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The development of high-temperature organic adhesive for bonding ultra-high-temperature ceramics with excellent thermal shock resistance has important significance to thermal protection systems for high-temperature environment application. In this study, high-temperature organic adhesive (HTOA) with carbon-fiber-SiC nanowires (CF-SiCNWs) binary phase enhancement structure was prepared. The method is that the SiCNWs grow on the chopped carbon-fiber surface and in the matrix of modified HTOA during high-temperature heat treatment with the help of a catalyst by a tip-growth way and with a vapor-liquid-solid (V-L-S) growth pattern. The results showed that the CF-SiCNWs binary phase enhancement structure plays a significant role in improving thermal shock resistance of high-temperature organic adhesive. The retention rate of the joint bond strength for the bonding samples after 20 cycles of thermal shock testing reaches 39.19%, which is higher than for the ones without CF, whose retain rate is only 6.78%. The shear strength of the samples with the CF-SiCNWs binary phase enhancement structure was about 10% higher than for those without the enhancement structure after 20 cycles of thermal shock.
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BACKGROUND: Recently, researchers have found that the tumour microenvironment plays an important role in tumours. We aimed to investigate the effects of plasma lipids on the prognosis of patients with pancreatic cancer and the infiltration of CD8+ T lymphocytes in tumour tissue. METHODS: We enrolled patients with pancreatic ductal adenocarcinoma (PDAC) who underwent pancreatic surgery between 2012 and 2021. Clinical pathological data were recorded; total cholesterol (TC) and triglyceride (TG) levels were measured; and tissue samples were collected. A tissue microarray was generated using collected tissue samples, and CD8 staining was performed to determine immunoreactive scores (IRSs). The correlations of TC and TG levels with clinicopathological characteristics and prognosis were analysed. Finally, the correlations of TC and TG levels with CD8+ T-cell infiltration were analysed. RESULTS: A total of 90 eligible PDAC patients were included. TC levels were significantly correlated with tumour grade and lymph node metastasis, and TG levels were significantly correlated with perineural invasion. The Kaplan-Meier survival analysis results indicated that the prognosis in the high TC group was significantly worse than that in the low TC group, and the prognosis in the high TG group was significantly worse than that in the low TG group. Cox multivariate analysis indicated that TC was an independent indicator of poor prognosis of pancreatic cancer patients after surgery. Spearman correlation analysis indicated that there were significant negative correlations between CD8 IRS and TC and between CD8 IRS and TG. CONCLUSIONS: TC and TG levels are significantly related to the prognosis of pancreatic cancer patients. They may be associated with tumour progression to higher grades, lymph node metastasis and/or nerve invasion. More importantly, TC and TG may reduce CD8+ T lymphocyte infiltration into pancreatic cancer tissue, affecting antitumour immune functions and immunotherapy efficacy.
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Carcinoma Ductal Pancreático , Neoplasias Pancreáticas , Humanos , Metástasis Linfática/patología , Linfocitos Infiltrantes de Tumor , Neoplasias Pancreáticas/patología , Pronóstico , Linfocitos T CD8-positivos , Lípidos , Microambiente Tumoral , Neoplasias PancreáticasRESUMEN
Our pre-investigation has revealed that long non-coding RNA (LncRNA) AL137789.1 has the potential to predict the survival of patients with pancreatic carcinoma (PCa). Accordingly, the mechanism underlying the implication of AL137789.1 in PCa is covered in the current study. The non-tumor and paired tumor tissues were collected. Kaplan-Meier curve was employed to estimate the survival of PCa patients with high or low expression of AL137789.1. The proliferation, migration, invasion, and cell cycle of PCa cells were determined, and the cytotoxicity of CD8+ T cells was evaluated as well. Levels of AL137789.1, E-cadherin, N-cadherin, and Vimentin were quantified. According to the experimental results, AL137789.1 was highly expressed in PCa and related to a poor prognosis of patients. Overexpressed AL137789.1 enhanced the proliferation, migration, and invasion of PCa cells, increased the cell population at G2/M and S phases yet decreased that in G0/G1 phase, and diminished the cytotoxicity of CD8+ T cells. Also, overexpressed AL137789.1 elevated levels of N-cadherin and Vimentin, while lessening E-cadherin levels. However, the silencing of AL137789.1 produced contrary effects. Collectively, lncRNA AL137789.1 plays a tumor-promotive role in PCa by enhancing the progression and immune escape.
