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1.
J Cell Physiol ; 2019 Oct 31.
Artigo em Inglês | MEDLINE | ID: mdl-31674024

RESUMO

Endometritis is an inflammatory change in the structure of the endometrium due to various causes and is a common cause of infertility. Studies have confirmed that microRNAs (miRNAs) play a key regulatory role in various inflammatory diseases. However, the miRNA-mediated mechanism of endometrial inflammation induced by lipopolysaccharides (LPS) remains unclear. In this study, real-time quantitative polymerase chain reaction, Western blot analysis, immunofluorescence and Rac family small GTPase 1 (Rac1) interference were used to reveal the overexpression of miR-488 in the LPS-induced bovine uterus, and the effect of protein kinase B κ-light chain enhancement of the nuclear factor-activated B cells (AKT/NF-κB) pathway in intimal epithelial cells. The results showed that the expression of inflammatory cytokines such as interleukin-1ß (IL-1ß), IL-6, and tumor necrosis factor-α in the experimental group was significantly lower than that in the control group when miR-488 was overexpressed. Similar results were observed in the expression levels of p-AKT, p-IKK, and p-p65 proteins. In addition, the dual-luciferase reporter system confirmed that miRNA-488 may directly target the 3'-untranslated region of Rac1. In turn, the expression of Rac1 was inhibited. Moreover, the nuclear translocation of NF-κB was inhibited, and meanwhile, the accumulation of reactive oxygen species (ROS) in the cells was reduced. Thus, we provide basic data for the negative regulation of miR-488 in LPS-induced inflammation by inhibiting ROS production and the AKT/NF-kB pathway in intimal epithelial cells.

2.
Sensors (Basel) ; 19(20)2019 Oct 09.
Artigo em Inglês | MEDLINE | ID: mdl-31600999

RESUMO

With the rapid development of marine IoT (Internet of Things), ocean MDTN (Mobile Delay Tolerant Network) has become a research hot spot. Long-term trajectory prediction is a key issue in MDTN. There are no long-term fine-grained trajectory prediction methods proposed for ocean vessels because a vessel's mobility pattern lacks map topology support and can be easily influenced by the fish moratorium, sunshine duration, etc. A traditional on-land trajectory prediction algorithm cannot be directly utilized in this field because trajectory characteristics of ocean vessels are far different from that on land. To address the problem above, we propose a novel long-term trajectory prediction algorithm for ocean vessels, called L-VTP, by utilizing multiple sailing related parameters and K-order multivariate Markov Chain. L-VTP utilizes multiple sailing related parameters to build multiple state-transition matrices for trajectory prediction based on quantitative uncertainty analysis of trajectories. Trajectories' sparsity of ocean vessels results in a critical state missing problem of a high-order state-transition matrix. L-VTP automatically traverses other matrices in a specific sequence in terms of quantitative uncertainty results to overcome this problem. Furthermore, the different mobility models of the same vessel during the day and the night are also exploited to improve the prediction accuracy. Privacy issues have been taken into consideration in this paper. A quantitative model considering Markov order, training metadata and privacy leak degree is proposed to help the participant make the trade-off based on their customized requirements. We have performed extensive experiments on two years of real-world trajectory data that include more than two thousand vessels. The experiment results demonstrate that L-VTP can realize fine-grained long-term trajectory prediction with the consideration of privacy issues. The average error of 4.5-hour fine-grained prediction is less than 500 m. In addition, the proposed method can be extended to 10-hour prediction with an average error of 2.16 km, which is also far less than the communication range of ocean vessel communication devices.

3.
Int J Biol Sci ; 15(11): 2308-2319, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31595149

RESUMO

Acute lung injury (ALI) is a common clinical disease with high incidence and mortality rate, which is characterized by severe inflammatory response and tissues damage. MicroRNAs (miRNAs) have been regarded as novel regulators of inflammation, and play an important role in various inflammatory diseases. However, it remains unknown whether the regulatory mechanisms mediated by miR-106a is involved in LPS-induced ALI. In this study, we found that expression of miR-106a was significantly decreased in lung tissues of ALI mice and LPS-stimulated macrophages. We also revealed that over-expression of miR-106a significantly decreased the production of pro-inflammatory cytokines, including IL-1ß, IL-6 and TNF-α, whereas this effect was reversed by the inhibition of miR-106a. Moreover, miR-106a inhibits NF-κB activation by targeting TLR4 expression. We further demonstrated that miR-106a inhibited TLR4 expression via binding directly to the 3'-UTR of TLR4. Taken together, the results of the present study illuminated that miR-106a is a negative feedback regulator in LPS-stimulated inflammation through TLR4/NF-κB signaling pathway.

