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Three-dimensional fluorescence spectra are often affected by scattering effects, traditional scattering elimination methods rely excessively on parameter settings and cannot automatically eliminate scattering in batches, thereby limiting the application of fluorescence spectroscopy technology in rapid online monitoring and analysis of samples. In this study, we have developed a model based on a deep learning CycleGAN to rapidly eliminate scattering from three-dimensional fluorescence spectra. The proposed model efficiently eliminates scattering by simply inputting single or batches of contaminated fluorescent spectra. By training the CycleGAN using a large dataset of simulated three-dimensional fluorescence spectra and employing data augmentation, to the model can transform fluorescence spectra with scattering into ones without scattering. To validate the effectiveness of the proposed methed, we confirmed its generalization and reliability by eliminating scattering from two sets of previously unseen real experimental three-dimensional fluorescence spectra. We evaluated the effectiveness of scattering elimination across various noise levels and scattering widths, using metrics such as the mean absolute error, peak signal-to-noise ratio, structural similarity and cosine similarity. Furthermore, we conducted a component analysis using PARAFAC on the spectra post-scattering elimination, yielding correlation coefficients of >0.97 when compared to that in case of actual components. Finally, we compared the proposed model with traditional mathematical methods, such as blank subtraction and Delaunay triangulation. Results showed that the proposed model can automatically and efficiently eliminate scattering from fluorescence spectra in batches, substantially improving the efficiency of scattering elimination.
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The establishment and utilization of preclinical animal models constitute a pivotal aspect across all facets of cancer research, indispensably contributing to the comprehension of disease initiation and progression mechanisms, as well as facilitating the development of innovative anti-cancer therapeutic approaches. These models have emerged as crucial bridges between basic and clinical research, offering multifaceted support to clinical investigations. This study initially focuses on the importance and benefits of establishing preclinical animal models, discussing the different types of preclinical animal models and recent advancements in cancer research. It then delves into cancer treatment, studying the characteristics of different stages of tumor development and the development of anti-cancer drugs. By integrating tumor hallmarks and preclinical research, we elaborate on the path of anti-cancer drug development and provide guidance on personalized cancer therapy strategies, including synthetic lethality approaches and novel drugs widely adopted in the field. Ultimately, we summarize a strategic framework for selecting preclinical safety experiments, tailored to experimental modalities and preclinical animal species, and present an outlook on the prospects and challenges associated with preclinical animal models. These models undoubtedly offer new avenues for cancer research, encompassing drug development and personalized anti-cancer protocols. Nevertheless, the road ahead continues to be lengthy and fraught with obstacles. Hence, we encourage researchers to persist in harnessing advanced technologies to refine preclinical animal models, thereby empowering these emerging paradigms to positively impact cancer patient outcomes.
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Microbial therapies have promising applications in the treatment of a broad range of diseases. However, effective colonization of the target region by therapeutic microorganisms remains a significant challenge owing to the complexity of the intestinal system. Here, we developed surface nanocoating-based universal platform (SNUP), which enabled the manipulation of controlled release and targeted colonization of therapeutic microbes in the digestive tract without the utilization of any targeting molecules. The system controlled the decomposition time of SNUP in the gut by regulating different modification layers and modification sequences on the microorganism's surface, so that the microorganism was released at a predetermined time and space. With the SNUP nanomodification technology, we could effectively deliver therapeutic microorganisms to specific complex intestinal regions such as the small intestine and colon, and protect the bioactivity of therapeutic microorganisms from destruction by both strong acids and digestive enzymes. In this study, we found that two layers SNUP-encapsulated Liiliilactobacillus salivarius (LS@CCMC) could efficiently colonize the small intestine and significantly improve the symptoms of a mouse model of Parkinson's disease through sustained secretion of γ-aminobutyric acid (GABA). This surface nanocoating-based universal platform system does not require the design of specific targeting molecules, providing a simple and universal method for colonized microbial therapy, target theranostics, precision medicine, and personalized medicine.