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BACKGROUND: Tumor-infiltrating lymphocytes (TILs) are major participants in the tumor microenvironment. The prognostic value of TILs in patients with pancreatic cancer is still controversial. METHODS: The aim of our meta-analysis was to determine the impact of FoxP3+Treg cells on the survival of pancreatic cancer patients. We searched for related studies in PubMed, EMBASE, Ovid, and Cochrane Library from the time the databases were established to Mar 30, 2017. We identified studies reporting the prognostic value of FoxP3+Treg cells in patients with pancreatic cancer. Overall survival (OS) and disease-free survival (DFS)/progression-free survival (PFS)/relapse-free survival (RFS) were investigated by pooling the data. The pooled hazard ratios (HRs) with 95% confidence intervals (95% CI) were used to evaluate the association between FoxP3+Treg cells and survival outcomes of pancreatic cancer patients. A total of 972 pancreatic cancer patients from 8 studies were included in our meta-analysis. RESULTS: High levels of infiltration with FoxP3+Treg cells were significantly associated with poor OS (HR=2.13; 95% CI 1.64-2.77; P<0.05) and poor DFS/PFS/RFS (HR=1.70; 95% CI 1.04 ~ 2.78; P< 0.05). Similar results were also observed in the peritumoral tissue; high levels of FoxP3+Treg cells were associated with poor OS (HR =2.1795% CI, CI 1.50-3.13). CONCLUSION: This meta-analysis indicated that high levels of intratumoral or peritumoral FoxP3+Treg cell infiltration could be recognized as a negative factor in the prognosis of pancreatic cancer.
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Adenocarcinoma , Neoplasias Pancreáticas , Factores de Transcripción Forkhead , Humanos , Linfocitos Infiltrantes de Tumor , Recurrencia Local de Neoplasia , Pronóstico , Linfocitos T Reguladores , Microambiente TumoralRESUMEN
BACKGROUND: It remains unclear whether lymph node dissection is necessary for patients with N0 gallbladder carcinoma (GBC). The objective of this study was to evaluate the effect of lymphadenectomy on the prognosis for N0 GBC patients. The secondary objective was to establish a prognostic model of survival for N0 GBC patients being founded on the large samples. METHODS: Patient data were obtained from the database named SEER (Surveillance, Epidemiology, and End Results database) between 2010 and 2014. Analyses of Kaplan-Meier survival and multivariate Cox regression were performed in subgroups based on regional lymph nodes removal (LNR) to calculate the excess risk of cause-specific death. A prognosis nomogram was constructed build on the results of a multivariate analysis to predict the specific survival time (CSS) rates of N0 GBC patients. RESULT: A total of 1406 N0 GBC patients were included in this research. The majority of N0 GBC patients undergoing cancer-directed surgery did not undergo LNR (64.5%). The results showed that LNR can improve the survival of N0 GBC patients, including those at the T1a and T1b stages, and a wider range of lymph node dissection (LNR2) compared to LNR1 was more conducive to the prognosis. Furthermore, multivariate regression analysis showed that LNR was an independent favorable prognostic factor of N0 GBC. Finally, a nomogram was constructed to accurately predict the prognosis of N0 gallbladder cancer patients. CONCLUSION: This study demonstrated a significant survival benefit for extended lymph nodes removed in N0 GBC patients. These results recommend that an extended lymph node dissection strategy is needed for N0 GBC patients.
