSCC. METHODS: Tumor tissues obtained from TSCC patients were implanted into immunodeficient mice to establish TSCC PDX models. Subsequently, the PDX models were used to evaluate the anti-tumor effects of plumbagin on TSCC. Furthermore, we conducted next-generation sequencing (NGS) and explored the mRNA expression profiles between the treatment and control groups. We selected eight mRNAs related to the characteristics and prognosis of TSCC patients for further analysis. RESULTS: Plumbagin could inhibit the growth of TSCC PDX models and inhibit expression of Akt/mTOR pathway. In addition, plumbagin was shown to increase drug sensitivity to cisplatin. The eight mRNAs selected for further analysis, AXL, SCG5, VOPP1, DCBLD2 and DRAM1 are cancer-promoting genes, DUSP1, AQP5 and BLNK are cancer suppressor genes. And they were related to the diagnosis, growth, prognosis, and immune cell infiltration in TSCC patients. CONCLUSION: Plumbagin exhibits an inhibitory effect on the growth of the PDX model of TSCC. Moreover, plumbagin enhances the inhibitory effects of cisplatin.

Plumbagin alleviates temporomandibular joint osteoarthritis progression by inhibiting chondrocyte ferroptosis via the MAPK signaling pathways.

AIMS: The acceleration of osteoarthritis (OA) development by chondrocytes undergoing ferroptosis has been observed. Plumbagin (PLB), known for its potent antioxidant and anti-inflammatory properties, has demonstrated promising potential in the treatment of OA. However, it remains unclear whether PLB can impede the progression of temporomandibular joint osteoarthritis (TMJOA) through the regulation of ferroptosis. The study aims to investigate the impact of ferroptosis on TMJOA and assess the ability of PLB to modulate the inhibitory effects of ferroptosis on TMJOA. MATERIALS AND METHODS: The study utilized an in vivo rat model of unilateral anterior crossbite (UAC)-induced TMJOA and an in vitro study of chondrocytes exposed to H2O2 to create an OA microenvironment. Various experiments including cell viability assessment, quantitative RT-PCR, western blot analysis, histology, and immunofluorescence were conducted to examine the impact of ferroptosis on TMJOA and evaluate the potential of PLB to mitigate the inhibitory effects of ferroptosis on TMJOA. Additionally, RNA-seq and bioinformatics analysis were performed to investigate the underlying mechanism by which PLB regulates ferroptosis in TMJOA. RESULTS: Fer-1 demonstrated its potential in mitigating the advancement of TMJOA through its inhibitory effects on ferroptosis and matrix degradation in chondrocytes, thereby substantiating the role of ferroptosis in the pathogenesis of TMJOA. Furthermore, the observed protective impact of PLB on cartilage implied that PLB can modulate the inhibition of ferroptosis in TMJOA by regulating the MAPK signaling pathways. CONCLUSIONS: PLB alleviates TMJOA progression by suppressing chondrocyte ferroptosis via MAPK pathways, indicating PLB to be a potential therapeutic strategy for TMJOA.

Corrigendum: MXene nanomaterials in biomedicine: a bibliometric perspective.

[This corrects the article DOI: 10.3389/fbioe.2023.1184275.].

Plumbagin Enhances the Anticancer Effects of PF Chemotherapy via Downregulation of the PI3K/AKT/mTOR/p70S6K Pathway in Human Tongue Squamous Cell Carcinoma.

