Anesthesia decision analysis using a cloud-based big data platform.

Big data technologies have proliferated since the dawn of the cloud-computing era. Traditional data storage, extraction, transformation, and analysis technologies have thus become unsuitable for the large volume, diversity, high processing speed, and low value density of big data in medical strategies, which require the development of novel big data application technologies. In this regard, we investigated the most recent big data platform breakthroughs in anesthesiology and designed an anesthesia decision model based on a cloud system for storing and analyzing massive amounts of data from anesthetic records. The presented Anesthesia Decision Analysis Platform performs distributed computing on medical records via several programming tools, and provides services such as keyword search, data filtering, and basic statistics to reduce inaccurate and subjective judgments by decision-makers. Importantly, it can potentially to improve anesthetic strategy and create individualized anesthesia decisions, lowering the likelihood of perioperative complications.

Anesthesia for mandibular yolk sac tumor in children after radiotherapy and chemotherapy: A case report.

Yolk sac tumor (YST), also known as endodermal sinus tumor, is a malignant germ cell tumor that usually affects children aged >3 years. It is commonly observed in the gonadal sites (testis or ovary) but is extremely rare in the mandibular regions. This study describes the anesthesia process for spontaneous ventilation bronchoscope intubation in the rare case of a 7-year-old child with extragonadal primary YST of the face, refractory to radiotherapy, and chemotherapy.

Noninvasive Detection of Arytenoid Cartilage Calcification Using Computed Tomography and Prediction of Prognosis in Laryngeal Contact Granuloma.

OBJECTIVE: Laryngeal contact granuloma (LCG) is a relatively uncommon disease with chronic inflammatory stimulation, and long-term reflux irritation is a vital factor for arytenoid cartilage calcification. Our investigation compared the severity of ipsilateral arytenoid cartilage calcification with the frequency of recurrence of LCG after surgical treatment. METHODS: A retrospective chart review of prospectively gathered data over five years from 327 patients, including 153 subjects without laryngeal lesions, were age- and sex-matched normal controls, 103 patients with various other vocal cord lesions were in the laryngeal lesion group and 71 LCG patients met the diagnostic criteria pathologically. All subjects underwent laryngeal high-resolution computed tomography (HRCT) prior to therapeutic interventions. The computed tomography (CT) value and arytenoid cartilage calcification were obtained using image data before surgery, and their clinical significance was further analyzed. RESULTS: Seventy-one patients with LCG, including sixty-two males, were enrolled in the study. Among these cases, there were 67 patients with unilateral vocal cord lesions. Of the 103 eligible patients in the laryngeal lesion group, 87 had unilateral lesions, which including eighty-seven men. Of the 153 average subjects, 105 were male. The rate of arytenoid cartilage calcification in the LCG group was dramatically higher in the lesion side than in the laryngeal lesions and normal group (P < 0.01). Furthermore, the CT value (P < 0.01) and range of calcification (P < 0.01) were significantly higher in patients with LCG than in those with laryngeal lesions. Importantly, patients with high CT values and the calcification range of lesions in the arytenoid cartilage displayed a greater lesion size and recurrence rate than patients with low CT values and lesion areas (P < 0.01). CONCLUSION: Our results suggest that most patients with LCG present with calcification of the arytenoid cartilage. The more severe the calcification in the arytenoid cartilage, the greater the risk of granuloma size and recurrence in LCG after surgical treatment. CT and bone density testing of the arytenoid cartilage may be an essential method to evaluate the prognosis of LCG.

miR-328-3p promotes migration and invasion by targeting H2AFX in head and neck squamous cell carcinoma.