4.
Biosci Rep ; 39(9)2019 Sep 30.
Artigo em Inglês | MEDLINE | ID: mdl-31471533

RESUMO

Nucleus pulposus (NP) cell senescence is involved in disc degeneration. The in situ osmolarity within the NP region is an important regulator of disc cell's biology. However, its effects on NP cell senescence remain unclear. The present study was aimed to investigate the effects and mechanism of hyper-osmolarity on NP cell senescence. Rat NP cells were cultured in the in situ-osmolarity medium and hyper-osmolarity medium. The reactive oxygen species (ROS) scavenger N-acetylcysteine (NAC) was added along with the medium to investigate the role of oxidative injury. Cell cycle, cell proliferation, senescence associated ß-galactosidase (SA-ß-Gal) activity, telomerase activity, expression of senescence markers (p16 and p53) and matrix molecules (aggrecan and collagen II) were tested to assess NP cell senescence. Compared with the in situ-osmolarity culture, hyper-osmolarity culture significantly decreased cell proliferation and telomerase activity, increased SA-ß-Gal activity and cell fraction in the G0/G1 phase, up-regulated expression of senescence markers (p16 and p53) and down-regulated expression of matrix molecules (aggrecan and collagen II), and increased intracellular ROS accumulation. However, addition of NAC partly reversed these effects of hyper-osmolarity culture on cellular senescence and decreased ROS content in NP cells. In conclusion, a hyper-osmolarity culture promotes NP cell senescence through inducing oxidative stress injury. The present study provides new knowledge on NP cell senescence and helps us to better understand the mechanism of disc degeneration.

5.
Int J Biometeorol ; 2019 Sep 14.
Artigo em Inglês | MEDLINE | ID: mdl-31520185

RESUMO

Although it is well-known and established that light plays important roles in plant development, up to now, there is no substantial improvements in how to deal with the light factor of spring phenology under natural condition. By monitoring the local meteorologic data and mature dates of two types (male and female) of flower from four pecan cultivars during 9 years, it was found that the complementary pattern of growing degree day and sunshine duration helped to maintain a threshold of driving force related to the maturity of pecan flower during 9 years. A novel photothermal time model based on the linear combination of growing degree day and sunshine duration was then proposed and validated to interpret the variance of mature dates of pecan cultivars. Comparative analysis showed that the new model had made extremely significant improvements to the traditional thermal time model. In addition, this model introduced the conversion coefficient K, which quantified the effect of light on the flowering drive, and revealed the differences of base temperature among cultivars. This was the first time that sunshine duration instead of photoperiod was adopted to develop into a verified model on spring phenological event of tree species. It will help to model the spring phenologies of other tree species more reasonably.

6.
Opt Express ; 27(16): 23593-23609, 2019 Aug 05.
Artigo em Inglês | MEDLINE | ID: mdl-31510634

RESUMO

Fiber-optic interferometric sensors (FOISs) are widely used in seismometers, hydrophones, and gyroscopes. The arctangent approach of phase-generated carrier (PGC-Arctan) demodulation algorithm is one of the key demodulation techniques in FOISs. The conventional PGC-Arctan demodulation algorithm requires the specific value of the phase modulation depth C to work properly. However, C will variate with laser wavelength, temperature, and humidity in the actual working environment, which leads to harmonic distortion and even demodulation failure. In this paper, a novel PGC demodulation algorithm called self-calibration PGC-Arctan (PGC-Arctan-SC) demodulation algorithm is presented. The proposed algorithm can jointly estimate the accurate C value by the elliptical parameters and C-related components while suppressing nonlinear distortion by ellipse fitting algorithm (EFA). Then C can be calibrated to the specific predefined optimal value by the closed-loop proportion integration differentiation (PID) module. The simulation results are consistent with theoretical analysis, and the all-digital PGC-Arctan-SC demodulation system is implemented on the embedded SoC. The experimental results show that C can be estimated and calibrated accurately in real time. The signal-to-noise and distortion ratio (SINAD) of the PGC-Arctan-SC demodulation output achieves 61.57 dB.