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Carcinoma/mortalidad , Carcinoma/patología , Neoplasias de la Vesícula Biliar/mortalidad , Neoplasias de la Vesícula Biliar/patología , Escisión del Ganglio Linfático/mortalidad , Anciano , Carcinoma/cirugía , Causas de Muerte , Femenino , Neoplasias de la Vesícula Biliar/cirugía , Humanos , Estimación de Kaplan-Meier , Masculino , Análisis Multivariante , Estadificación de Neoplasias , Nomogramas , Pronóstico , Modelos de Riesgos Proporcionales , Programa de VERFRESUMEN
Pancreatic cancer (PC) is a highly malignant tumor type with a high early metastasis rate and no obvious symptoms. Gemcitabine is a first-line chemotherapeutic drug for PC. Since there is no distinct method to determine the efficacy of chemotherapy with gemcitabine in patients with PC, the purpose of the present study was to determine whether positivity for circulating tumor cells (CTCs) in patients with advanced PC is associated with response to gemcitabine chemotherapy and to explore whether CTCs may be used as a predictor of prognosis of patients with advanced PC undergoing chemotherapy. First, immunomagnetic microspheres (magnetic beads; MIL) were prepared to detect CTCs. The patients' clinical characteristics and survival data, as well as efficacy and adverse effects of chemotherapy, were prospectively obtained and their association with CTCs was analyzed. The results indicated that CTC-positive patients with advanced PC had a higher probability of developing resistance to gemcitabine chemotherapy than CTC-negative patients. Survival in the CTC-negative group was significantly higher than in the CTC-positive group (χ2=14.58, P<0.001). CTC-positive patients with advanced PC also had shorter progression-free survival (PFS) after chemotherapy with gemcitabine (P=0.01). In conclusion, CTC-positive patients with PC are more likely to develop gemcitabine resistance, have poor PFS and low incidence of thrombocytopenia. CTCs are expected to become a prognostic indicator for chemotherapy response in patients with PC.
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A quartz crystal resonator (QCR) is an indispensable electronic component in the field of the modern electronics industry. By designing and depositing electrodes of different shapes and thicknesses on a quartz wafer with a certain fundamental frequency, the desired target frequency can be obtained. Affected by factors such as the deposition equipment, mask, wafer size and placement position, it is difficult to accurately obtain the target frequency at a given time, especially for mass-produced QCRs. In this work, a laser with a wavelength of 532 nm was used to thin the electrodes of a QCR with a fundamental frequency of 10 MHz. The electrode surface was etched through a preset processing pattern to form a processing method of local thinning of the electrode surface. At the same time, the effect of laser etching on silicon dioxide and resonator performance was analyzed. Satisfactory trimming frequency-increasing results were achieved, such as a frequency modulation accuracy of 1 ppm, frequency distribution with good consistency and equivalent parameters with small changes, by the laser partial etching of the resonator electrode. However, when the surface electrode was etched into using through-holes, the attenuation amplitude of the equivalent parameter became larger, especially in terms of the quality factor (Q), which decreased from 63 K to 1 K, and some resonators which had a serious frequency drift of >40%. In this case, a certain number of QCRs were no longer excited to vibrate, which was due to the disappearance of the piezoelectric effect caused by the local thermal phase change in the quartz wafer.
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Pancreatic cancer (PAAD) is a common malignancy with a poor survival rate. The identification of novel biomarkers could improve clinical outcomes for patients with PAAD. Here we evaluated the expression and clinical significance of PPP1CB in PAAD. PPP1CB expression was higher in PAAD tissue than in matched paracancerous tissue (P < 0.05). We predicted a network of regulatory targets and protein interaction partners of PPP1CB, and identified a PPI network consisting of 39 node genes. The expression of 33 node genes was higher in PAAD tissue than in matching paracancerous tissue. High expression of the node genes ACTN4, ANLN, CLTB, IQGAP1, SPTAN1, and TMOD3 was associated with improved overall survival (P < 0.05). SiRNA knockdown of PPP1CB significantly reduced the migration and invasion of PAAD cells. A PPP1CB immunohistochemical staining was performed using a tissue microarray (TMA), consisting of tumor samples collected from 91 patients with PAAD (88 of which contained matched paracancerous tissues). The expression of PPP1CB in PAAD was significantly higher than in the matched paracancerous tissue, (P = 0.016). High PPP1CB expression was associated with patient sex (P = 0.048), alcohol use (P = 0.039), CEA (P= 0.038), N stage (P = 0.001), and invasion of nerve (P = 0.036). Furthermore, high PPP1CB expression was associated with significantly poorer overall survival (P = 0.022). Our data demonstrate that PPP1CB is associated with the migration and invasion of PAAD cells, and may be useful as an independent prognostic indicator for clinical outcome in patients with PAAD.