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Propiedades de Superficie , Animales , Ratones , Tracto Gastrointestinal/microbiología , Tracto Gastrointestinal/metabolismo , Tamaño de la Partícula , ClostridialesRESUMEN
Background: Advanced lung cancer that contributes to a heavy burden on medical institutions is the leading cause of cancer-related death and is often accompanied by metabolic disorders. In this study, we aimed to explore the biomarkers of diagnosis and radiotherapy response in non-small-cell lung cancer (NSCLC) patients by plasma lipidomics analysis. Method: Using triple-quadrupole mass spectrometer analysis, our research characterized the plasma lipid metabolomics profile of 25 healthy controls and 31 advanced NSCLC patients in each of three different radiotherapy phases. Results: The results showed altered lipid elements and concentrations among NSCLC patients with different radiotherapy phases, NSCLC subtypes, and different radiotherapeutic responses. We found that compared to the healthy controls, myelin-associated glycoprotein (MAG), phosphatidylinositol (PI), and phosphatidylserine (PS) were mainly and significantly altered lipid elements (> twofold, and p < 0.05) among NSCLC patients with different radiotherapy phases. Through comparison of lipid elements between bad and good responses of NSCLC patients with radiotherapy, the obviously declined phosphatidylglycerol (PG 18 : 0/14 : 0, 18 : 1/18 : 3, and 18 : 0/20 : 1) or markedly elevated PI (20 : 0/22 : 5 and 18 : 2/22 : 4) and phosphatidic acid (PA 14 : 0/20 : 4, 14 : 0/20 : 3, and 18 : 2/22 : 4) could indicate poor therapeutic response for NSCLC patients. The results of ROC curve analysis suggested that PG (18 : 0/20 : 1 and 18 : 0/14 : 0) could clearly predict the radiotherapeutic response for NSCLC patients, and PS (18 : 0/20 : 0) and cholesterol were the first two lipid components with the most potential for the diagnosis of advanced NSCLC. Conclusion: Our results indicated that plasma lipidomics profiling might have a vital value to uncover the heterogeneity of lipid metabolism in healthy people and advanced NSCLC patients with different radiotherapy phase, and further to screen out radiotherapeutic response-specific biomarkers.
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Autophagy, a complex and highly regulated cellular process, is critical for the maintenance of cellular homeostasis by lysosomal degradation of cellular debris, intracellular pathogens, and dysfunctional organelles. It has become an interesting and attractive topic in cancer because of its dual role as a tumor suppressor and cell survival mechanism. As a highly conserved pathway, autophagy is strictly regulated by diverse non-coding RNAs (ncRNAs), ranging from short and flexible miRNAs to lncRNAs and even circRNAs, which largely contribute to autophagy regulatory networks via complex RNA interactions. The potential roles of RNA interactions during autophagy, especially in cancer procession and further anticancer treatment, will aid our understanding of related RNAs in autophagy in tumorigenesis and cancer treatment. Herein, we mainly summarized autophagy-related mRNAs and ncRNAs, also providing RNA-RNA interactions and their potential roles in cancer prognosis, which may deepen our understanding of the relationships between various RNAs during autophagy and provide new insights into autophagy-related therapeutic strategies in personalized medicine.