7.
J Cell Physiol ; 2019 Sep 20.
Artigo em Inglês | MEDLINE | ID: mdl-31541458

RESUMO

Breast cancer is a common malignancy that is highly lethal with poor survival rates and immature therapeutics that urgently needs more effective and efficient therapies. MicroRNAs are intrinsically involved in different cancer remedies, but their mechanism in breast cancer has not been elucidated for prospective treatment. The function and mechanism of microRNA-188-5p (miR-188) have not been thoroughly investigated in breast cancer. In our study, we found that the expression of miR-188 in breast cancer tissues was obviously reduced. Our findings also revealed the abnormal overexpression of miR-188 in 4T1 and MCF-7 cells significantly suppressed cell proliferation and migration and also enhanced apoptosis. miR-188 induced cell cycle arrest in the G1 phase. To illuminate the molecular mechanism of miR-188, Rap2c was screened as a single target gene by bioinformatics database analysis and was further confirmed by dual-luciferase assay. Moreover, Rap2c was found to be a vital molecular switch for the mitogen-activated protein kinase signaling pathway in tumor progression by decreasing apoptosis and promoting proliferation and migration. In conclusion, our results revealed that miR-188 is a cancer progression suppressor and a promising future target for breast cancer therapy.

8.
World Neurosurg ; 2019 Sep 03.
Artigo em Inglês | MEDLINE | ID: mdl-31491573

RESUMO

OBJECTIVE: To compare the change in cervical range of motion (CROM) after the 2 most widely used techniques for multilevel cervical spondylotic myelopathy (CSM): anterior cervical corpectomy and fusion (ACCF) and laminoplasty. METHODS: Patients with multilevel CSM treated in our hospital between 2014 and 2018 were divided into an ACCF group and a laminoplasty (LAMP) group according to the treatment received. Their demographic data, preoperative and postoperative Japanese Orthopedic Association (JOA) scores, and CROM, measured using the Coda Motion system, were analyzed and compared. RESULTS: A total of 53 patients were enrolled, including 29 patients in the ACCF group and 24 patients in the LAMP group. Age, sex, duration of follow-up, and preoperative and postoperative JOA scores were comparable in the 2 groups. Compared with preoperative measurements, ACCF group lost an average of 9.8%, 28.5%, 8.9%, 9.9%, 10.6%, and 7.8% of their CROM in flexion, extension, left and right lateral flexion, and left and right rotation, respectively, at the latest follow-up. For the LAMP group, these average losses were 3.5%, 16.4%, 3.2%, 6.3%, 7.0%, and 5.7%, respectively. Thus, the ACCF group exhibited greater average CROM loss than the LAMP group in all directions at the latest follow-up. CONCLUSIONS: Both ACCF and laminoplasty cause significant CROM loss in patients with multilevel CSM. The laminoplasty technique preserved more CROM than ACCF in all 6 directions after at least 1 year of follow-up. These results can be used when counseling patients undergoing surgery.

9.
Microb Pathog ; 136: 103721, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31494298

RESUMO

Acute lung Injury (ALI) is the clinical syndrome of parenchymal lung disease, leading to an extremely high mortality. The pathogenesis of ALI is suggested to be a consequence of uncontrolled inflammation. Lipopolysaccharide (LPS)-induced ALI mice model is often used for the mechanism. Studies show that TGF-beta activated kinase 1 (MAP3K7) binding protein 1/2 (TAB2) plays a crucial role in LPS-induced inflammation response. Furthermore, microRNA-142a-3p (miR-142a-3p) has been observed to be involved in inflammation-induced disease. Thus, we investigated the role of miR-142a-3p and TAB2 on LPS-induced ALI, which involved the TLR4/TAB2/NF-κB signaling. ALI and normal lung tissues were collected to access the relative expression of pro-inflammatory cytokines and miR-142a-3p. Histopathological examination and Wet to Dry weight ratios of lung tissues were used to access the establishment of ALI models. Raw264.7 cells were transfected with si-TAB2 or miR-142a-3p mimics to elucidate the role of TAB2 or miR-142a-3p in the inflammatory cascade in ALI. Additionally, the relationship between miR-142a-3p and TAB2 was validated by dual-luciferase report system. Our study discovered that miR-142-3p was up-regulated both in LPS-induced ALI mice model and RAW264.7 cells model. MiR-142a-3p mimics group experienced significant decrease in the secretion of pro-inflammatory cytokines as a result of the inhibition of NF-κB signaling pathway. Bioinformatics database showed that the adaptor protein, TAB2, was critical in this pathway and it is the target gene of miR-142a-3p. Their relation was first confirmed by us via dual-luciferase report system. Results of our study demonstrated that miR-142a-3p exerts as a protective role in LPS-induced ALI through down-regulation of NF-κB signaling pathway.

