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OBJECTIVE: MicroRNAs (miRNAs) are endogenous, non-coding RNAs, which exert crucial functions in regulating biological progressions. Previous studies have demonstrated the anti-tumor effect of miRNA-215-5p. However, its specific role in influencing the progression of prostate cancer (PCa) remains unclear. This study aims to uncover the regulatory effect of miRNA-215-5p on the metastasis and prognosis of PCa. PATIENTS AND METHODS: MiRNA-215-5p levels in collected PCa tissues (n=52) and paracancerous tissues (n=52) were determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The relationship between miRNA-215-5p level and pathological indexes, as well as overall survival of PCa patients, was analyzed. Regulatory effects of miRNA-215-5p on proliferative and metastatic capacities of LNCaP and DU-145 cells were evaluated through cell counting kit-8 (CCK-8) and transwell assay, respectively. Bioinformatics prediction was performed to search for the target genes of miRNA-215-5p and PGK1 was selected. The biological role of PGK1 in the progression of PCa was finally clarified by a series of rescue experiments. RESULTS: MiRNA-215-5p was lowly expressed in PCa tissues and cell lines. Low level of miRNA-215-5p predicted poor prognosis in PCa patients. The silence of miRNA-215-5p enhanced viability, migratory, and invasive capacities of LNCaP cells, while the overexpression of miRNA-215-5p yielded the opposite trends in DU-145 cells. PGK1 was predicted to be the target of miRNA-215-5p. PGK1 was upregulated in PCa tissues and cell lines and its high level predicted poor prognosis of PCa. Moreover, PGK1 level was negatively correlated to that of miRNA-215-5p in PCa tissues. PGK1 was able to reverse the regulatory effects of miRNA-215-5p on metastatic potentials of PCa cells. CONCLUSIONS: Downregulated miRNA-215-5p in PCa is closely related to distant metastasis and poor prognosis of affected patients. MiRNA-215-5p alleviates the malignant progression of PCa by targeting and downregulating PGK1. [ABSTRACT FROM AUTHOR]

Verticillium wilt, an infection caused by the soilborne fungus Verticillium dahliae, is one of the most serious diseases in cotton. No effective control method against V. dahliae has been established, and the infection mechanism of V. dahliae in upland cotton remains unknown.GFP‐tagged V. dahliae isolates with different pathogenic abilities were used to analyse the colonisation and infection of V. dahliae in the roots and leaves of different upland cotton cultivars, the relationships among infection processes, the immune responses and the resistance ability of different cultivars against V. dahliae.Here, we report a new infection model for V. dahliae in upland cotton plants. V. dahliae can colonise and infect any organ of upland cotton plants and then spread to the entire plant from the infected organ through the surface and interior of the organ.Vascular tissue was found to not be the sole transmission route of V. dahliae in cotton plants. In addition, the rate of infection of a V. dahliae isolate with strong pathogenicity was notably faster than that of an isolate with weak pathogenicity. The resistance of upland cotton to Verticillium wilt was related to the degree of the immune response induced in plants infected with V. dahliae. These results provide a theoretical basis for studying the mechanism underlying the interaction between V. dahliae and upland cotton. These results provide a theoretical basis for studying the mechanism underlying the interaction between V. dahliae and upland cotton. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To investigate the expression of long noncoding RNA (LncRNA) MIRG and its potential functions in regulating osteoclastogenesis and bone resorption function through modulating miR-1897 in bone marrow macrophages (BMMs). MATERIALS AND METHODS: qRT-PCR was performed to detect the expressions of MIRG and its co-expression mRNA NFATc1 at different stages during osteoclastogenesis. The CCK-8 assay was performed to evaluate cell proliferation and differentiation. The correlation between miR-1897 and MIRG was detected by statistical analysis. Bioinformatics and luciferase assay were performed to explore the interaction and binding site of MIRG and miR- 1897. We also cloned the mice NFATc1 3'-UTR into the luciferase reporter vector and constructed miR-1897 binding mutants to validate the inhibited regulation of miR-1897 to the expression of NFATc1. RESULTS: Results showed that expressions of MIRG and NFATc1 were upregulated during osteoclastogenesis. qRT-PCR and CCK-8 assay showed that MIRG expression is associated with osteoclastogenesis and bone resorption. The bioinformatics prediction and luciferase assay suggested that by interacting with miR-1897, MIRG acts as a molecular sponge for the miR- 1897 target NFATc1, to partly modulate the inhibitory effect of miR-1897 on NFATc1. CONCLUSIONS: We found that lncRNA-MIRG was upregulated in osteoclasts, which could promote osteoclastogenesis and bone resorption function as a molecular sponge by modulating the inhibitory effect of miR-1897 on NFATc1. [ABSTRACT FROM AUTHOR]

