Objective:To investigate the expression and role of DEAD-box RNA helicases 5(DDX5 helicases)in head and neck squamous carcinoma(HNSCC).Methods:Tissue microarray microarray was used to assess relevant mRNA expression profile data,and R software was used to screen differential mRNAs(DEGs).The expression level of DDX5 was predicted using GEPIA 2,TCGA databases,and detected by immunohistochemistry,western blot and RT-qPCR in the HNSCC tissue and cell lines.Based on high-throughput sequencing data of DECs,differentially expressed miRNAs(DEMIs)relevant DDX5 competitive endogenous RNA network(ceRNA)was constructed.The software cytoscape was used to visualize the ceRNA network map and further screen the regulatory ax-is.Results:The results of microarray screening revealed that DDX5 expression in HNSCC was upregulated.Immunohistochemistry ver-ified that DDX5 was stronger expressed in the nuclei of squamous carcinoma cells.qPCR results suggested that significant expression of DDX5 mRNA at the tissue and cellular levels(P＜0.05).Western blot results showed high expression of DDX5 protein in the tissues.The ceRNA network was constructed,from which the relevant HNSCC axis circRNA-039626-miR-222-5p-DDX5 was identified.Con-clusion:DDX5 is highly expressed in HNSCC,and the circRNA-039626-miR-222-5p-DDX5 axis may be a potential regulatory axis for the development of HNSCC.

Objective To study whether emodin,a natural product,can affect the level of histone acetylation in HpG2 hepatocellular carcinoma cells(HCC),and then accelerate the occurrence of pyroptosis and apoptosis in hepatocellular carcinoma cells,so as to provide a new target for the treatment of liver cancer.Methods CCK-8 method was used to detect the effect of different concentrations of emodin on the viability of HpG2 cells.Bioinformatics was used to analyze histone acetylation-related genes in patients with liver cancer in TCGA database.The correlation between the candidate gene lysine acetyltransferase 2A(KAT2A)and the apoptosis pathway was verified.qPCR method was used to detect the mRNA level of KAT2A in HepG2 cells and L02 cells.The effects of emodin on histone acetyltransferase(HAT)and histone deacetyltransferase(HDAC),interleukin 1β(IL-1β)and interleukin 18(IL-18)in HpG2 cells were detected by ELISA.The effect of emodin on the apoptosis of liver cancer cells was detected by flow cytometry.The expression level of cell apoptosis,pyroptosis-associated protein B lymphocytoma-2(Bcl-2),Bcl-2-related X protein(Bax),NOD-like receptor thermal protein domain-related protein 3(NLRP3),Caspase-1,Gasdermin family member DN terminal(GSDMD-N)and KAT2A were detected by Western blot assay.Results Emodin could reduce the activity of HpG2 cells,and the confidence interval of IC5095%was 58.12-66.52μmol/L.Compared with normal liver tissue,the expression of histone acetylation related gene mRNA was increased in HCC tissue,and the change of KAT2A was the highest[log2(Fold Change)=2.010,P＜0.01].In HCC tissue,the expression of KAT2A mRNA was negatively correlated with apoptosis pathway(rs=-0.230,P＜0.01).Compared with L02 cells,the expression of KAT2A mRNA in HepG2 was higher(P＜0.05).Compared with the control group,expression levels of HAT and HDAC decreased in the 60μmol/L emodin intervention group,expression levels of IL-18 and IL-1β increased,the apoptosis rate increased,expression levels of KAT2A and BAX decreased,and expression levels of Bcl-2,NLRP3,GSDMD-N and Caspase-1 increased(P＜0.05).Conclusion Emodin could inhibit the viability of hepatoma cells,accelerate apoptosis and pyroptosis,and its mechanism may be related to the regulation of KAT2A expression.

DDX5 helicase (DEAD box helicases 5), also known as P68, is an important member of an ATP dependent RNA helicase.Studies have shown that DDX5 is abnormally expressed in a variety of cancers, targeting a variety of tumor related signal pathways, regulating upstream and downstream factors to affect the occurrence, invasion and migration of tumor cells. This article describes the biological role of DDX5 in malignant tumors and provides prospects for targeted treatment of tumors.

