ObjectiveTo summarize the role of circular RNA (circRNAs) in thyroid papillary carcinoma (PTC) and the emphasis of future research.MethodRelevant literatures in recent years about the biological function of circRNA and its role in PTC were reviewed.ResultscircRNAs had abnormal expression in PTC tissues. Besides, by working as miRNA sponges or interacting with RNA-binding proteins, circRNAs regulated the expression of proteins that were associated with cell proliferation, apoptosis, invasion, and metastasis, which could affect the biological characteristics of tumor cells.ConclusioncircRNAs are expected to be the biomarkers for early diagnosis of PTC or potential targets for PTC therapy and provid therapeutic bases to prevent PTC.
ObjectiveTo evaluate the monitoring value of brain injury biomarkers in the patients during extracorporeal membrane oxygenation (ECMO). MethodsWe searched PubMed, EMbase, the Cochrane Library, CNKI, and CBM from inception of each database to May 2015 to identify randomized controlled trials, or case-control trials, or cohort trials of brain injury biomarkers predict brain injury during ECMO. Data were extracted independently by two reviewers. Meta-analysis was conducted using STATA 12.0 software. ResultsFour retrospective trials were included. The results showed that compared with patients without brain injury, the patients with brain injury had a higher level of S100B protein (P < 0.05). The incidence of major neurological events was higher for high neuron-specific enolase level patients than mild-to-moderate neuron-specific enolase level patients (85% vs. 29%, P=0.01). The incidence of brain injury was higher for normal glial fibrillary acidic protein level than patients with glial fibrillary acidic protein > 0.436 ng/ml (OR=11.5, 95%CI 1.3-98.3). ConclusionsBrain injury biomarkers may be used as an indicator for earlier diagnosis of brain injury in patients during ECMO.
ObjectiveTo explore the clinical value of immunotherapeutic drugs represented by programmed cell death-1 (PD-1) / programmed cell death ligand-1 (PD-L1) blockades for treatment of advanced gastric cancer. MethodThe latest literatures about the clinical studies of PD-1/PD-L1 blockades for the treatment of advanced gastric cancer were retrieved and reviewed. ResultsThe corresponding clinical trials relevant to PD-1/PD-L1 blockades had been conducted in the treatment, biomarkers, and resistance to drugs for advanced gastric cancer. The PD-1/PD-L1 blockades single drug or its in combination with chemical drugs or (and) targeted drugs for the treatment of advanced gastric cancer or gastroesophageal junction cancer had shown a good efficacy in some patients. The patients who benefited from PD-1/PD-L1 blockades might be a population with specific molecular characteristics, but the resistance to drugs during the therapy process affected its therapeutic effect. ConclusionFrom the progress of this review, PD-1/PD-L1 blockades bring benefits to some patients with advanced gastric cancer, but more biomarkers which can predict the therapeutic effect need to be found to optimize the drug regimen, and the resistance to drugs mechanism needs to be further studied.
Although great progress has been achieved in the techniques and materials of cardiopulmonary bypass (CPB), cardiac surgery under CPB is still one of the surgeries with the highest complication rate. The systemic inflammatory response is an important cause of complications, mainly characterized by activation of innate immune cells and platelets, and up-regulation of inflammatory cytokines. After activation, a variety of molecules on the membrane surface are up-regulated or down-regulated, which can amplify tissue inflammatory damage by releasing cytoplasmic protease and reactive oxygen species, and activate multiple inflammatory signaling pathways in the cell, ultimately leading to organ dysfunction. Therefore, the expression of these cell membrane activation markers is not only a marker of cell activation, but also plays an important role in the process of vital organ injury after surgery. Identification of these specific activation markers is of great significance to elucidate the mechanisms related to organ injury and to find new prevention and treatment methods. This article will review the relationship between these activated biomarkers in the innate immune cells and vital organ injuries under CPB.