Migration and invasion are the initial step in the metastatic process, while metastasis is responsible for the poor prognosis of head and neck squamous cell carcinoma (HNSCC). Since miRNA has been found as an important regulator of gene expression at the post-transcriptional level in various diseases including carcinoma, exploring the role of miRNA in cancer metastasis will facilitate the target therapy of advanced HNSCC. MiR-328-3p has been reported to be an onco-miRNA or a tumor suppressor in several cancers. However, the role of miR-328-3p in HNSCC migration and invasion remains undefined. In this study, we first demonstrated that miR-328-3p enhanced migration and invasion of HNSCC in vitro, accompanying with a promotion of epithelial-mesenchymal transition (EMT) and mTOR activity. Meanwhile, we confirmed that miR-328-3p directly targeted the 3'UTR of H2A histone family, member X (H2AFX), which served as a tumor suppressor in migration and invasion of HNSCC. Moreover, H2AFX could partially reverse the migration and invasion of HNSCC caused by miR-328-3p. Overall, our results indicated that miR-328-3p enhanced migration and invasion of HNSCC through targeting H2AFX and activated the mTOR pathway.

Elevated expression of MKRN3 in squamous cell carcinoma of the head and neck and its clinical significance.

BACKGROUND: Squamous cell carcinoma of the head and neck (SCCHN) is one of the most common types of cancer that cause a substantial number of cancer-related deaths. Our previous study has revealed that makorin ring finger protein 3 (MKRN3) may act as a key regulator of the SCCHN tumorigenesis; however, its specific role in SCCHN progression has not been reported. METHODS: The Cancer Genome Atlas (TCGA) data analysis and quantitative polymerase chain reaction (qPCR) were used to quantify the MKRN3 mRNA expression levels in SCCHN; immunohistochemical staining or immunoblotting analyses were performed to detect MKRN3 protein expression. Kaplan-Meier plotter was used to assess the prognostic values of MKRN3 in terms of overall survival and disease-free survival. The expression differences based on various clinicopathological features were evaluated using subgroup analysis and forest map analysis. The regulatory mechanism of MKRN3 was further investigated using gene ontology and Kyoto Encyclopedia of Genes and Genomes analyses. Subsequently, STRING was used to perform a co-expression and enrichment analysis for MKRN3. Homologous modeling, molecular docking, and western blot analyses were performed to investigate the relationship between MKRN3 and its potential target gene P53. RESULTS: MKRN3 was ectopically expressed between cancerous and noncancerous SCCHN tissues, and its expression level was tightly associated with high T classifications as well as advanced clinical stages. qPCR analysis revealed that MKRN3 was upregulated in the SCCHN cell line. Moreover, Kaplan-Meier and Cox regression analyses indicated that SCCHN patients with high MKRN3 expression had poorer prognosis and that MKRN3 was a potential prognostic marker for SCCHN. Using gene ontology and Kyoto Encyclopedia of Genes and Genomes analyses, we determined that MKRN3 may be involved in the regulation of synthesis and metabolism and cell growth, death and motility, as well as cancer pathways associated with SCCHN progression. Mechanism investigation further revealed that P53, a potential target of MKRN3, may be involved in the SCCHN tumorigenesis mediated by MKRN3. CONCLUSIONS: We performed a comprehensive evaluation of the clinical significance of MKRN3 and explored its underlying mechanisms. We concluded that MKRN3 represents a valuable predictive biomarker and potential therapeutic target in SCCHN.

miR-3187-3p enhances migration and invasion by targeting PER2 in head and neck squamous cell carcinomas.

Invasion and metastasis are major contributors to treatment failure in patients with head and neck squamous cell carcinomas (HNSCCs) and microRNAs (miRNAs) are reported to play important roles in tumor progression. Our study therefore try to find the crucial miRNAs and reveal their molecular and functional mechanisms involved in migration and invasion of HNSCCs. Through The Cancer Genome Atlas (TCGA) data analysis, we screened out miR-3187-3p and its biological function and specific mechanism were further analyzed. The wound-healing and transwell invasion assay demonstrated that miR-3187-3p promoted the capacity of migration and invasion of HNSCCs in vitro. Luciferase reporter assays showed that PER2 was a direct target of miR-3187-3p, which could reverse the effect of miR-3187-3p in HNSCCs. Furthermore, we found that miR-3187-3p / PER2 axis activated the Wnt / ß-catenin signaling pathway in HNSCCs. Altogether, our study indicated that miR-3187-3p enhanced migration and invasion by targeting PER2 in HNSCCs.