OBJECTIVE: The aim of this study was to detect the relationship between long-chain non-coding RNA (lncRNA) NEAT1 and microRNA-1224 (miR-1224) in lung cancer and to explore its underlying mechanism. MATERIALS AND METHODS: The expression levels of lncRNA NEAT1 and miR-1224 in lung cancer tissues and cells were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The interaction between lncRNA NEAT1 with miR-1224, miR-1224, and KLF3 was detected by Dual-Luciferase Reporter Gene Assay. MTT 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide and flow cytometry were used to detect the changes in the proliferative and apoptosis abilities of lung cancer cells after silencing lncRNA NEAT1 or up-regulating miR-1224, respectively. RESULTS: Compared with adjacent normal tissues, lncRNA NEAT1 was significantly up-regulated, while miR-1224 was significantly down-regulated in lung cancer tissues. LncRNA NEAT1 could specifically bind to the 3'UTR of miR-1224 and regulate its expression. The inhibition of lncRNA NEAT1 remarkably reduced the proliferation and enhanced the apoptosis of lung cancer cells. However, the upregulation of the expression of miR-1224 level could significantly inhibit proliferation and promote the apoptosis rate of lung cancer cells. Furthermore, miR-1224 could downregulate KLF3 expression by directly binding to its 3'UTR. CONCLUSIONS: LncRNA NEAT1 can sponge the expression of miR-1224, thereby affecting the proliferation and apoptosis of lung cancer. [ABSTRACT FROM AUTHOR]

OBJECTIVE: The aim of this study was to explore the expression of long non-coding RNA (lncRNA) KCNQ1OT1 in nonsmall cell lung cancer (NSCLC), and to elucidate its clinical significance. PATIENTS AND METHODS: The quantitative Real Time-Polymerase Chain Reaction (qRTPCR) was used to detect the expression of lncRNA KCNQ1OT1 in NSCLC tissues and para-cancer tissues (5 cm or above away from the tumor). The relation between lncRNA KCNQ1OT1 expression and the clinical pathological data was analyzed by the multivariate logistic regression analysis. Furthermore, the survival analysis was performed by the Kaplan-Meier method. RESULTS: The expression of lncRNA KCNQ1OT1 increased significantly in NSCLC tissues than that of in para-cancer tissues. According to the median expression of lncRNA KCNQ1OT1, NSCLC patients were divided into two groups, including high expression group and low expression group. Meanwhile, the lncRNA KCNQ1OT1 expression was correlated with tumor size, tumor node metastasis (TNM) staging, and lymph node metastasis of NSCLC patients. Both univariate analysis and multivariate analysis indicated that the high expression of lncRNA KCNQ1OT1 was closely related to TNM staging and lymph node metastasis. In addition, the Kaplan-Meier analysis showed that the overall survival and progression-free survival time of patients with higher lncRNA KCNQ1OT1 expression were significantly worse than those with lower lncRNA KCNQ1OT1 expression. CONCLUSIONS: LncRNA KCNQ1OT1 might contribute to the development of NSCLC. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To study the effect of promethazine on neuronal apoptosis in rats with cerebral infarction (CI) through the phosphatidylinositol 3-hydroxy kinase/protein kinase B (PI3K/Akt) signaling pathway. MATERIALS AND METHODS: A total of 36 Sprague-Dawley rats were randomly divided into the sham group (n=12), model group (n=12), and promethazine group (n=12). The external carotid artery was only exposed in the model group, and the ischemia-reperfusion model after CI was established using the suture method in the other two groups. After modeling, the normal saline was intraperitoneally injected in the sham group and model group, while promethazine was intraperitoneally injected in the promethazine group. The rats were sampled after 1 week of intervention. The neurological deficits of rats were evaluated using the