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Search Results: 1 - 10 of 120180 matches for " Junru Wang "
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The Research on the Methods of Diagnosing the Steam Turbine Based on the Elman Neural Network  [PDF]
Junru Gao, Yuqing Wang
Journal of Software Engineering and Applications (JSEA) , 2013, DOI: 10.4236/jsea.2013.63B019
Abstract: This paper introduces a kind of diagnosis principle and learning algorithm of steam turbine fault diagnosis which based on Elman neural network. Comparing the results of the Elman neural network and the traditional BP neural network diagnosis, the results shows that Elman neural network is an effective way to improve the learning speed , effectively suppress the minimum defects that the traditional neural network easily trapped in, and shorten the autonomous learning time. All these proves that the Elman neural network is an effective way to diagnose the steam turbine.
Evaluating on Performance of Single-source Single-relay Sr-carq protocol in Tdma Networks with Raleigh Fading
Suoping Li,Junru Wang,Yongqiang Zhou
International Journal of Computer Science Issues , 2012,
Abstract: This paper analyzes the performance of single-source and single-relay SR-CARQ protocol in TDMA wireless communication system. We establish its M/G/1 queuing model with vacations, and provide the expressions of its system time delay and saturation throughput. Then the analysis of theory and simulation results under the slow Raleigh fading channel show that under what conditions the SR-CARQ protocol is superior to its non-cooperative counterpart.
Spiro[cyclopropane-1,3′-indolin]-2′-one
Maosen Yuan,Qi Wang,Yuejun Zhang,Junru Wang
Acta Crystallographica Section E , 2011, DOI: 10.1107/s1600536811034167
Abstract: In the title molecule, C10H9NO, the dihedral angle between the mean plane of the cyclopropane ring and the essentially planar [maximum deviation = 0.032 (2) ] indole ring system is 87.65 (17)°. In the crystal, intermolecular N—H...O hydrogen bonds link molecules into one-dimensional chains along [100].
Global Transcriptome Profiling of Salicornia europaea L. Shoots under NaCl Treatment
Jinbiao Ma, Meiru Zhang, Xinlong Xiao, Jinjin You, Junru Wang, Tao Wang, Yinan Yao, Changyan Tian
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0065877
Abstract: Background Soil salinity is a major abiotic stress that limits agriculture productivity worldwide. Salicornia europaea is well adapted to extreme saline environments with more than 1,000 mM NaCl in the soil, so it could serve as an important model species for studying halophilic mechanisms in euhalophytes. To obtain insights into the molecular basis of salt tolerance, we present here the first extensive transcriptome analysis of this species using the Illumina HiSeq? 2000. Principal Findings A total of 41 and 39 million clean reads from the salt-treated (Se200S) and salt-free (SeCKS) tissues of S. europaea shoots were obtained, and de novo assembly produced 97,865 and 101,751 unigenes, respectively. Upon further assembly with EST data from both Se200S and SeCKS, 109,712 high-quality non-redundant unigenes were generated with a mean unigene size of 639 bp. Additionally, a total of 3,979 differentially expressed genes (DEGs) were detected between the Se200S and SeCKS libraries, with 348 unigenes solely expressed in Se200S and 460 unigenes solely expressed in SeCKS. Furthermore, we identified a large number of genes that are involved in ion homeostasis and osmotic adjustment, including cation transporters and proteins for the synthesis of low-molecular compounds. All unigenes were functionally annotated within the COG, GO and KEGG pathways, and 10 genes were validated by qRT-PCR. Conclusion Our data contains the extensive sequencing and gene-annotation analysis of S. europaea. This genetic knowledge will be very useful for future studies on the molecular adaptation to abiotic stress in euhalophytes and will facilitate the genetic manipulation of other economically important crops.