Optical coherence tomography (OCT) is a new technique applied in cardiovascular system. It can detect vessel intimal, small structure of plaque surface and discover small lesions with its high axial resolution and quantification character. Especially with the application of OCT in characterization of coronary atherosclerotic plaque, diagnosis and treatment strategy making, optimizing percutaneous coronary intervention therapy and assessment after stent planting make the OCT become an efficient tool for cardiovascular disease diagnosis and treatment. This paper presents a novel coronary vessel intimal sequence extraction method based on prior boundary constraints in OCT image. On the basis of conventional Chan-Vese model, we modified the evolutionary weight function to control the evolutionary rate of boundary by adding local information of boundary curve. At the same time, we added the gradient energy term and intimal boundary constraint term based on priori boundary condition to further control the evolutionary of boundary curve. At last, coronary vessel intimal is extracted in a sequence way. The comparison with vessel intimal, manual segmented by clinical scientists (golden standard), indicates that our coronary vessel intimal extraction method is robust to intimal boundary blur, distortion, guide wire shadow and plaque disturbs. The results of this study can be applied to clinical aid diagnosis and precise diagnosis and treatment.

Objective: To explore the potential genetic target of Stephania terandra in the therapy for hypertension based on inte-grated pharmacology platform to study the molecular mechanism of Chinese medicines in treating hypertension. Methods: Using the functional prediction modules of integrated pharmacology platform and the functional modules of network construction, the component-target network of Stephania terandra was calculated, and the target network of anti-hypertension was further calculated, and the target molecules related to hypertension were explored. Results: A total of 198 targets related to hypertension were obtained from the hyper-tension prevention. Among them, there were 59 potential action nodes and 20 known action nodes. The nodes with direct action were type-2 angiotensin Ⅱ receptor ( AGTR2), type-1 angiotensin Ⅱ receptor ( AGTR1), prostacyclin receptor ( PTGIR), solute carrier family 12 member 3 (SLC12A3) and endothelin-1 (EDN1). The GO enrichment and KEGG pathway enrichment of Stephania terandra chemical components showed a close correlation with hypertension, and the molecular mechanism of the target was clear. Conclusion:Through the integration of pharmacology platform, the targets of Stephania terandra-disease are deeply explored, and its potential mo-lecular mechanism as well as potential factors is studied.

PURPOSE: The aim of this study was to investigate the association of telomere length with breast cancer risk. We simultaneously explored the association between telomerase reverse transcriptase gene polymorphisms and telomere length. METHODS: We used real-time quantitative polymerase chain reaction to measure relative telomere length (RTL) in genomic DNA extracted from peripheral blood from 183 breast cancer cases and 191 healthy controls. Genotyping was performed using the Sequenom MassARRAY platform. RESULTS: Our results show that breast cancer patients had significantly shorter RTLs than control subjects (p < 0.05). When the RTLs were categorized into tertiles, we found that the lowest RTL was significantly associated with increased breast cancer risk compared with the highest RTL (odds ratio [OR], 2.33; 95% confidence interval [CI], 1.40–3.90; p=0.001). Subgroup analyses indicated that risk of breast cancer was also significantly increased in the lowest RTL compared with the highest RTL in age >40 years (OR, 2.41; 95% CI, 1.31–4.43; p=0.005), body mass index ≤24 kg/m2 (OR, 2.81; 95% CI, 1.55–5.10; p=0.001), and postmenopausal women (OR, 3.94; 95% CI, 1.63–9.51; p=0.002), respectively. In addition, individuals with the AA genotype of rs2853677 have longer telomeres than those of breast cancer patients with the AG genotype (p=0.011). CONCLUSION: Our results suggest that shorter RTL was associated with an increased risk of breast cancer. An association was found between the AA genotype of rs2853677 and longer RTLs in the case group. Functional studies are warranted to validate this association and further investigate our findings.
Asian Continental Ancestry Group* ; Body Mass Index ; Breast Neoplasms* ; Breast* ; Case-Control Studies* ; DNA ; Female ; Genotype ; Humans ; Polymerase Chain Reaction ; Real-Time Polymerase Chain Reaction ; Telomerase ; Telomere*