Cisplatin plus 5-fluorouracil (PF) is used as the standard neoadjuvant chemotherapy (also called preoperative chemotherapy) in the treatment of tongue squamous cell carcinoma (TSCC). Although PF chemotherapy reduces the distant metastasis of TSCC, the five-year survival rate has not significantly improved. In recent years, components considered in traditional Chinese medicine have been researched as adjuvant drugs for radiotherapy and chemotherapy. Plumbagin (PB) is a quinone component isolated from Plumbago zeylanica L. Notably, PB demonstrates numerous anticancer properties. In order to examine the chemosensitization effect of PB on PF and its associated mechanisms, in vitro experiments using TSCC Cal27 and cisplatin (CDDP)-resistant Cal27/CDDP cells were carried out in the present study, and the results were subsequently verified using nude mice xenografts. Results of the present study demonstrated that PB enhanced the anticancer effects of PF on the proliferation, migration, and invasion of Cal27 and Cal27/CDDP cells. Cell cycle assays demonstrated that both Cal27 and Cal27/CDDP cells were arrested in the S phase following the combined treatment of PF and PB. Moreover, the PF and PB combination group induced higher levels of apoptosis in Cal27 and Cal27/CDDP cells compared with the group treated with PF alone. In addition, the results of the present study demonstrated that combined PB and PF inhibited the PI3K/AKT/mTOR/p70S6K pathway in TSCC cells. Moreover, the weight and volumes of tumors in nude mice were reduced following treatment with a combination of PF and PB. Results of the present study also demonstrated that the expression levels of Ki67 were markedly reduced in the combined treatment group compared with the group treated with PF alone. In summary, the results of the present study demonstrated that PB enhanced the PF sensitivity of TSCC through induction of S-phase arrest and apoptosis via the PI3K/AKT/mTOR/p70S6K pathway.

MXene nanomaterials in biomedicine: A bibliometric perspective.

Purpose: MXene is two-dimensional (2D) nanomaterials that comprise transition metal carbides, nitrides, and carbonitrides. Their unique nanostructure attributes it a special role in medical applications. However, bibliometric studies have not been conducted in this field. Therefore, the aim of the present study was to conduct a bibliometric analysis to evaluate the global scientific output of MXene in biomedical research, explore the current situation of this field in the past years and predicte its research hotpots. Methods: We utilized visual analysis softwares Citespace and Bibliometrix to analyze all relevant documents published in the period of 2011-2022. The bibliometric records were obtained from the Web of Science Core Collection. Results: A total of 1,489 publications were analyzed in this study. We observed that China is the country with the largest number of publications, with Sichuan University being the institution with the highest number of publications in this field. The most publications on MXene medicine research in the past year were found primarily in journals about Chemistry/Materials/Physics. Moreover, ACS Applied Materials and Interfaces was found to be the most productive journal in this field. Co-cited references and keyword cluster analysis revealed that #antibacterial# and #photothermal therapy# are the research focus keyword and burst detection suggested that driven wearable electronics were newly-emergent research hot spots. Conclusion: Our bibliometric analysis indicates that research on MXene medical application remains an active field of study. At present, the research focus is on the application of MXene in the field of antibacterial taking advantage of its photothermal properties. In the future, wearable electronics is the research direction of MXene medical application.

Isoorientin ameliorates H2O2-induced apoptosis and oxidative stress in chondrocytes by regulating MAPK and PI3K/Akt pathways.

Osteoarthritis (OA) is a chronic and complicated degenerative disease for which there is currently no effective treatment. Isoorientin (ISO) is a natural plant extract that has antioxidant activity and could be used to treat OA. However, due to a lack of research, it has not been widely used. In this study, we investigated the protective effects and molecular mechanisms of ISO on H2O2-induced chondrocytes, a widely used cell model for OA. Based on RNA-seq and bioinformatics, we discovered that ISO significantly increased the activity of chondrocytes induced by H2O2, which was associated with apoptosis and oxidative stress. Furthermore, the combination of ISO and H2O2 significantly reduced apoptosis and restored mitochondrial membrane potential (MMP), which may be achieved by inhibiting apoptosis and mitogen-activated protein kinase (MAPK) signaling pathways. Moreover, ISO increased superoxide dismutase (SOD), heme oxygenase 1 (HO-1) and quinone oxidoreductase 1 (NQO-1) and reduced malondialdehyde (MDA) levels. Finally, ISO inhibited H2O2-induced intracellular reactive oxygen species (ROS) in chondrocytes by activating the nuclear factor erythroid 2-related factor 2 (Nrf2) and phosphatidylinositol 3 kinase/protein kinase B (PI3K/Akt) signaling pathways. This study establishes a theoretical framework for ISO's ability to inhibit OA in vitro models.

Glandular Odontogenic Cyst Associated with Odontoma: A Rare Case Report.