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MicroARNs , Neoplasias , ARN Largo no Codificante , Humanos , ARN no Traducido/genética , MicroARNs/genética , MicroARNs/metabolismo , Neoplasias/genética , ARN Mensajero/genética , ARN Largo no Codificante/genética , ARN Largo no Codificante/metabolismo , Autofagia/genéticaRESUMEN
BACKGROUND: Burning mouth syndrome (BMS) is an oral-facial pain disorder involving the central and peripheral nervous systems, but the evidence for altered pain sensitivity remains inconclusive. The aim of this study was to investigate pain sensitivity and oral health-related quality of life (OHRQoL) in patients with BMS and to assess the relationship between them. METHODS: Fifty Chinese patients with BMS (57.82 ± 11.2 years) and fifty age- and gender-matched healthy subjects (55.64 ± 10.1 years) participated in the study. The Pain Sensitivity Questionnaire (PSQ) was used to assess participants' pain sensitivity. The Oral Health Impact Profile (OHIP-14) was used to evaluate participants' OHRQoL. RESULTS: The PSQ total score (p = 0.009), the PSQ minor score (p = 0.003) and the OHIP-14 score (p<0.05) of patients with BMS were significantly higher than those of the healthy subjects. Simple linear regression showed that the PSQ minor score was significantly associated with the OHIP-14 score in patients with BMS (ß = 0.338, p = 0.016). CONCLUSION: Patients with BMS have higher pain sensitivity than healthy subjects. Reducing pain sensitivity might help to improve the quality of life of patients with BMS.
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Síndrome de Boca Ardiente , Calidad de Vida , Humanos , Pueblos del Este de Asia , Dolor Facial , Persona de Mediana Edad , AncianoRESUMEN
Cancer is the second leading cause of death in the world, and chemotherapy is one of the main methods of cancer treatment. However, the resistance of cancer cells to chemotherapeutic drugs has always been the main reason affecting the therapeutic effect. Synthetic lethality has emerged as a promising approach to augment the sensitivity of cancer cells to chemotherapy agents. Synthetic lethality (SL) refers to the specific cell death resulting from the simultaneous mutation of two non-lethal genes, which individually allow cell survival. This comprehensive review explores the classification of SL, screening methods, and research advancements in SL inhibitors, including Poly (ADP-ribose) polymerase (PARP) inhibitors, Ataxia telangiectasia and Rad3-related (ATR) inhibitors, WEE1 G2 checkpoint kinase (WEE1) inhibitors, and protein arginine methyltransferase 5 (PRMT5) inhibitors. Emphasizing their combined use with chemotherapy drugs, we aim to unveil more effective treatment strategies for cancer patients.
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Esophageal squamous cell carcinoma (ESCC) is an aggressive malignancy of the digestive system with increasing incidence and mortality rates. The biological roles of microRNA (miR)-378a-3p in tumor cells remain contested, and the mechanisms underlying the functions, energy metabolism, and cell survival mechanisms in ESCC cells are yet to be fully elucidated. In the present study, miR-378a-3p overexpression and negative control plasmids were transfected into ECA-109 cells using electroporation. Western blotting was used to detect the relative expression of proteins, and flow cytometry was used to detect cell apoptosis. Subsequently, ELISA assays were performed to determine enzyme activity, and an ATP detection kit was used to measure ATP content. Dual-luciferase reporter assays were performed to identify the target genes of miR-378a-3p. The results of the present study demonstrated that miR-378a-3p inhibited the gene expression and enzyme activities of glucose transporter protein 1 (GLUT-1), Aldolase A (ALDOA), and pyruvate kinase M2 (PKM2), all of which are involved in the glycolytic pathway of cells. Energy metabolism was suppressed by miR-378a-3p by reducing ATP content, and this downregulated the expression of Bcl-2 and Survivin. Moreover, increased miR-378a-3p expression promoted cell apoptosis in the early stages by increasing the expression levels and the activity of Bad and Caspase-3, while inhibiting the expression levels of Bcl-2 and Survivin. The results of the present study also demonstrated that GLUT-1/ALDOA/PKM2 were target genes of miR-378a-3p. Notably, miR-378a-3p blocked energy production and promoted the apoptosis of tumor cells via the downregulation of glycolytic enzyme expression and by reducing the mitochondrial membrane potential in ESCC. Bad, Caspase-3, Survivin, and Bcl-2 may be associated with blocking energy production and promoting apoptosis via miR-378a-3p in ESCC cells.