Objective This study aimed to investigate whether the copy numbers of the CCL3L1 (Chemokine C-C-Motif Ligand 3 Like Protein 1) gene were associated with susceptibility to ankylosing spondylitis (AS). Methods A total of 806 Chinese individuals including 405 AS patients and 401 healthy controls were enrolled. The CCL3L1 gene copy number was measured by a custom-by-design Multiplex AccuCopyTM Kit based on a multiplex fluorescence competitive polymerase chain reaction (PCR) principle, and 50 samples were randomly selected using the fluorescent quantitative PCR method to verify copy number. Main statistical method was t test, chi-square test and logistic regression model. Results There were no statistically significant differences between the case group and control group in age and gender ( t=1.77, P=0.076, χ2=1.14, P=0.289). The copy number of CCL3L1 gene ranged from 0 to 13 in both AS patients and the controls. After copy numbers were classified into 3 categories by 3, we did not find significant difference between the two groups ( χ2=0.591, P=0.669). And regression analyses also did not support the hypothesis that CCL3L1 gene copy number variation (CNV) could be an impact factor to the severity or function indexes of AS patients ( χ2=0.341, P=0.804 and χ2=0.472, P=0.774, respectively). Conclusion We suggest that the copy number of the CCL3L1 gene does not have a role in the susceptibility and the severity or function to AS.

Objective To study the therapeutic effect of IGF?1R inhibitor TAE226 on malignant pleural effusion ( MPE) in nude mice. Methods Human lung carcinoma A549 cells were injected into the pleural cavity of nude mice to establish MPE model. The mice were randomly divided into model group and treatment group, and were orally administered with distilled water and TAE226 ( 20 mg/kg ) in the same volume, respectively. The volume of pleural effusion and tumor weight of the two groups were observed. HE staining was used to reveal the histological changes and enzyme?linked immunosorbent assay ( ELISA) was used to detect the IGF?1R protein expression. IGF?1R mRNA level in the tumor tissue was determined by RT?PCR. Microvessel density (MVD) and cell proliferation index (PI) were assessed by immunohistochemical analysis. The protein expression levels of IGF?1R, p?IGF?1R, PI3K and p?PI3K in the tumor tissue were determined by Western blotting. Results The volumes of pleural effusion were ( 241. 4 ± 89. 7 ) μl and (121.7±78.8) μl in the model and treatment groups, respectively (P<0.05). The tumor weight of treatment group was (316.7±186.3) mg, significantly lower than that of the model group (671.4±281.4) mg (P<0.05) . RT?PCR analysis showed that IGF?1R mRNA level was 0. 914 ± 0. 029 in the treatment group, significantly lower than that of the model group (1.152±0.037, P<0.01). The ELISA data revealed that IGF?1R protein expression level of the model group was significantly higher than that of the treatment group [(41.0±4.7) μg/L vs. (24.0±3.1) μg/L, P<0.01]. Immunohistochemical analysis showed that there were significant differences between MVD and PI in the model and treatment groups [ MVD, 34. 75 ± 3. 49 vs. 22.25±3.63;PI, (75.25±7.15)% vs. (45.75±5.12)%;P<0.01 for both). Western blot data showed that IGF?1R and PI3K protein expression levels were not significantly different between the model and treatment groups (1.03±0.33 vs. 0.98±0.37 and 1.05±0.28 vs. 0.98±0.19), respectively (P>0.05), but p?IGF?1R and p?PI3K protein expression levels had significant differences between the two groups (1.08±0.10 vs. 0.51± 0.08 and 1.12±0.09 vs. 0.86±0.09), respectively (P<0.01 for both). Conclusions The IGF?1R inhibitor can effectively inhibit the formation of malignant pleural effusion. Its mechanism may be related to the suppression of tumor cell proliferation, invasion and angiogenesis through inhibition of PI3K signaling. TAE226 treatment may be a potential therapeutic regimen of treating malignant pleural effusion.