UBE2O Promotes Progression and Epithelial-Mesenchymal Transition in Head and Neck Squamous Cell Carcinoma.

BACKGROUND: UBE2O, as a member of the ubiquitin-conjugating enzyme family, is abnormally expressed and exhibits abnormal functions in human malignancies. However, the function of UBE2O in head and neck squamous cell carcinoma (HNSCC) remains unknown. Therefore, our study aims to investigate the role of UBE2O in HNSCC progression and the underlying mechanisms. METHODS: The expression of UBE2O in HNSCC patients was investigated with data from the Cancer Genome Atlas (TCGA) and from a separate primary tumor cohort. The function of UBE2O in HNSCC cells was studied by cell viability assay, colony formation assay, wound healing assay, and cell migration and invasion chamber assay. The effect of UBE2O on tumor growth in vivo was determined in a subcutaneous xenograft model of HNSCC. RESULTS: TCGA data showed that UBE2O mRNA expression was dramatically increased in HNSCC tissues and that patients with high expression of UBE2O transcripts had a worse survival prognosis than patients with low expression of UBE2O transcripts. Gain-of-function and loss-of-function analyses revealed that oncogenic UBE2O enhanced the proliferation, migration and invasion of HNSCC cells in vitro. Further, mechanistic analysis revealed that UBE2O induced the epithelial-mesenchymal transition (EMT) phenotype and also potentiated TGF-ß1-induced EMT, and thus leading to an enhanced capacity of migration and invasion in HNSCC. Finally, xenograft models showed that UBE2O knockout obviously inhibited the occurrence of EMT, angiogenesis and tumor growth in HNSCC in vivo. CONCLUSION: Our study indicates that UBE2O acts as an oncogene to promote the malignant progression and EMT of HNSCC.

miR-93-5p enhances migration and invasion by targeting RGMB in squamous cell carcinoma of the head and neck.

Invasion and metastasis represent the primary causes of therapeutic failure in patients diagnosed with squamous cell carcinoma of the head and neck (SCCHN). Therefore, disease prediction and inhibition of invasion and metastasis are critical for enhancing the survival of patients with SCCHN. Our previous study revealed that increased expression of miR-93-5p is associated with poor prognosis in SCCHN; however, the mechanism underlying the oncogenic functions of miR-93-5p in SCCHN migration and invasion remains unclear. Using qPCR analyses, transwell assays, and scratch tests, we demonstrated that expression of ectopic miR-93-5p induced the migration and invasion of SCCHN, and this was accompanied by corresponding alterations in biomarkers and transcription factors specific for epithelial-mesenchymal transition (EMT). Luciferase reporter assays were used to demonstrate that miR-93-5p directly targeted the 3' UTR of RGMB, and we further found that the tumor-promoting functions of miR-93-5p were partly mediated by targeting RGMB, whose downregulation also promoted the migration and invasion of SCCHN. Overall, our results indicate that miR-93-5p acts as an oncogene in the regulation of migration and invasion by suppressing RGMB in SCCHN. These findings provide novel evidence that miR-93-5p may serve as a valuable predictive biomarker and potential intervention target in patients with SCCHN.

miR-30e-5p represses angiogenesis and metastasis by directly targeting AEG-1 in squamous cell carcinoma of the head and neck.

Metastasis is a critical determinant for the treatment strategy and prognosis in patients with squamous cell carcinoma of the head and neck (SCCHN). However, the mechanisms underlying SCCHN metastasis are poorly understood. Our study sought to determine the key microRNA and their functional mechanisms involved in SCCHN metastasis. For The Cancer Genome Atlas (TCGA) data analysis, quantitative PCR was used to quantify the level of miR-30e-5p in SCCHN and its clinical significance was further analyzed. A series of in vitro and in vivo experiments were applied to determine the effects of miR-30e-5p and its target AEG-1 on SCCHN metastasis. A mechanism investigation further revealed that AEG-1 was implicated in the angiogenesis and metastasis mediated by miR-30e-5p. Overall, our study confirms that miR-30e-5p is a valuable predictive biomarker and potential therapeutic target in SCCHN metastasis.