10.
Artigo em Inglês | MEDLINE | ID: mdl-31502744

RESUMO

The study of palladium(IV) species has great implications for PdII /PdIV -mediated catalysis. However, most of the PdIV complexes rapidly decompose under ambient conditions, which makes the isolation, characterization and further reactivity study very challenging. The reported ancillary ligand platforms to stabilize PdIV species are dominated by chelating N-donors such as bipyridines. In this work, we present two PdIV complexes with scarcely used C-donors as the supporting platform. The anionic aryl donor and MIC (MIC=mesoionic carbene) are combined in a [CC'C]-type pincer framework to access a series of ambient-stable PdIV tris(halido) complexes. Their synthesis, solid-state structures, stability, and reactivity are presented. To the best of our knowledge, the work presented herein reports the first isolated PdIV -MIC as well as the first PdIV carbene-based aryl pincer.

11.
Pathol Res Pract ; 215(10): 152569, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31421977

RESUMO

AIM: Previous studies have confirmed that overexpression of the long non-coding RNA prostate cancer gene expression marker 1 (PCGEM1) contributes to the invasion and metastasis of gastric cancer (GC) cells. However, the expression of circulating PCGEM1 in the plasma of GC patients and its clinical value remain unclear. METHODS: A total of 317 patients with GC and 100 healthy subjects were enrolled in this study. Circulating PCGEM1 was detected by reverse transcription-polymerase chain reaction. The diagnostic value of plasma PCGEM1 was evaluated by receiver operating characteristic curves and the area under the curve (AUC) value. RESULTS: The expression level of PCGEM1 in the GC group was significantly higher than that in the healthy control subjects. In addition, the PCGEM1 expression level was associated with tumor differentiation and TNM stage. The AUC value of PCGEM1 was higher than that of other conventional tumor markers (CEA, CA12-5, CA72-4, AFP, and CA19-9), although the combination of all markers showed the highest predictive value. CONCLUSION: Plasma PCGEM1 may be a potential novel circulating biomarker for GC diagnosis and prognosis.

12.
Biomed Res Int ; 2019: 9749751, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31467922

RESUMO

Gastric cancer (GC) is a common tumor-associated lethal disease, and invasiveness and metastasis are primary challenges in its clinical treatment. Hypoxia microenvironment cannot be ignored in the process of metastasis. Hypoxia inducible factor-1α (HIF-1α) is the core component of the hypoxia signaling pathway. The aim of this study was to identify potential hub genes and signaling pathways associated with HIF-1α. We explored the invasiveness- and metastasis-associated phenotype of GC via bioinformatics analysis and molecular studies. Differentially expressed genes (DEGs) were identified in GC cells and HIF-1α-knockdown GC cells. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed, and a protein-protein interaction (PPI) network was constructed. Hub genes were identified via centrality analysis and Molecular Complex Detection (MCODE) module analysis. The findings suggested that prolyl 4-hydroxylase beta polypeptide (P4HB) has strong associations with HIF-1α. Further, we observed that HIF-1α and P4HB were upregulated in SGC-7901 and BGC-823 cells. In addition, inhibition of HIF-1α expression reduced invasion and metastasis in GC cells; this effect was partially reversed by P4HB overexpression. Our results confirm that P4HB plays a significant role in the regulatory network of HIF-1α. Therefore, HIF-1α and P4HB may be considered potential biomarkers of GC.