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Neoplasias Pancreáticas , Proteína Fosfatasa 1/genética , Biomarcadores de Tumor/genética , Biomarcadores de Tumor/metabolismo , Biología Computacional , Femenino , Humanos , Masculino , Persona de Mediana Edad , Neoplasias Pancreáticas/diagnóstico , Neoplasias Pancreáticas/genética , Neoplasias Pancreáticas/metabolismo , Neoplasias Pancreáticas/mortalidad , Pronóstico , Proteína Fosfatasa 1/metabolismo , Transcriptoma/genéticaRESUMEN
BACKGROUND: Spontaneous bladder rupture is relatively rare, and common causes of spontaneous bladder rupture include bladder diverticulum, neurogenic bladder dysfunction, gonorrhea infection, pelvic radiotherapy, etc. Urinary bladder perforation caused by urinary catheterization mostly occurs during the intubation process. CASE SUMMARY: Here, we describe an 83-year-old male who was admitted with 26 h of middle and upper abdominal pain and a history of long-term catheterization. Physical examination and computed tomography of the abdomen supported the diagnosis of diffuse peritonitis, most likely from a perforated digestive tract organ. Laparoscopic exploration revealed a possible digestive tract perforation. Finally, a perforation of approximately 5 mm in diameter was found in the bladder wall during laparotomy. After reviewing the patient's previous medical records, we found that 1 year prior the patient underwent an ultrasound examination showing that the end of the catheter was embedded into the mucosal layer of the bladder. Therefore, the bladder perforation in this patient may have been caused by the chronic compression of the urinary catheter against the bladder wall. CONCLUSION: For patients with long-term indwelling catheters, there is a possibility of bladder perforation, which needs to be dealt with quickly.
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Pancreatic adenocarcinoma (PAAD) is a common and highly malignant tumor. The identification of prognostic biomarkers for PAAD could provide invaluable information for clinical treatment. AMPactivated protein kinase family member 5 (ARK5) is a member of the AMPK family that mediates the migration of PAAD cells. In the present study, ARK5 expression was evaluated using bioinformatics analysis in public datasets from The Cancer Genome Atlas. The expression levels of ARK5 in PAAD tumor tissue were significantly increased, compared with matched noncancerous tissues. ARK5 target genes were then predicted and Gene Ontology Biological Processes, Kyoto Encyclopedia of Genes and Genomes pathway analysis and Reactome gene sets were used to determine the functions associated with the target genes. A proteinprotein interaction network was also constructed to find out the node genes and observe their association with the overall survival rate of PAAD. A total of nine node genes were identified in the PPI network, of which six were significantly upregulated in PAAD tissue, compared with matched normal tissue. The prognostic value of each node gene was evaluated by comparing the overall survival in patients with PAAD stratified according to the expression levels of these genes. Overall survival was significantly reduced in patients with high pololike kinase1 (PLK1) or protein phosphatase 1 catalytic subunit ß (PPP1CB) expression, compared with patients with low expression of these genes. To further evaluate the relationship between PAAD and ARK5, ARK5 immunohistochemical staining was performed in a tissue microarray consisting of 112 tumor samples from patients with PAAD and adjacent normal tissue samples. ARK5 protein expression in PAAD tissue was markedly increased, compared with noncancerous tissue (P=7.631x1011). Moreover, ARK5 protein levels were associated with N stage (P=0.018). The overall survival of patients with PAAD with high ARK5 protein expression levels was reduced (P=0.014), compared with patients with low expression. In conclusion, these findings suggested that ARK5 may represent an independent prognostic indicator of PAAD.