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Dysregulated expression of specific non-coding RNAs (ncRNAs) has been strongly linked to tumorigenesis, cancer progression, and therapeutic resistance. These ncRNAs can act as either oncogenes or tumor suppressors, thereby serving as valuable diagnostic and prognostic markers. Numerous studies have implicated the participation of ncRNAs in the regulation of diverse signaling pathways, including the pivotal Wnt/ß-catenin signaling pathway that is widely acknowledged for its pivotal role in embryogenesis, cellular proliferation, and tumor biology control. Recent emerging evidence has shed light on the capacity of ncRNAs to interact with key components of the Wnt/ß-catenin signaling pathway, thereby modulating the expression of Wnt target genes in cancer cells. Notably, the activity of this pathway can reciprocally influence the expression levels of ncRNAs. However, comprehensive analysis investigating the specific ncRNAs associated with the Wnt/ß-catenin signaling pathway and their intricate interactions in cancer remains elusive. Based on these noteworthy findings, this review aims to unravel the intricate associations between ncRNAs and the Wnt/ß-catenin signaling pathway during cancer initiation, progression, and their potential implications for therapeutic interventions. Additionally, we provide a comprehensive overview of the characteristics of ncRNAs and the Wnt/ß-catenin signaling pathway, accompanied by a thorough discussion of their functional roles in tumor biology. Targeting ncRNAs and molecules associated with the Wnt/ß-catenin signaling pathway may emerge as a promising and effective therapeutic strategy in future cancer treatments.
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Background: An increasing number of clinicians are experimenting with high-dose radiation. This study focuses on the genomic effects of high-dose single-shot radiotherapy and aims to provide a dynamic map for non-small cell lung cancer (NSCLC). Methods: We used whole-transcriptome sequencing to understand the evolution at molecular levels in A549 and H1299 exposed to 10 Gy X-rays at different times (2, 6, 12, 24, and 48 h) in comparison with the no radiation group. Ingenuity pathway analysis, ceRNA analysis, enrichment analysis, and cell cycle experiments are performed for molecular analyses and function analyses. Results: Whole-transcriptome sequencing of NSCLC showed a significant dynamic change after radiotherapy within 48 h. MiR-219-1-3p and miR-221-3p, miR-503-5p, hsa-miR-455-5p, hsa-miR-29-3p, and hsa-miR-339-5p were in the core of the ceRNA related to time change. GO and KEGG analyses of the top 30 mRNA included DNA repair, autophagy, apoptosis, and ferroptosis pathways. Regulation of the cell cycle-related transcription factor E2F1 might have a key role in the early stage of radiotherapy (2.6 h) and in the later stage of autophagy (24 and 48 h). Functions involving different genes/proteins over multiple periods implied a dose of 10 Gy was related to the kidney and liver pathway. Radiation-induced cell cycle arrest at the G2/M phase was evident at 24 h. We also observed the increased expression of CCNB1 at 24 h in PCR and WB experiments. Conclusion: Our transcriptomic and experimental analyses showed a dynamic change after radiation therapy in 48 h and highlighted the key molecules and pathways in NSCLC after high-dose single-shot radiotherapy.