Objective To study the therapeutic effect of IGF?1R inhibitor TAE226 on malignant pleural effusion ( MPE) in nude mice. Methods Human lung carcinoma A549 cells were injected into the pleural cavity of nude mice to establish MPE model. The mice were randomly divided into model group and treatment group, and were orally administered with distilled water and TAE226 ( 20 mg/kg ) in the same volume, respectively. The volume of pleural effusion and tumor weight of the two groups were observed. HE staining was used to reveal the histological changes and enzyme?linked immunosorbent assay ( ELISA) was used to detect the IGF?1R protein expression. IGF?1R mRNA level in the tumor tissue was determined by RT?PCR. Microvessel density (MVD) and cell proliferation index (PI) were assessed by immunohistochemical analysis. The protein expression levels of IGF?1R, p?IGF?1R, PI3K and p?PI3K in the tumor tissue were determined by Western blotting. Results The volumes of pleural effusion were ( 241. 4 ± 89. 7 ) μl and (121.7±78.8) μl in the model and treatment groups, respectively (P<0.05). The tumor weight of treatment group was (316.7±186.3) mg, significantly lower than that of the model group (671.4±281.4) mg (P<0.05) . RT?PCR analysis showed that IGF?1R mRNA level was 0. 914 ± 0. 029 in the treatment group, significantly lower than that of the model group (1.152±0.037, P<0.01). The ELISA data revealed that IGF?1R protein expression level of the model group was significantly higher than that of the treatment group [(41.0±4.7) μg/L vs. (24.0±3.1) μg/L, P<0.01]. Immunohistochemical analysis showed that there were significant differences between MVD and PI in the model and treatment groups [ MVD, 34. 75 ± 3. 49 vs. 22.25±3.63;PI, (75.25±7.15)% vs. (45.75±5.12)%;P<0.01 for both). Western blot data showed that IGF?1R and PI3K protein expression levels were not significantly different between the model and treatment groups (1.03±0.33 vs. 0.98±0.37 and 1.05±0.28 vs. 0.98±0.19), respectively (P>0.05), but p?IGF?1R and p?PI3K protein expression levels had significant differences between the two groups (1.08±0.10 vs. 0.51± 0.08 and 1.12±0.09 vs. 0.86±0.09), respectively (P<0.01 for both). Conclusions The IGF?1R inhibitor can effectively inhibit the formation of malignant pleural effusion. Its mechanism may be related to the suppression of tumor cell proliferation, invasion and angiogenesis through inhibition of PI3K signaling. TAE226 treatment may be a potential therapeutic regimen of treating malignant pleural effusion.

Objective To detect the level of CD64 and serum procalcitonin (PCT ) and investigate the diagnosis value of CD64 and serum PCT in cirrhosis patients with spontaneous bacterial peritonitis (SBP) .Methods Participants were categorized in‐to three groups including liver cirrhosis with SBP(45 patients) ,liver cirrhosis without SBP(93 patients) and health personnel(50 persons) .CD64 was detected by flow cytometry and serum PCT was measured by electroc hemiluminescence immunoassay .The li‐mosis vein blood samples were obtained from the patients with SBP at the time of 24 h after admission ,before antibacterial drugs use and 7 days after the effective treatment of antibacterial drugs .The CD64 and serum PCT were detected with the limosis vein blood samples .At the same time ,the complete blood count ,liver ,kidney and blood coagulate functions were tested .The participants in other two groups were detected the CD64 ,serum PCT ,complete blood count ,liver ,kidney and blood coagulate functions at the same time .Results The level of CD64 and serum PCT in cirrhosis patients with SBP were significantly higher than those in liver cirrhosis without SBP and normal controls (P< 0 .01) .ROC curve analysis showed that the sensitivity and specificity of CD64 and serum PCT were 95 .5% ,93 .8% and 96 .1% ,85 .2% respectively .Conclusion CD64 and serum PCT can be determined as the im‐portant indicator in early diagnosis and efficacy criterion .