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Adenocarcinoma/patología , Biomarcadores de Tumor/genética , Biomarcadores de Tumor/metabolismo , Neoplasias Pancreáticas/patología , Proteínas Quinasas/genética , Proteínas Quinasas/metabolismo , Proteínas Represoras/genética , Proteínas Represoras/metabolismo , Adenocarcinoma/genética , Adenocarcinoma/metabolismo , Femenino , Perfilación de la Expresión Génica , Regulación Neoplásica de la Expresión Génica , Ontología de Genes , Redes Reguladoras de Genes , Humanos , Masculino , Estadificación de Neoplasias , Neoplasias Pancreáticas/genética , Neoplasias Pancreáticas/metabolismo , Pronóstico , Mapas de Interacción de Proteínas , Análisis de Supervivencia , Análisis de Matrices Tisulares , Regulación hacia ArribaRESUMEN
Immunotherapy based on the tumor microenvironment is a feasible method for treating cancer; therefore, it is necessary to investigate the immune microenvironment of pancreatic cancer and the influencing factors of the immune microenvironment. Chemokines are an important factor affecting the tumor immune microenvironment. In the present study, chemokines or chemokine receptors were screened to identify those differentially expressed in pancreatic cancer compared with normal controls and associated with patient prognosis. Chemokines or chemokine receptors that are differentially expressed in pancreatic cancer tumor tissues were initially screened using the Gene Expression Omnibus database. Next, survival analysis was performed using GEPIA, a website based on The Cancer Genome Atlas (TCGA) database. Immunohistochemical staining of CXCL5 was performed in tissue microarrays (TMAs) containing 119 cases of pancreatic cancer. Histochemistry score (H-SCORE) was used to evaluate the expression of CXCL5. Next, association analysis of the H-SCORE of CXCL5 and the clinical characteristics of patients was performed, as well as Kaplan-Meier survival and Cox multivariate regression analyses. The results of the bioinformatics analysis demonstrated that CXCL5 was highly expressed in pancreatic cancer tissues. High expression of CXCL5 in pancreatic cancer tissues was associated with a poor prognosis in patients in TCGA cohort. The expression level of CXCL5 in tumor tissues was significantly higher compared with that in adjacent peritumoral normal tissues in the immunohistochemical analysis. There was no significant association between CXCL5 expression in pancreatic cancer tumor tissues and clinicopathological factors. Patients with pancreatic cancer with high CXCL5 expression had a poor prognosis, as determined by Kaplan-Meier survival analysis based on the TMA dataset. The results of Cox multivariate regression analysis showed that CXCL5 was an independent factor for a poor prognosis in patients with pancreatic cancer. In conclusion, the results of the present study revealed that the chemokine CXCL5 was highly expressed in pancreatic cancer tissues; high CXCL5 expression was associated with a poor prognosis in patients with pancreatic cancer.
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Proper vacancy engineering is considered as a promising strategy to improve intrinsic activity, but it is challenging to construct rich vacancies by a simple strategy. Herein, Fe doped Ni5P4 nanosheet arrays with rich P vacancies are developed via a facile phase transformation strategy. Based on systematic investigations, we have demonstrated that an optimized surface electronic structure, abundant active sites and improved charge transport capability can be effectively achieved by vacancy engineering. Consequently, Fe doped Ni5P4 with rich vacancies show remarkable catalytic performances with 94.5 mV for the hydrogen evolution reaction (HER) and 217.3 mV for the oxygen evolution reaction (OER) at 10 mA cm-2, respectively, as well as good durability. When directly employed as working electrodes, the as-obtained Fe doped Ni5P4 with rich vacancies can attain 10 mA cm-2 at a low voltage of 1.59 V. This work demonstrates a feasible strategy for rationally fabricating electrocatalysts with rich vacancies via a simple phase transformation.
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Owing to low-cost and 3d electronic configurations, Co3O4 material is considered as promising candidate for oxygen evolution reaction (OER) electrocatalyst, but the intrinsically low conductivity and limited active site exposure greatly limit the electrocatalytic performances, Herein, we successfully achieve modulation of Co3O4 arrays by Mn and S dual-doping for OER. Results demonstrate that Mn doping modifies the electronic structure of Co center to boost the intrinsic activity of active site in Co3O4, while inducing S in Co3O4 increases the electrical conductivity and provides ample S sites for proton adsorption. In addition, Mn and S dual-doping effectively increase the proportion of Co3+, resulting in facilitating the four-electron transfer and thus higher electrochemical activities. Consequently, the optimal Mn and S dual-doping Co3O4 presents low overpotentials of 330, 407 and 460â¯mV at 10, 100 and 300â¯mAâ¯cm-2 for OER, as well as a low Tafel slope of 68â¯mVâ¯dec-1 and a good durability after 20â¯h. Current work highlights a feasible strategy to design electrocatalysts via dual-doping and maximizing the high-valence transition metal ions.
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Designing and constructing bifunctional electrocatalysts is vital for water splitting. Particularly, the rational interface engineering can effectively modify the active sites and promote the electronic transfer, leading to the improved splitting efficiency. Herein, free-standing and defect-rich heterogeneous MoS2/NiS2 nanosheets for overall water splitting are designed. The abundant heterogeneous interfaces in MoS2/NiS2 can not only provide rich electroactive sites but also facilitate the electron transfer, which further cooperate synergistically toward electrocatalytic reactions. Consequently, the optimal MoS2/NiS2 nanosheets show the enhanced electrocatalytic performances as bifunctional electrocatalysts for overall water splitting. This study may open up a new route for rationally constructing heterogeneous interfaces to maximize their electrochemical performances, which may help to accelerate the development of nonprecious electrocatalysts for overall water splitting.