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OBJECTIVES: Radiosensitivity Index (RSI) can predict intrinsic radiotherapy sensitivity. We analyzed multiomics characteristics in lung squamous cell carcinoma between high and low RSI groups, which may help understand the underlying molecular mechanism of radiosensitivity and guide optional treatment for patients in the future. METHODS: The Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO) data were used to download clinical data, mRNA, microRNA, and lncRNA expression. Differential analyses, including mRNA, miRNA, lncRNA, and G.O. and KEGG, and GSVA analyses, were performed with R. Gene set enrichment analysis was done by GSEA. miRNA-differentially expressed gene network and ceRNA network were analyzed and graphed by the Cytoscape software. RESULTS: In TCGA data, 542 patients were obtained, including 171 in the low RSI group (LRSI) and 371 in the high RSI group (HRSI). In RNAseq, 558 significantly differentially expressed genes (DEGs) were obtained. KRT6A was the most significantly upregulated gene and IDO1 was the most significantly downregulated gene. In miRNAseq, miR-1269a was the most significantly upregulated. In lncRNAseq, LINC01871 was the most upregulated. A 66-pair interaction between differentially expressed genes and miRNAs and an 11-pair interaction between differential lncRNAs and miRNAs consisted of a ceRNA network, of which miR-184 and miR-490-3p were located in the center. In the GEO data, there were 40 DEGs. A total of 17 genes were founded in both databases, such as ADAM23, AHNAK2, BST2, COL11A1, CXCL13, FBN2, IFI27, IFI44L, MAGEA6, and PTGR1. GSVA analysis revealed 31 significant pathways. GSEA found 87 gene sets enriched in HRSI and 91 gene sets in LRSI. G.O. and KEGG of RNA expression levels revealed that these genes were most enriched in T cell activation and cytokine-cytokine receptor interaction. CONCLUSIONS: Patients with lung squamous cell carcinoma have different multiomics characteristics between two groups. These differences may have an essential significance with radiotherapy effect.
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Biomarcadores de Tumor/metabolismo , Carcinoma de Células Escamosas/patología , Metilación de ADN , Perfilación de la Expresión Génica , Regulación Neoplásica de la Expresión Génica , Neoplasias Pulmonares/patología , Tolerancia a Radiación , Anciano , Biomarcadores de Tumor/genética , Carcinoma de Pulmón de Células no Pequeñas/genética , Carcinoma de Pulmón de Células no Pequeñas/metabolismo , Carcinoma de Pulmón de Células no Pequeñas/patología , Carcinoma de Pulmón de Células no Pequeñas/radioterapia , Carcinoma de Células Escamosas/genética , Carcinoma de Células Escamosas/metabolismo , Carcinoma de Células Escamosas/radioterapia , Femenino , Humanos , Neoplasias Pulmonares/genética , Neoplasias Pulmonares/metabolismo , Neoplasias Pulmonares/radioterapia , Masculino , MicroARNs/genética , Mapas de Interacción de Proteínas , ARN Largo no Codificante/genética , ARN Mensajero/genética , ARN Mensajero/metabolismo , TranscriptomaRESUMEN
Objective: We aimed to explore the prognostic implication for non-small cell lung cancer (NSCLC) based on the expression profiles of circadian clock-related genes (CCRGs), and describe the changes of immune infiltration and cell functions of related to the circadian rhythm. Methods: Univariate and multivariate Cox proportional hazard regression were performed to determine a CCRGs risk-score significantly correlated with overall survival (OS) of the training set and validation set. GO, KEGG, and GSVA indicated discrepant changes in cellular processes and signaling pathways associated with these CCRGs. Immune cell infiltration and mutation rates were investigated by the online analysis platform and the algorithm provided by works of literature. Results: The signature-based on ten-gene signatures could independently predict the OS both in TCGA lung adenocarcinoma (p < 0.001, HR: 1.228, 95% CI: 1.158 to 1.302) and lung squamous cell carcinoma (p < 0.001, HR: 2.501, 95% CI: 2.010 to 3.117), respectively. The circadian oscillations driven by CCRGs could disturb the metabolism and cellular functions of cancer cells. The infiltration level of critical cells in specific anti-tumor immunity process was suppressed apparently. In contrast, the infiltrating of inflammatory cells and immune cells with negative regulatory effects were promoted in the high-risk group. CCRGs were evolutionarily conserved with low mutation rates, which brought difficulties to explore therapeutic targets. Conclusion: We identified and validated a circadian rhythm signature to described clinical relevance and tumor microenvironment of NSCLC, which revealed that circadian rhythms might play an influential role in the NSCLC.