13.
Langmuir ; 35(33): 10890-10899, 2019 Aug 20.
Artigo em Inglês | MEDLINE | ID: mdl-31373500

RESUMO

Polyimide (PI) fibers pose potential problems in applications. Their low surface activity causes poor interfacial wettability, easy agglomeration in aqueous solutions, and poor dispersibility. Therefore, this work proposes a method of surface modification of alkali-treated PI fibers with cellulose nanocrystals (CNCs) under the combined catalytic action of a Lewis acid and a crosslinker. The dispersion degree of PI fibers in aqueous solution before and after CNC modification and the contact angle of the PI fiber paper are measured. The results show that the wettability of the PI fibers improved. Furthermore, the structure and properties of PI fibers before and after CNC treatment are characterized via scanning electron microscopy, Fourier transform infrared spectroscopy, X-ray photoelectron spectroscopy, and thermogravimetric analysis. The pore-size distribution of the PI-fiber paper is measured by a porous-material pore-size analyzer. Compared with the original PI fibers, the oxygen content of the fiber surfaces increases after CNC treatment because of the esterification reaction and crosslinking that occur on the surfaces. The increase in the number of oxygen-containing polar groups and the increased surface roughness of the PI fiber improve its wettability. The contact angle of the PI fiber paper in deionized water is reduced by 14.9° and that in ethanol by 4.8°; the fiber dispersion degree is increased by 45%. These results indicate that the fibers have remarkably improved hydrophilicity and dispersion in the aqueous phase. Therefore, the method developed herein is to prepare high-performance organic fibers and corresponding composite materials.

14.
Biochem Biophys Res Commun ; 517(3): 445-451, 2019 Sep 24.
Artigo em Inglês | MEDLINE | ID: mdl-31378368

RESUMO

Nutlin-3 shows a potent antitumor efficacy through downregulation of the cancerogenic ether à go-go 1 (Eag1) channel. However, the molecular mechanisms responsible for the regulation of Eag1 by Nutlin-3 in cancer cells remain unclear. In this study, we propose a novel anticancer mechanism of Nutlin-3, in which Nutlin-3 acts through the p53-Eag1-PI3K/AKT pathway. We first confirmed that Eag1 was downregulated through the activation of p53 by Nutlin-3. We then revealed that the inhibition of Eag1 electrophysiological function resulted in the decrease of viability, migration and invasion of HeLa cells. It is worth noting that the antitumor effect of Nutlin-3 was abolished in the Eag1 knockdown HeLa cell lines by siRNA. And Nutlin-3 can decrease the cell viability of H8 cells which were stably transfected with Eag1, but has no obvious inhibitory effect on blank H8 cells. Finally, we demonstrated that the decrease in Eag1 channel activity induced by Nutlin-3 treatment exerts anticancer activity by inhibiting the PI3K/AKT pathway. Our study therefore fills the gap between p53 pathway and its cellular function mediated by Eag1, shedding light on the new anti-cancer mechanism of Nutlin-3.

15.
CNS Neurosci Ther ; 2019 Aug 14.
Artigo em Inglês | MEDLINE | ID: mdl-31411808

RESUMO

INTRODUCTION: The occurrence of circadian rhythm disorder in patients with Alzheimer's disease (AD) is closely related to the abnormal deposition of amyloid-ß (Aß), and d-Ser2-oxyntomodulin (Oxy) is a protease-resistant oxyntomodulin analogue that has been shown to exert neuroprotective effects. AIMS: This study aimed to explore whether Oxy, a new GLP-1R/GCGR dual receptor agonist, can improve the Aß-induced disrupted circadian rhythm and the role of GLP-1R. METHODS: A mouse wheel-running experiment was performed to explore the circadian rhythm, and western blotting and real-time PCR were performed to assess the expression of the circadian clock genes Bmal1 and Per2. Furthermore, a lentivirus encoding an shGLP-1R-GFP-PURO was used to interfere with GLP-1R gene expression and so explore the role of GLP-1R. RESULTS: The present study has confirmed that Oxy could restore Aß31-35-induced circadian rhythm disorders and improve the abnormal expression of Bmal1 and Per2. After interfering the GLP-1R gene, we found that Oxy could not improve the Aß31-35-induced circadian rhythm disorder and abnormal expression of clock genes. CONCLUSION: This study demonstrated that Oxy could improve Aß31-35-induced circadian rhythm disorders, and GLP-1R plays a critical role. This study thus describes a novel target that may be potentially used in the treatment of AD.