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Constructing heterointerfaces in heterostructures could effectively enlarge the electroactive sites and enhance the interfacial charge transfer, and thus improve the electrocatalytic performances. Herein, free-standing porous Ni2P-Ni5P4 heterostructured arrays are successfully prepared through in situ phosphating Ni(OH)2 arrays by simply tuning the reaction temperatures. Contributing from the interfacial coupling effects of two phases, large surface areas, highly conductive support of carbon cloth substrates and unique free-standing arrays, Ni2P-Ni5P4 heterostructured arrays show the enhanced kinetics and electrocatalytic performances for the hydrogen evolution reaction, oxygen evolution reaction and overall water splitting. Our research might offer insight into constructing heterophase junctions for efficient overall water splitting.
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Rational design of efficient bifunctional electrocatalysts is highly imperative but still a challenge for overall water splitting. Herein, we construct novel freestanding Mo-doped NiCoP nanosheet arrays by the hydrothermal and phosphation processes, serving as bifunctional electrocatalysts for overall water splitting. Notably, Mo doping could effectively modulate the electronic structure of NiCoP, leading to the increased electroactive site and improved intrinsic activity of each site. Furthermore, an electrochemical activation strategy is proposed to form Mo-doped (Ni,Co)OOH to fully boost the electrocatalytic activities for oxygen evolution reaction. Benefiting from the unique freestanding structure and Mo doping, Mo-doped NiCoP and (Ni,Co)OOH show the remarkable electrochemical performances, which are competitive among current researches. In addition, an overall water splitting device assembled by both electrodes only requires a cell voltage of 1.61 V to reach a current density of 10 mA cm-2. Therefore, this work opens up new avenues for designing nonprecious bifunctional electrocatalysts by Mo doping and in situ electrochemical activation.
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Herein, we successfully design and construct core-shell nanostructured NiCo2S4@Ni3S2 directly on Ni foam by a scalable and effective one-step strategy. Further, through simply and accurately controlling the concentration of sulfur source, various nanostructures of NiCo2S4@Ni3S2 arrays in situ on Ni foam are successfully synthesized. The intriguing core-shell structures and integrated electrode configurations endow NiCo2S4@Ni3S2 electrode a large electroactive sites, fast electron transport path and sufficient contacts with electrolyte. Serving as free-standing electrode, as-fabricated NiCo2S4@Ni3S2 arrays exhibit the high specific capacity (4.55â¯Câ¯cm-2 at 5â¯mAâ¯cm-2), good rate performance and good cycling stability. Impressively, current research provides a general, scalable and effective one-step strategy for constructing core-shell nanostructures for energy storage devices.
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A growing body of evidence confirms that long noncoding RNAs (lncRNAs) have an important role in biological processes by regulating gene expression at multiple levels. Dysregulated lncRNAs may be potential prognostic biomarkers or targets for the development of cancer treatments. However, the prognostic role of an lncRNA signature in pancreatic cancer has not been investigated. Pancreatic cancer lncRNA expression profiles from The Cancer Genome Atlas (TCGA) were analyzed in the current study. The prognostic value of differentially expressed lncRNAs (DElncRNAs) was evaluated via the KaplanMeier method. A risk score model was established based on the potential prognostic lncRNAs. The biological functions of lncRNAs were predicted by functional enrichment analysis. Then, an lncRNAmRNA coexpression network was established and predicted the function of the lncRNAs. Seven DElncRNAs that were significantly associated with the prognosis of pancreatic cancer were identified. Patients were classified into highrisk and lowrisk groups using a risk score based on a threelncRNA signature. There was a significant difference in overall survival (OS) between the groups (median OS 1.33 vs. 3.65 years; logrank test, P=0.0000). Cox regression analysis and ROC curves demonstrated that the threelncRNA signature may be an effective independent prognostic biomarker in patients with pancreatic. The functional enrichment analysis showed that lncRNA AL137789.1, one component of the threelncRNA signature, may be associated with tumor immune responses. In the present study, a novel threelncRNA signature that was established that may be useful in predicting survival among patients with pancreatic cancer. These lncRNAs may be involved in tumor immunity and thus affect the prognosis of patients.