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Long non-coding RNAs (lncRNAs) have been considered as novel regulators in oral squamous cell carcinoma (OSCC). Enhancer of zeste homolog 2 (EZH2) can act as an oncogene in OSCC. This study intended to investigate whether lncRNA prostatic androgen-regulated transcription 1 (PART1) can exert its role in OSCC by regulating EZH2. The expression of PART1 in OSCC samples, tumour tissues or OSCC cell lines was detected by qRT-PCR. The proliferation and apoptosis of OSCC cells were detected by CCK-8 and flow cytometry assays, respectively. The expression of PART1 and EZH2 was highly expressed in clinical OSCC tumours and cell lines. The expression level of PART1 was positively correlated to the size, clinical stage and node metastasis of OSCC patients. Functionally, PART1 knockdown inhibited proliferation and facilitated apoptosis of OSCC cells. Mechanically, fused in sarcoma/translocated in liposarcoma (FUS) interacted with PART1 and EZH2. In addition, PART1 knockdown reduced the mRNA expression of EZH2, which was offset by FUS overexpression. The overexpression of FUS abrogated the effects of PART1 silence on proliferation and apoptosis of OSCC cells. The in vivo experiment revealed that PART1 knockdown inhibited tumour growth of OSCC cells in nude mice. This study indicated that PART1 exerts a carcinogenic role in OSCC by enhancing the stability of EZH2 protein.
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Biomarcadores de Tumor/metabolismo , Carcinoma de Células Escamosas/patología , Proteína Potenciadora del Homólogo Zeste 2/metabolismo , Regulación Neoplásica de la Expresión Génica , Neoplasias de la Boca/patología , ARN no Traducido/genética , Animales , Apoptosis , Biomarcadores de Tumor/genética , Carcinoma de Células Escamosas/genética , Carcinoma de Células Escamosas/metabolismo , Proliferación Celular , Proteína Potenciadora del Homólogo Zeste 2/genética , Femenino , Humanos , Masculino , Ratones , Ratones Endogámicos BALB C , Ratones Desnudos , Persona de Mediana Edad , Neoplasias de la Boca/genética , Neoplasias de la Boca/metabolismo , Pronóstico , Tasa de Supervivencia , Células Tumorales Cultivadas , Ensayos Antitumor por Modelo de XenoinjertoRESUMEN
BACKGROUND: Lung cancer is the leading cause of cancer-related death, and countries all over the world have given considerable support to lung cancer research. However, analysis on the status of funding in the field of lung cancer is still lacking. METHODS: We visited the National Natural Science Foundation of China (NSFC) and National Institutes of Health (NIH) official websites to gather lung cancer research information between 2008 and 2020. RSTCM6 software was used to extract the keywords of funded projects which were then imported into CiteSpace software for visual analysis of word frequency. RESULTS: A total of 1,745 and 5,939 search results were finally obtained from the NSFC and NIH websites, respectively. The amount of NSFC funding for projects in the field of lung cancer increased steadily from 2008 to 2012, while the NIH funding for lung cancer was significantly higher in even years than in odd years between 2008 to 2018. The Shanghai Jiaotong University, Sun Yat-sen University, and Guangzhou Medical University were the top three research institutions that had received the most projects funded by the NSFC. Apoptosis, proliferation, invasion, metabolism, the pathogenesis of lung cancer, cell signal transduction, epithelial-mesenchymal transformation (EMT), and immune-related research were the most frequently funded research areas by the NSFC. Biomarkers, targeted therapy, signal pathway, genomics, and immune-related research were funded most the most frequently funded research areas by the NIH. Both the NIH and NSFC funding for lung cancer immune-related research has increased in recent years. CONCLUSIONS: NIH funding in the United States is decreasing year by year, whereas NSFC funding is increasing in China. There are some differences in research focus in lung cancer research funding between China and the United States. However, both countries have increased the support for immune-related research in recent years.