Objective To explore the change of serum levels of neutrophil gelatinase-associated lipocalin (NGAL), tissue inhibitor of metalloproteinases-2 (TIMP-2), and insulin-like growth factor-binding protein 7 (IGFBP-7) in the early stage of multiple trauma, and their predictive efficacy for acute kidney injury (AKI). Methods The multiple trauma patients admitted between February 2020 and July 2021 were prospectively selected, and they were divided into AKI group and non-AKI group according to whether they developed AKI within 72 h after injury. The serum levels of NGAL, TIMP-2, and IGFBP-7 measured at admission and 12, 24, and 48 h after injury, the Acute Pathophysiology and Chronic Health Evaluation Ⅱ(APACHE Ⅱ) score, intensive care unit duration, rate of renal replacement therapy, and 28-day mortality rate were compared between the two groups. Results A total of 51 patients were included, including 20 in the AKI group and 31 in the non-AKI group. The APACHE Ⅱ at admission (20.60±3.57 vs. 11.61±3.44), intensive care unit duration [(16.75±2.71) vs. (11.13±3.41) d], rate of renal replacement therapy (35.0% vs. 0.0%), and 28-day mortality rate (25.0% vs. 3.2%) in the AKI group were higher than those in the non-AKI group (P<0.05). The serum levels of NGAL and IGFBP-7 at admission and 12, 24, and 48 h after injury in the AKI group were all higher than those in the non-AKI group (P<0.05). For the prediction of AKI, the areas under receiver operating characteristic curves and 95% confidence intervals of serum NGAL, TIMP-2 and IGFBP-7 12 h after injury were 0.98 (0.96, 1.00), 0.92 (0.83, 1.00), and 0.87 (0.78, 0.97), respectively. Conclusion Serum NGAL, TIMP-2, and IGFBP-7 have high predictive efficacy for AKI secondary to multiple trauma, and continuous monitoring of serum NGAL can be used for early prediction of AKI secondary to multiple trauma.
ObjectiveTo summarize the research progress of long non-coding RNA (lncRNA) in the regulation of malignant biological behavior of gallbladder cancer so as to provide references for its related research.MethodThe relevant literatures about studies of lncRNA in gallbladder cancer in recent years were reviewed.ResultsThe recent studies had shown that 19 lncRNAs associated with gallbladder cancer had played the important roles in regulating tumor cell proliferation, migration, invasion, apoptosis, “sponge” miRNAs, chemoresistance, and tumor metastasis. Among them, most lncRNAs tended to have carcinogenic properties, only a few had anticarcinogenic effect. Although the research suggested the mechanism and role of lncRNA to promote or inhibit the occurrence and development of gallbladder cancer, the current research on its mechanism was still limited. In addition, some lncRNAs were found to be specifically expressed in the serum of patients with gallbladder cancer, so which were expected to become biomarkers for tumor diagnosis and prognosis.ConclusionslncRNAs associated with gallbladder cancer have carcinogenic or anticarcinogenic effect, or chemoresistance. They play potential roles in diagnosis, prognosis, and (or) treatment of tumors, but molecular mechanisms of their effects are still limited.
Tripartite motif 5 (TRIM5) plays a significant function in autophagy and involves in immune and tumor processes. While the function of TRIM5 remains poorly understood in glioma. We purpose to evaluate the possible prognostic role of TRIM5 in glioma via bioinformatics analyses. The database clinical samples of glioma in this study included low grade glioma (LGG) and glioblastoma multiforme (GBM). TRIM5 expression in glioma tissues were explored in Oncomine, GEPIA and The Cancer Genome Atlas (TCGA) databases. Survival analysis and the multivariate Cox regression analysis of TRIM5 based on TCGA were used to evaluate the prognostic role of TRIM5. The protein networks of TRIM5 was detected by STRING database. KEGG enrichment analyses were performed to predict the potential molecular pathways of TRIM5 in glioma. In addition, immune infiltration analysis was conducted by CIBERSORT and TIMER databases. We found that TRIM5 was strongly increased in glioma samples compared with normal samples in Oncomine, GEPIA and TCGA databases. Higher TRIM5 was significantly contributed to worse overall survival (OS) in LGG+GBM patients and LGG patients, while was no correlated with OS of GBM patients. Interaction networks analysis identified that IRF3, IRF7, OAS1, OAS2, OAS3, OASL, GBP1, PML, BTBD1 and BTBD2 proteins were contacted with TRIM5. Moreover, KEGG revealed that apoptosis and cancer- and immune-related pathways were enriched with elevated TRIM5. Specifically, TRIM5 could influence the immune infiltration levels, such as activated NK cells, monocytes, activated mast cells and macrophages in glioma. In conclusion, our data indicated that TRIM5 was upregulated in glioma tissues and associated with poor prognosis and immune infiltration. TRIM5 may be acted as a biomarker in prognosis and immunotherapy guidance of glioma.