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Biomarcadores de Tumor/metabolismo , Regulación Neoplásica de la Expresión Génica/inmunología , Neoplasias Pancreáticas/genética , Neoplasias Pancreáticas/mortalidad , ARN Largo no Codificante/metabolismo , Biomarcadores de Tumor/genética , Biomarcadores de Tumor/inmunología , Conjuntos de Datos como Asunto , Femenino , Perfilación de la Expresión Génica , Humanos , Estimación de Kaplan-Meier , Masculino , Persona de Mediana Edad , Neoplasias Pancreáticas/inmunología , Pronóstico , ARN Largo no Codificante/genética , ARN Largo no Codificante/inmunología , Curva ROCRESUMEN
BACKGROUND The aim of this study was to explore the risk factors for post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis and investigate the effect of octreotide combined with nonsteroidal anti-inflammatory drugs on preventing its occurrence. MATERIAL AND METHODS A total of 139 patients undergoing ERCP in our hospital from May 2016 to April 2017 were retrospectively analyzed, and divided into an observation group (n=67) (octreotide + indomethacin) and a control group (n=72) (no preventive drugs). The preoperative and postoperative inflammatory cytokines such as tumor necrosis factor-α (TNF)-α, interleukin-6 (IL-6) and IL-8, and serum amylase levels were measured, and the incidence of pancreatitis and hyper amylasemia were monitored. RESULTS Serum amylase level was increased significantly 3 hours after operation in both groups with significantly higher level in the control group compared to the observation group. After 24 hours, serum amylase in the observation group was decreased to preoperative level, whereas it was still higher than preoperative in the control group (P<0.05). Regarding the levels of TNF-α, IL-6, IL-8, and visual analogue scale, they were significantly increased in both groups after operation with significantly higher levels in the control group compared to the observation group (P<0.05). Furthermore, logistic regression analysis showed that difficult intubation, pancreatic duct angiography, surgery for a long time, and the history of previous pancreatitis were risk factors for post-ERCP pancreatitis (P<0.05). CONCLUSIONS Difficult intubation, pancreatic duct angiography, surgery for a long time, and the history of previous pancreatitis were risk factors for post-ERCP pancreatitis. Octreotide combined with non-steroidal anti-inflammatory drugs can reduce the pain of patients with abdominal pain as well as the incidence of postoperative pancreatitis, indicating that they might be effective preventative approaches for pancreatitis.
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Colangiopancreatografia Retrógrada Endoscópica/efectos adversos , Octreótido/uso terapéutico , Pancreatitis/prevención & control , Dolor Abdominal/etiología , Adulto , Anciano , Amilasas/sangre , Antiinflamatorios no Esteroideos/uso terapéutico , China , Quimioterapia Combinada/métodos , Femenino , Humanos , Indometacina/farmacología , Indometacina/uso terapéutico , Interleucina-6/sangre , Interleucina-8/sangre , Masculino , Persona de Mediana Edad , Octreótido/farmacología , Estudios Retrospectivos , Factores de Riesgo , Factor de Necrosis Tumoral alfa/sangreRESUMEN
Yes-associated protein (YAP) serves an essential role in tumorigenesis. However, the potential role and the molecular mechanism underlying the effect of YAP on hepatocellular carcinoma (HCC) cells have not been elucidated. In the current study, it was revealed that YAP expression was increased significantly in HCC cancer tissues and its overexpression was associated with tumor differentiation. The silencing of YAP by small interferring RNA led to the inhibition of HCC cell growth, which was associated with the promotion of apoptosis. The silencing of YAP also decreased the invasive potential of HCC cells and the activity of the phosphoinositide 3-kinase (PI3K)/AKT serine/threonine kinase (AKT) signaling pathway. Furthermore, silencing of YAP increased the chemosensitivity of HCC cells to cisplatin (CDDP) through inactivation of the PI3K/AKT signaling pathway. In vivo studies using PDTX model suggested a promotive role for YAP in the growth of HCC and knockdown of YAP increased the anti-tumor activity of CDDP. Taken together, these results revealed that YAP is overexpressed in HCC, and promotes proliferation, invasion and drug resistance of HCC cells. Inhibition of YAP, alone or in combination with traditional chemotherapy, may effectively combat HCC.