Background: Glandular odontogenic cyst (GOC) is an extremely rare developmental jawbone cyst, tending to recurrence owing to its aggressive behavior. There has been no reported case of presence of GOC simultaneous with odontoma. We presented a case of GOC associated with odontoma with special reference to the diagnostic imaging and the histopathological features. Case Presentation: A 42-year-old Chinese man presented with swelling and pain in the anterior mandible for the past 3 months. Panoramic scan showed a large multiocular well-circumscribed radiolucency accompanied by toothlike morphological abnormality. Histological findings confirmed a GOC associated with odontoma. Conclusion: This case demonstrates GOC with multiple clinical spectrum, and its association with odontoma might enhance the existing knowledge of this rare jawbone cyst.

Construction of prognostic signature of patients with oral squamous cell carcinoma based on pyroptosis-related long non-coding RNAs.

Background and objective: Oral squamous cell carcinoma (OSCC) is the most common malignant tumor in the head and neck, and its morbidity and mortality are increasing year by year. Changes in key genes are thought to be closely related to the occurrence and development of OSCC. Pyroptosis is an inflammatory form of programmed cell death that has been implicated in malignancies and inflammatory diseases. Changes in the expression of long noncoding RNAs may also affect tumorigenesis and progression. In this study, our main objective was to evaluate the association between pyroptosis-related lncRNAs and prognosis in patients with OSCC. Methods: The RNA-seq data and clinicopathological data of OSCC patients are from The Cancer Genome Atlas database. The pyroptosis gene set is obtained from Gene Set Enrichment Analysis database. Univariate COX, Lasso and multivariate COX regression analyses were used for the construction of risk prognostic models of OSCC, eight lncRNAs were incorporated into prognostic models. The Kaplan-Meier method and log-rank test were used to evaluate the differences of overall survival between patients in high-risk and low-risk groups. The reliability of predictions across the dataset was analyzed by receiver operating characteristic (ROC) curves. The immune signature score was calculated using the single-sample gene set enrichment analysis. Results: Eight pyroptosis-related lncRNAs were used to construct prognostic signature of OSCC, including AC136475.2, AC024075.2, JPX, ZFAS1, TNFRSF10A-AS1, LINC00847, AC099850.3 and IER3-AS1. According to this prognostic signature, patients with OSCC were divided into high-risk and low-risk groups. Kaplan-Meier survival analysis showed that the survival rate of the high-risk group was significantly lower than the low-risk group. ROC area for risk score was 0.716, and ROC area of the 8 lncRNAs are all between 0.5 and 1, implied that these lncRNAs had high accuracy in predicting the prognosis of OSCC patients. Immune Infiltration findings suggested that these lncRNAs affected immune responses in the microenvironment of OSCC. Conclusion: The prognostic signature based on pyroptosis-related lncRNAs potentially serves as an independent prognostic indicator for OSCC patients. And this signature facilitates research on targeted diagnosis and treatment of patients diagnosed with OSCC.

The osteogenic effects of porous Tantalum and Titanium alloy scaffolds with different unit cell structure.

Porous scaffolds have long been regarded as optimal substitute for bone tissue repairing. In order to explore the influence of unit cell structure and inherent material characteristics on the porous scaffolds in terms of mechanical and biological performance, selective laser melting (SLM) technology was used to fabricate porous tantalum (Ta) and titanium alloy (Ti6Al4V) with diamond (Di) or rhombic dodecahedron (Do) unit cell structure. The mechanical strength of all the porous scaffolds could match that of trabecular bone, while the biological performance of each scaffold was diverse from each other. Moreover, the ILK/ERK1/2/Runx2 signaling pathway had been verified to be involved in the osteogenic differentiation of rat bone mesenchymal stem cells (rBMSCs) cultured on those porous scaffolds. Unit cell structure and material characteristics of the porous Ta and Ti6Al4V scaffolds can synergistically modulate this axis and further impact on the osteogenic effects. Our results hence illustrate that porous Ta scaffold with diamond unit cell structure possesses excellent osteogenic effects and moderate mechanical strength and porous Ti6Al4V scaffold with rhombic dodecahedron unit cell structure has the highest mechanical strength and moderate osteogenic effects. Both porous Ta and Ti6Al4V can be applied in different settings requiring either better biological performance or higher mechanical demand.