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HEADINGS AIMS: To establish a microsatellite instability (MSI) predictive model in pan-cancer and compare the multi-omics characterization of MSI-related molecular features. MATERIALS AND METHODS: We established a 15-gene signature for predicting MSI status and performed a systematic assessment of MSI-related molecular features including gene and miRNA expression, DNA methylation, and somatic mutation, in approximately 10,000 patients across 30 cancer types from The Cancer Genome Atlas, Gene Expression Omnibus database, and our institution. Then we identified common MSI-associated dysregulated molecular features across six cancers and explored their mutual interfering relationships and the drug sensitivity. KEY FINDINGS: we demonstrated the model's high prediction performance and found the samples with high-MSI were mainly distributed in six cancers: BRCA, COAD, LUAD, LIHC, STAD, and UCEC. We found RPL22L1 was up-regulated in the high-MSI group of 5/6 cancer types. CYP27A1 and RAI2 were down-regulated in 4/6 cancer types. More than 20 miRNAs and 39 DMGs were found up-regulated in MSI-H at least three cancers. We discovered some drugs, including OSI-027 and AZD8055 had a higher sensitivity in the high MSI-score group. Functional enrichment analysis revealed the correlation between MSI score and APM score, HLA score, or glycolysis score. The complicated regulatory mechanism of tumor MSI status in multiple dimensions was explored by an integrated analysis of the correlations among MSI-related genes, miRNAs, methylation, and drug response data. SIGNIFICANCE: Our pan-cancer study provides a valuable predictive model and a comprehensive atlas of tumor MSI, which may guide more precise and personalized therapeutic strategies for tumor patients.
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Inestabilidad de Microsatélites , Repeticiones de Microsatélite/genética , Neoplasias/genética , Colestanotriol 26-Monooxigenasa , Metilación de ADN , Bases de Datos Genéticas , Expresión Génica/genética , Regulación Neoplásica de la Expresión Génica/genética , Genómica/métodos , Humanos , Péptidos y Proteínas de Señalización Intercelular , MicroARNs , Repeticiones de Microsatélite/fisiología , Modelos Teóricos , Mutación , Neoplasias/metabolismo , Proteómica/métodos , Proteínas Ribosómicas , Transcriptoma/genéticaRESUMEN
OBJECTIVE: To investigate the effect of three anatomical parameters (maxillary sinus width, maxillary sinus angle, and residual bone height) on the outcomes of transcrestal sinus lift with simultaneous implant placement. METHODS: A total of 60 maxillary sinuses in 42 patients were included in this study. All patients were treated with transcrestal sinus lift procedure associated with simultaneous implant placement using a composite graft material of autogenous bone and Bio-Oss. For each patient, beam computed tomography (CBCT) scans were performed preoperatively, immediately after surgery, and 6 months after surgery. The parameters were measured on the preoperative and postoperative CBCT images. The correlation of three anatomical parameters with graft resorption was analyzed using Pearson's correlation test. RESULTS: The average residual bone height was (4.46±1.55) mm. The average width of maxillary sinus was (13.86±2.71) mm. The average sinus angle was 78.09°±10.27°. A significant positive correlation was observed between maxillary sinus width and graft resorption (P<0.01). A positive association was also found between sinus angle and graft resorption (P<0.01). CONCLUSIONS: The findings show that graft bone resorption in elevated sinus has a positive correlation with the sinus width and sinus angle.