16.
Mol Ther ; 27(10): 1758-1771, 2019 Oct 02.
Artigo em Inglês | MEDLINE | ID: mdl-31405809

RESUMO

Emerging evidence has revealed that excessive activation of macrophages may result in an adverse lung inflammation involved in sepsis-related acute lung injury (ALI). However, it has never been clearly identified whether peripheral circulating serum exosomes participate in the pathogenesis of sepsis-related ALI. Therefore, the purposes of our study were to investigate the effect of serum exosomes on macrophage activation and elucidate a novel mechanism underlying sepsis-related ALI. Here we found that exosomes were abundant in the peripheral blood from ALI mice and selectively loaded microRNAs (miRNAs), such as miR-155. In vivo experiments revealed that intravenous injection of serum exosomes harvested from ALI mice, but not control mice, increased the number of M1 macrophages in the lung, and it caused lung inflammation in naive mice. In vitro, we demonstrated that serum exosomes from ALI mice delivered miR-155 to macrophages, stimulated nuclear factor κB (NF-κB) activation, and induced the production of tumor necrosis factor alpha (TNF-α) and interleukin (IL)-6. Furthermore, we also showed that serum exosome-derived miR-155 promoted macrophage proliferation and inflammation by targeting SHIP1 and SOCS1, respectively. Collectively, our data suggest the important role of circulating exosomes secreted into peripheral blood as a key mediator of septic lung injury via exosome-shuttling miR-155.

17.
BMC Urol ; 19(1): 71, 2019 Jul 29.
Artigo em Inglês | MEDLINE | ID: mdl-31357972

RESUMO

BACKGROUND: In this case report, giant calculus in the urethral diverticulum was found through ureteroscopy investigation, the pneumatic lithotripsy combined with ultrasound lithotripsy (PLCUL) was successfully performed to break down this rare and giant urethral calculus in the diverticulum without open surgery. CASE PRESENTATION: A 82-year-old male presented to the urology department, complaining of frequent urination and dysuria. One giant, dark brown stone (6.5 × 6 × 5.5 cm) was revealed in the diverticulum of the anterior urethra using combination of local ultrasound, pelvic Computer Tomography (CT) and Magnetic Resonance Imaging (MRI). The stone was then successfully broken down via the PLCUL, and the emptied anterior urethral diverticulum was left untreated. In the 18 months' follow-up, no new calculus was found in urethral tract, anterior diverticula became gradually smaller, eventually disappeared. CONCLUSION: In the treatment of giant calculus in the urethral diverticulum, this case report provides an effective method of lithotripsy in the clinical trials.

18.
J Physiol Biochem ; 75(3): 379-389, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31290116

RESUMO

N6-Methyladenosine (m6A) is the most common posttranscriptional modification of RNA and plays critical roles in cancer pathogenesis. However, the biological function of long noncoding RNA (lncRNA) methylation remains unclear. As a demethylase, ALKBH5 (alkylation repair homolog protein 5) is involved in mediating methylation reversal. The purpose of this study was to investigate lncRNA m6A modification and its role in gastric cancer (GC). Bioinformatics predicted interactions of ALKBH5 with lncRNAs. Five methods were employed to assess the function of nuclear paraspeckle assembly transcript 1 (NEAT1), including gene silencing, RT-PCR, separation of nuclear and cytoplasmic fractions, scrape motility assays, and transwell migration assays. Then, m6A RNA immunoprecipitation and immunofluorescence were used to detect methylated NEAT1 in GC cells. Rescue assays were performed to define the relationship between NEAT1 and ALKBH5. NEAT1 is a potential binding lncRNA of ALKBH5. NEAT1 was overexpressed in GC cells and tissue. Additional experiments confirmed that knockdown of NEAT1 significantly repressed invasion and metastasis of GC cells. ALKBH5 affected the m6A level of NEAT1. The binding of ALKBH5 and NEAT1 influences the expression of EZH2 (a subunit of the polycomb repressive complex) and thus affects GC invasion and metastasis. Our findings indicate a novel mechanism by which ALKBH5 promotes GC invasion and metastasis by demethylating the lncRNA NEAT1. They may be potential therapeutic targets for GC.