Wnt3a promotes radioresistance via autophagy in squamous cell carcinoma of the head and neck.

The canonical Wnt/ß-catenin signalling pathway and autophagy play critical roles in cancer progression. However, the role of Wnt-mediated autophagy in cancer radioresistance remains unclear. In this study, we found that irradiation activated the Wnt/ß-catenin and autophagic signalling pathways in squamous cell carcinoma of the head and neck (SCCHN). Wnt3a is a classical ligand that activated the Wnt/ß-catenin signalling pathway, induced autophagy and decreased the sensitivity of SCCHN to irradiation both in vitro and in vivo. Further mechanistic analysis revealed that Wnt3a promoted SCCHN radioresistance via protective autophagy. Finally, expression of the Wnt3a protein was elevated in both SCCHN tissues and patients' serum. Patients showing high expression of Wnt3a displayed a worse prognosis. Taken together, our study indicates that both the canonical Wnt and autophagic signalling pathways are valuable targets for sensitizing SCCHN to irradiation.

Autophagy inhibition impairs the epithelial-mesenchymal transition and enhances cisplatin sensitivity in nasopharyngeal carcinoma.

Drug resistance restricts the efficacy of cisplatin in the treatment of nasopharyngeal carcinoma (NPC). Increasing evidence indicates that autophagy and the epithelial-mesenchymal transition (EMT) participate in cancer progression and drug sensitivity. The aim of the present study was to investigate the function of autophagy and EMT in cisplatin treatment, and to reveal the underlying impact of autophagy on the EMT process in NPC. Transmission electron microscopy assays and western blot analyses confirmed that cisplatin activates autophagy in NPC cells. Alterations in cell morphology and biomolecular markers confirmed that cisplatin induces the EMT phenotype in NPC cells. Cell viability assays showed that the combination of the autophagy inhibitor chloroquine (CQ) increased the cytotoxicity of cisplatin in NPC cells and that the EMT inducer transforming growth factor ß1 promoted the resistance to cisplatin in NPC cells. Moreover, autophagy inhibition by CQ and microtubule-associated protein 1 light chain 3B-knockdown reversed the EMT phenotype in NPC cells. In conclusion, autophagy and the EMT process promote cisplatin resistance in NPC cells, while the inhibition of autophagy impairs the EMT process.

miR-324-3p suppresses migration and invasion by targeting WNT2B in nasopharyngeal carcinoma.

BACKGROUND: Nasopharyngeal carcinoma (NPC) is a malignant epithelial carcinoma of the head and neck with strong ability of invasion and metastasis. Our previous study indicated that miR-324-3p, as a tumor-suppressive factor, could regulate radioresistance of NPC cells by targeting WNT2B. The purpose of this study is to investigate the role of miR-324-3p on migration and invasion in NPC cells. METHODS: Quantitative real time PCR was applied to measure the expression level of miR-324-3p and WNT2B mRNA in both cells and tissues, and the expression level of WNT2B protein was determined by western blotting. The capacity of migration and invasion were tested by using wound healing and transwell invasion assay. RESULTS: Ectopic expression of miR-324-3p or silencing its target gene WNT2B could dramatically suppress migration and invasion capacity of NPC cells. Meanwhile, the alterations of miR-324-3p in NPC cells could influence the expression level of the biomarkers of epithelial-mesenchymal transition (EMT), including E-cadherin and Vimentin. Moreover, the expression of miR-324-3p was obviously downregulated and WNT2B was significantly upregulated in NPC tissues. The expression levels of miR-324-3p and WNT2B were closely correlated with T stage, clinic stage and cervical lymph node metastasis of NPC (P < 0.05). CONCLUSION: miR-324-3p could suppress the migration and invasion of NPC by targeting WNT2B and the miR-324-3p/WNT2B pathway possibly provide new potential therapeutic clues for NPC.