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Resorción Ósea , Implantes Dentales , Elevación del Piso del Seno Maxilar , Implantación Dental Endoósea , Humanos , Seno Maxilar/diagnóstico por imagen , Seno Maxilar/cirugía , Tomografía Computarizada por Rayos XRESUMEN
Osteoclast differentiation-mediates bone resorption is the key biological basis of orthodontic treatment while the specific mechanism of osteoclastogenesis remains unclear. This study aims to explore the underlying mechanism of the osteoclast differentiation from the perspective of long non-coding RNA (LncRNA). In the present study, the osteoclast differentiation of CD14+ peripheral blood mononuclear cells (PBMCs) was induced by recombinant human macrophage colony-stimulating factor (M-CSF) and receptor activator of nuclear factor κB ligand (RANKL), and LncRNA TUG1 expression was dramatically elevated during this process. Functionally, the silence of TUG1 in CD14+ PBMCs decreased tartrate-resistant acid phosphatase (TRAP)-positive cell numbers and the protein levels of TRAP, nuclear factor of activated T cell c1 (NFATc1), and osteoclast-associated receptor (OSCAR), whereas increased V-maf musculoaponeurotic fibrosarcoma oncogene homolog B (MafB) protein level. The subsequent experiments confirmed that TUG1 lessened the MafB protein level via accelerating its degradation. Then, the interference of MafB reversed the inhibitory effect of si-TUG1 on osteoclastogenesis, including increased the TRAP-positive cell numbers and up-regulated the protein levels of osteoclast markers. Finally, the in vivo experiments displayed that the increased TUG1 levels could promote tooth movement and bone resorption via facilitating osteoclast differentiation in the rat model of orthodontic tooth movement. In summary, TUG1 overexpressed during the process of osteoclast differentiation and positively regulated osteoclast differentiation by targeting MafB.
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Diferenciación Celular/genética , Regulación de la Expresión Génica , Factor de Transcripción MafB/genética , Osteoclastos/citología , Osteoclastos/metabolismo , Interferencia de ARN , ARN Largo no Codificante/genética , Humanos , Leucocitos Mononucleares/citología , Leucocitos Mononucleares/metabolismo , Factor Estimulante de Colonias de Macrófagos/metabolismo , Factor Estimulante de Colonias de Macrófagos/farmacología , Osteoclastos/efectos de los fármacos , Ligando RANK/metabolismo , Ligando RANK/farmacologíaRESUMEN
BACKGROUND: Both radiotherapy and surgery are now recommended for early stage glottic laryngeal squamous cell carcinoma (LSCC), and both have their own advantages in patients with different characteristics. For each patient, it is hard to determine whether radiotherapy or surgery is more appropriate. METHODS: Patients with T1-2N0M0 glottic LSCC who received radiotherapy or surgery in the 2004-2016 SEER database were reviewed, then randomly divided into training and validation cohorts. Propensity score matching was used to eliminate the baseline variations, and competing risk analyses helped to exclude the effects of other causes of death. Based on univariate and multivariate analyses, we built two nomograms to visually predict the survival of each patient with different characteristics who received radiotherapy or surgery, then validated the accuracy in both training and validation cohorts. Using nomogramEx, we quantified the algorithms of the nomograms and put the nomograms on the websites. RESULTS: A total of 6538 patients in the SEER database were included. We found that therapy (p = 0.004), T stage (p < 0.001), age (p < 0.001), race (p < 0.044), grade (p = 0.001), and marital status (p < 0.001) were independent prognostic factors. Two nomograms were built to calculate the survival for each patient who received radiotherapy (C-index = 0.668 ± 0.050 in the training cohort and 0.578 ± 0.028 in the validation cohort) or underwent surgery (C-index = 0.772 ± 0.045 in the training cohort and 0.658 ± 0.090 in the validation cohort). Calibration plots showed the accuracy of the nomograms. Using the nomograms, we found that 3872 patients (59.22%) had no difference between the two therapies, 706 patients (10.80%) who received radiotherapy had better survival outcomes, and 1960 patients (29.98%) who underwent surgery had better survival outcome. CONCLUSION: Nomograms were used to comprehensively calculate independent factors to determine which treatment (radiotherapy or surgery) is better for each patient. A website was used to offer guidance regarding surgery or radiation for patients and physicians.