ObjectiveTo explore the prognostic value of serum cystatin C (Cys C) in patients with congenital heart disease-associated pulmonary arterial hypertension (PAH-CHD).MethodsA retrospective cohort study was conducted on adult PAH-CHD patients who were hospitalized for the first time in the First Affiliated Hospital of Xinjiang Medical University from January 2010 to January 2020. The serum Cys C and other related data of patients were collected. The median follow-up time was 57 months. The main end event was all-cause death. According to the prognosis, the patients were divided into a survival group and a death group. Cox regression was used to analyze the risk factors for all-cause death in patients with PAH-CHD.ResultsA total of 456 patients were enrolled, including 160 males and 296 females, aged 38.99±14.72 years. The baseline data showed that there were statistical differences in resting heart rate, serum Cys C, creatinine, NT-proB-type natriuretic peptide (NT-proBNP), high-sensitivity cardiac troponin T (hs-cTnT), high-sensitivity C reactive protein (hs-CRP), New York Heart Association (NYHA) cardiac function classification and serum potassium between the survival group and the death group. Univariate Cox regression analysis showed that serum Cys C, NT-proBNP, hs-cTnT, creatinine and NYHA cardiac function classification were related risk factors for all-cause death in patients with PAH-CHD. Multivariate Cox regression analysis showed that serum Cys C (HR=3.820, 95%CI 2.053-7.108, P<0.001), NYHA grade Ⅲ (HR=2.234, 95%CI 1.316-3.521, P=0.010), NYHA grade Ⅳ (HR=4.037, 95%CI 1.899-7.810, P=0.002) and NT-proBNP (HR=1.026, 95%CI 1.013-1.039, P<0.001) were independent risk factors for all-cause death in patients with PAH-CHD and had a good predictive value.ConclusionAs a new cardiac marker, serum Cys C can predict all-cause death in patients with PAH-CHD and is an independent risk factor.
ObjectiveTo understand the clinical value of centromere proteins (CENPs) in hepatocellular carcinoma and their influence on the malignant biological behavior of hepatocellular carcinoma, and to provide theoretical references for related research in this field. MethodDomestic and international databases were searched for relevant literatures on the study of CENPs in hepatocellular carcinoma in recent years to be analyzed and reviewed. ResultsA total of 11 CENPs closely related to hepatocellular carcinoma had been summarized, which were differentially expressed in hepatocellular carcinoma and correlated with prognosis. CENPs might regulate various malignant biological behaviors such as hepatocellular carcinoma proliferation, metastasis, apoptosis, and resistance to radiotherapy and thus participate in the development of hepatocellular carcinoma via multiple mechanisms. The roles and mechanisms of some CENPs in hepatocellular carcinoma remained unclear. ConclusionsCENPs play an essential role in the diagnosis, treatment, and prognosis of hepatocellular carcinoma. They are involved in multiple malignant biological behaviors of hepatocellular carcinoma and are expected to be potential therapeutic targets for hepatocellular carcinoma. However, their roles and mechanisms in hepatocellular carcinoma remain to be investigated.
ObjectiveTo explore the metabolic changes during the differentiation of 3T3-L1 adipocytes caused by the treatment of the transient receptor potential vanilloid 4 (TRPV4)-specific agonist GSK1016790A basing on ultra-performance liquid chromatography-mass spectrometry technology. MethodsMouse 3T3-L1 cells were treated with GSK1016790A at different concentrations (0.1, 1, and 10 μmol/L), and the effect of drugs on cell proliferation was detected by cell counting kit-8 method. A mature adipocyte model was constructed, and GSK1016790A was used to activate TRPV4 channel protein activity and verify the expression levels of TRPV4 and triglycerides. Cell metabolites were collected for metabolomic studies, differential metabolites were screened between groups, and related metabolic pathways were analyzed. Results After GSK1016790A intervened in mature adipocytes, the expression levels of TRPV4 mRNA and triglycerides in cells were significantly upregulated (P<0.05). Metabolomics detection found that GSK1016790A screened a total of 45 differential metabolites such as 2-amino-1,3,4-octadecanetriol, linoleic acid, sphingosine, sphinganine, sn-glycerol-3-phosphate and uridine, mainly involving 13 possible metabolic pathways such as sphingolipid metabolism and biosynthesis of unsaturated fatty acids. Conclusion GSK1016790A may promote adipogenesis in adipocytes by activating TRPV4 channel protein activity, and at the same time participate in regulating metabolic pathways such as the biosynthesis of unsaturated fatty acids pathway and sphingolipid metabolism pathway, affecting lipid metabolism in adipocytes.