Zea-Longa score, and the cognitive function, the spatial learning, and memory of rats were detected via the water maze test. Moreover, the expressions of B-cell lymphoma-2 (Bcl-2) and Bcl-2 associated X protein (Bax) in brain tissues were detected via immunohistochemistry, and the relative protein expressions of PI3K p85, PI3K p110, and p-Akt were detected via Western blotting. The mRNA expressions of Bax and Bcl-2 were detected via quantitative Polymerase Chain Reaction (qPCR), and the apoptosis was detected via terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. RESULTS: The Zea-Longa score was significantly increased in the model group and promethazine group compared with that in the sham group (p<0.05), while it significantly declined in the promethazine group compared with that in the model group (p<0.05). The escape latency was significantly prolonged and the times of crossing platform were significantly reduced in the model group and promethazine group compared with those in the sham group (p<0.05), while the escape latency was significantly shortened and the times of crossing platform were significantly increased in the promethazine group compared with those in the model group (p<0.05). Compared with those in the sham group, the positive expression of Bax was significantly increased, while the positive expression of Bcl-2 was remarkably decreased in the model group and promethazine group (p<0.05). Compared with those in the model group, the positive expression of Bax was significantly decreased, while the positive expression of Bcl- 2 was remarkably increased in the promethazine group (p<0.05). Besides, the model group and promethazine group had evidently higher relative protein expressions of PI3K p85, PI3K p110, and p-Akt than the sham group (p<0.05), while the promethazine group also had evidently higher relative protein expressions of PI3K p85, PI3K p110, and p-Akt than the model group (p<0.05). Compared with the sham group, model group, and promethazine group had remarkably increased relative mRNA expression of Bax, and remarkably decreased relative mRNA expression of Bcl-2 (p<0.05). Compared with those in the model group, the relative mRNA expression of Bax was remarkably decreased, while the relative mRNA expression of Bcl-2 was remarkably increased in the promethazine group (p<0.05). Finally, the apoptosis rate was significantly higher in the model group and promethazine group than that in the sham group (p<0.05), while it was significantly lower in the promethazine group than that in the model group (p<0.05). CONCLUSIONS: Promethazine inhibits neuronal apoptosis in CI rats by upregulating the PI3K/Akt signaling pathway, thereby exerting a protective effect. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To study the efficacy of transarterial chemoembolization (TACE) combined with high-intensity focused ultrasound (HIFU) in patients with middle-advanced liver cancer. PATIENTS AND METHODS: A total of 100 patients with middle-advanced liver cancer treated in our hospital from January 2015 to January 2018 were selected and randomly divided into TACE group (control group, n=50) and TACE combined with HIFU group (experimental group, n=50) according to different therapeutic regimens. The efficacy was observed after the operation, the blood was collected to detect the postoperative liver function indexes aspartate aminotransferase (AST) and alanine aminotransferase (ALT), the postoperative complications were observed. Also, the immune indexes cluster of differentiation 3+ (CD3+), CD4+, and CD8+ were determined. Moreover, the quality of life (QOL) score was compared between the two groups, the 1-, 2-, 3-, and 5-year survival rates were observed after the operation. Also, the changes in the levels of tumor markers α-L-fucosidase (AFU), alpha- fetoprotein (AFP), carbohydrate antigen 19- 9 (CA19-9), and carcinoembryonic antigen (CEA) were observed. RESULTS: In experimental group, the levels of AST, ALT, and blood urea nitrogen (BUN) after the operation were significantly decreased (p<0.05), while the postoperative efficacy was significantly superior to that in control group (p<0.05). The incidence of postoperative complications was significantly reduced (p<0.05), the levels of CD3+, CD4+, CD8+, and natural killer (NK) cells were markedly increased (p<0.05). Also, the QOL score was evidently better than that in control group (p<0.05) and the 1-, 2-, 3-, and 5- year survival rates after the operation were evidently higher than those in control group (p<0.05). After treatment, the levels of AFU, AFP, CA19-9, and CEA were remarkably lower than those before treatment in both groups, while they were remarkably lower in experimental group than those in control group (p<0.05). CONCLUSIONS: TACE combined with HIFU in the treatment of patients with middle-advanced liver cancer can restore the hepatic metabolism, enhance the immunity, improve the QOL, prolong the survival time of patients, and significantly reduce the tumor markers. Also, it has fewer adverse reactions and definite overall efficacy, which is worthy of popularization and application. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To explore the effect of micro-ribonucleic acid (miR)-29c on renal fibrosis in diabetic rats through the adenosine 5'-monophosphate-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) signaling pathway, and to investigate its related mechanism by the research on the effect of miR-29c on the expression of fibrosis-related genes. MATERIALS AND METHODS: The rat model of diabetic nephropathy (DN) was established, and the levels of fasting blood glucose (FBG), 24 h urine protein (24h-Pro), blood urea nitrogen (BUN), and serum creatinine (sCr) were monitored. After the rats were executed, kidney tissues were dissected, stained with paraffin and embedded in hematoxylin and eosin (H&E). Then, Western blotting was used to detect the levels of miR-29c, phosphorylated-AMPK (p-AMPK), α-smooth muscle actin (α-SMA), tumor necrosis factor-α (TNF-α), and macrophage migration inhibitory factor (MIF). The human renal tubular epithelial HK-2 cell line was treated with high glucose (HG) to simulate DN cell status in vivo. After that, the expressions of miR-29c and the renal fibrosis marker α-SMA were examined via Western blotting. Finally, the level of α-SMA was measured by Western blotting after HG treatment combined with miR-29c silencing. RESULTS: The levels of FBG, BUN, sCr, and 24h-Pro in DN model rats were significantly higher than those in rats of control group. The data manifested that the DN model was successfully established. The expression level of miR-29c in DN model rats was markedly increased and that of the downstream protein p-AMPK also exhibited a significantly increasing trend. In addition, the levels of α-SMA, TNF-α, and MIF were elevated. The expression levels of miR-29c and α-SMA were increased markedly after the human renal tubular epithelial HK-2 cell line was treated with HG, but the expression of α-SMA was reduced after HG treatment combined with miR-29c silencing for 24 h. CONCLUSIONS: MiR-29c is probably related to the occurrence and development of DN. Besides, miR-29c silencing may inhibit the DN renal fibrosis through AMPK/mTOR signals, so miR-29c may be an effective target for the treatment of DN renal fibrosis. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To investigate the association between bone morphogenetic protein 4 (BMP4) expression and clinical pathology, computed tomography (CT) characteristics and prognosis of patients with non-small cell lung cancer (NSCLC). PATIENTS AND METHODS: A total of 76 NSCLC patients treated in our hospital from July 2012 to March 2015 were enrolled. The paired NSCLC and para-carcinoma tissues, as well as their CT image data were collected. The messenger ribonucleic acid (mRNA) and protein levels of BMP4 in NSCLC were detected via quantitative polymerase chain reaction (qPCR) and immunohistochemistry (IHC). The association between BMP4 level and clinicopathological indexes of NSCLC patients was analyzed. Moreover, Kaplan-Meier method was introduced for analyzing the progression- free survival (PFS) and overall survival (OS) in NSCLC patients with high-level or low-level BMP4. The correlation between CT manifestations and BMP4 level in NSCLC patients was analyzed using the Chi-square test. RESULTS: The mRNA level of BMP4 in NSCLC tissues was 2.15 times higher than that in para-carcinoma tissues (p<0.05). IHC results revealed 59.21% (45/76) of BMP4-positive NSCLC tissues and 40.79% (31/76) in para-carcinoma tissues. BMP4 level was higher in NSCLC patients with lymph node metastasis and those in clinical stage III and IV than those without lymph node metastasis and in clinical stage I and II (p<0.05). Besides, BMP4 level was not correlated to the gender, age and differentiation degree of NSCLC patients (p>0.05). According to the Kaplan-Meier survival curve, both PFS and OS were significantly shortened in NSCLC patients with high level of BMP4 compared with patients with low level of BMP4 (PFS: 13.28 months vs. 19.34 months, Log-rank test, p=0.016; OS: 15.14 months vs. 22.08 months, Log-rank test, p=0.027). BMP4 level was associated with lobulation sign, spinous process sign, tumor diameter and mediastinal lymph node metastasis in CT findings (p<0.05), rather than spiculation sign, ground glass sign, calcification lesion and CT enhancement value of lung cancer (p>0.05). CONCLUSIONS: BMP4 overexpression is closely associated with the occurrence and development of NSCLC and CT signs. Detection of BMP4 is helpful for evaluating the malignant degree and prognosis of NSCLC. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To investigate the effect of micro ribonucleic acid (miR)-101a on myocardial cell apoptosis in the rat model of acute myocardial infarction (AMI) and its regulatory mechanism. MATERIALS AND METHODS: A total of 30 Sprague-Dawley (SD) rats were randomly divided into the Sham group, Model group, and miR- 101a mimic group, with 10 rats in each group. The rat model of AMI was established by the ligation of the anterior descending coronary artery. The rat left ventricular end-diastolic volume (LVEDV) and left ventricular end-systolic volume (LVESV) were detected using a color Doppler ultrasonic apparatus. Subsequently, the miRNA online database (TargetScan) was adopted to predict miRNAs that could be able to regulate TGF-ß1. Hematoxylin and eosin (H&E) staining was conducted to reveal the histopathological morphology changes in the rat heart. The serum levels of cysteinyl aspartate specific proteinase-3 (Caspase-3) and Bcl-2-associated X protein (Bax) in rats were detected via enzyme-linked immunosorbent assay (ELISA). Moreover, the expression levels of the transforming growth factor-beta l (TGF-ß1) and c-Jun N-terminal kinase (JNK) in rat heart were measured via Western blotting. RESULTS: Through searching miRNA database, miR-101a and TGF-ß1 messenger RNAs (mRNAs) had binding sites in the 3' untranslated region (3'UTR). Compared with those in Sham group, the rat LVEDV and LVESV were notably elevated, the histopathological morphology of the heart was seriously damaged, the apoptotic rate of myocardial cells and the levels of TGF-ß1 and JNK proteins significantly increased in the Model group. Additionally, compared with those in the Model group, the LVEDV and LVESV of rats in miR-101a mimic group were significantly reduced, the histopathological morphology of the heart was markedly improved, and the apoptotic rate and the levels of TGF-ß1 and JNK in rat heart were remarkably decreased. CONCLUSIONS: The myocardial cell apoptosis in AMI rats can be suppressed by overexpression of miR-101a by inhibiting the TGF-ß1/JNK signaling pathway. [ABSTRACT FROM AUTHOR]

The corrosion behavior of a 304 oxide dispersion strengthened (ODS) austenitic stainless steel after being exposed to supercritical water (SCW) with dissolved oxygen of 300 ppb at 600 °C/25 MPa was studied. By the means of a least-square fit, the weight gain (Δ w) of the samples as a function of exposure time ( t) could be described by the equation Δ w = 8.011 × t0.459. An approximately parabolic time law in this specified SCW environment can be assumed. A triple protective oxide layer formed on the surface of the metal with the exposure time up to 1000 h. Furthermore, the result of slow-strain rate tensile (SSRT) test indicated that the 304-ODS austenitic stainless steel was not susceptible to stress corrosion cracking (SCC) in SCW at 600 °C/25 MPa. [ABSTRACT FROM AUTHOR]

In order to eliminate the effects of flow regimes on phase concentration measurements, electrical capacitance tomography (ECT) was employed to improve the measurement accuracy. The solid particle distribution in the flow pipelines were characterized by measuring capacitance to obtain flow patterns. An improved offline iteration online reconstruction (OIOR) algorithm was proposed as the image reconstruction for the ECT system and a method of two-dimension maximum entropy threshold image segmentation was used for further image processing. Dynamic experiments were carried out for gas/solid two-phase flows. First, the flow regime was identified by the ECT, and the results were used to trace the fluctuation of the dynamic two-phase flow online. The volume concentrations were then calculated based on the reconstructed results. The experimental results indicate that the average relative error of the concentration measurements was about 1.5% over a pulverized coal volume concentration range 0.96–4.97%. [ABSTRACT FROM PUBLISHER]