19.
Lancet Gastroenterol Hepatol ; 4(9): 686-697, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31279647

RESUMO

BACKGROUND: Angioplasty recanalisation is recommended as the first-line interventional procedure for Budd-Chiari syndrome, but subsequent restenosis is common. We aimed to test whether use of routine, non-selective stenting in angioplasty could improve patency and treatment efficacy with adequate safety in Budd-Chiari syndrome. METHODS: We did a randomised controlled trial, for which patients aged 18-75 years with Budd-Chiari syndrome with membranous obstruction or short-length stenosis (≤4 cm), and a Child-Pugh score of less than 13 were considered eligible. Patients were excluded if they had obstruction not amenable to angioplasty, were recommended to be treated with transjugular intrahepatic portosystemic shunt or liver transplantation, or had contraindications for angioplasty. Eligible patients were randomly assigned (1:1) to an angioplasty-only group or an angioplasty plus routine stenting group, with use of a web-based allocation system (Pocock and Simon's minimisation method, stratified by obstruction features and Child-Pugh score). Recanalisation procedures were done within 24 h of randomisation. The statistician and investigators responsible for data collection data and endpoint assessment were masked to group allocation. The primary outcome was the proportion of patients free of restenosis, analysed in the intention-to-treat population. The study is registered on ClinicalTrials.gov (NCT02201485) and is completed. FINDINGS: Between July 28, 2014, and Sept 29, 2017, 88 (59%) of 150 screened patients were enrolled and assigned either the angioplasty-only group (n=45) or the angioplasty plus routine stenting group (n=43). During a median follow-up period of 27 months (IQR 19-41), the angioplasty plus routine stenting group had significantly higher proportion of patients free of restenosis (42 [98%] of 43 patients) than did the angioplasty-only group (27 [60%] of 45 patients; p<0·0001). In the survival analysis, 3-year restenosis-free survival was 96·0% (95% CI 88·6-100·0) in the routine stenting group versus 60·4% (46·4-78·7) in the angioplasty-only group (log-rank p<0·0001). The hazard ratio for restenosis was 0·04 (95% CI 0·01-0·31) in favour of routine stenting, with an absolute risk reduction of 35·6% (95% CI 24·2-55·0). Two (5%) patients in the angioplasty plus routine stenting group and one (2%) patient in the angioplasty-only group died during follow-up. One (2%) patient from the angioplasty plus routine stenting group had puncture site haematoma, which was not related to stenting. No stent fracture or migration occurred. Anticoagulation-related adverse events occurred in five (11%) patients from angioplasty alone group and five (12%) patients from angioplasty plus routine stenting group. INTERPRETATION: Routine stenting with angioplasty is superior to angioplasty alone for preventing restenosis in patients with Budd-Chiari syndrome with short-length stenosis and is safe to use as part of first-line invasive treatment. Further validation is needed in similar settings and other regions in which different characteristics of Budd-Chiari syndrome are more prevalent. FUNDING: National Natural Science Foundation of China, National Key Technology R&D Programme, Optimised Overall Project of Shaanxi Province, Boost Programme of Xijing Hospital.

20.
Int Immunopharmacol ; 75: 105749, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31306981

RESUMO

Acute lung injury (ALI) is a pulmonary diffuse dysfunction disease caused by immoderate inflammatory response breaking the coordination of physiological structures and functions, and there are very few effective treatments to reduce high morbidity of ALI in critical patients. Glycitin is a natural ingredient derived from the seeds of leguminous plants and may have potent anti-inflammation features. The purpose of this study was to investigate the anti-inflammation effect of glycitin on LPS-induced ALI in mice and elucidate its possible anti-inflammatory mechanisms. The results of histopathological changes, the wet/dry weight ratio as well as the myeloperoxidase (MPO) activity indicated that glycitin obviously alleviated the lung injury induced by LPS. In addition, qPCR and ELISA results found that glycitin could dose-dependently decrease the expressions of pro-inflammatory cytokines IL-1ß, IL-6, and TNF-α. Western blotting was performed to revealed that glycitin inhibited the activation of NF-κB and MAPKs signaling pathways by suppressing the expression of TLR4 protein and the phosphorylation of IKKß, IκBα, p65, p38, ERK, and JNK. All data indicated that glycitin could protect lung tissues from LPS-induced inflammation via inhibiting TLR4-mediated NF-κB and MAPKs signaling pathways.

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