Pharmacological Induction of Transforming Growth Factor-Beta1 in Rat Models Enhances Radiation Injury in the Intestine and the Heart
Marjan Boerma, Junru Wang, Vijayalakshmi Sridharan, Jean-Marc Herbert, Martin Hauer-Jensen
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0070479
Abstract: Radiation therapy in the treatment of cancer is dose limited by radiation injury in normal tissues such as the intestine and the heart. To identify the mechanistic involvement of transforming growth factor-beta 1 (TGF-β1) in intestinal and cardiac radiation injury, we studied the influence of pharmacological induction of TGF-β1 with xaliproden (SR 57746A) in rat models of radiation enteropathy and radiation-induced heart disease (RIHD). Because it was uncertain to what extent TGF-β induction may enhance radiation injury in heart and intestine, animals were exposed to irradiation schedules that cause mild to moderate (acute) radiation injury. In the radiation enteropathy model, male Sprague-Dawley rats received local irradiation of a 4-cm loop of rat ileum with 7 once-daily fractions of 5.6 Gy, and intestinal injury was assessed at 2 weeks and 12 weeks after irradiation. In the RIHD model, male Sprague-Dawley rats received local heart irradiation with a single dose of 18 Gy and were followed for 6 months after irradiation. Rats were treated orally with xaliproden starting 3 days before irradiation until the end of the experiments. Treatment with xaliproden increased circulating TGF-β1 levels by 300% and significantly induced expression of TGF-β1 and TGF-β1 target genes in the irradiated intestine and heart. Various radiation-induced structural changes in the intestine at 2 and 12 weeks were significantly enhanced with TGF-β1 induction. Similarly, in the RIHD model induction of TGF-β1 augmented radiation-induced changes in cardiac function and myocardial fibrosis. These results lend further support for the direct involvement of TGF-β1 in biological mechanisms of radiation-induced adverse remodeling in the intestine and the heart.
An In Vivo Study of the Effects on Serum Glucose, Amylase and Histopathology of the Feline Pancreatic Tissue Treated by Focused Ultrasound
Ying Mao, Liaoqiong Fang, Liang Ai, Chongyan Li, Zhibiao Wang, Junru Wu, Jin Bai, Faqi Li
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0088815
Abstract: Pancreatic cancer is one of the most malignant neoplasms originating in the digestive system. Focused ultrasound (FUS) treatment instead of the surgery operation has been used to treat Pancreatic cancer noninvasively in clinical trials. The endocrine and exocrine glands in pancreas provide the two unique functions for a person to be healthy. It is critically important to find out if the FUS treatment can still keep the normal functions of the two glands. The goal of this study is to examine and analyze changes in histopathology and serum glucose and amylase levels of the targeted in-vivo felines after the FUS treatment. Various percentage volumes of pancreas of felines were insonified. The FUS treatment (7.5 MHz of central frequency; 5 W of acoustical power; transducer f-number = 0.33; 6 s insonification time per point) effectively generated coagulative necrosis at the insonified site while leaving tissue outside the insonified site intact. It was also observed that all felines endured well with the FUS treatment; changes introduced to pancreatic tissue after up to 50% of a pancreas by volume was insonified by the FUS procedure did not affect its normal endocrine and exocrine functions.
Laser Capture Microdissected Mucosa versus Whole Tissue Specimens for Assessment of Radiation-Induced Dynamic Molecular and Pathway Changes in the Small Intestine
Junying Zheng, Sarita Garg, Junru Wang, David S. Loose, Martin Hauer-Jensen
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0053711
Abstract: Background The intestinal mucosa is the compartment that sustains the most severe injury in response to radiation and is therefore of primary interest. The use of whole gut extracts for analysis of gene expression may confound important changes in the mucosa. On the other hand, laser capture microdissection (LCM) is hampered by the unstable nature of RNA and by a more complicated collection process. This study assessed, in parallel samples from a validated radiation model, the indications for use of LCM for intestinal gene expression analysis. Methodology/Principal Findings RNA was extracted from mouse whole intestine and from mucosa by LCM at baseline and 4 h, 24 h, and 3.5 d after total body irradiation and subjected to microarray analysis. Among mucosal genes that were altered > = 2-fold, less than 7% were present in the whole gut at 4 and 24 h, and 25% at 3.5 d. As expected, pathway analysis of mucosal LCM samples showed that radiation activated the coagulation system, lymphocyte apoptosis, and tight junction signaling, and caused extensive up-regulation of cell cycle and DNA damage repair pathways. Using similar stringent criteria, regulation of these pathways, with exception of the p53 pathway, was undetectable in the whole gut. Radiation induced a dramatic increase of caspase14 and ectodysplasin A2 receptor (Eda2r), a TNFα receptor, in both types of samples. Conclusions/Significance LCM-isolated mucosal specimens should be used to study cellular injury, cell cycle control, and DNA damage repair pathways. The remarkable increase of caspase14 and Eda2r suggests a novel role for these genes in regulating intestinal radiation injury. Comparative gene expression data from complex tissues should be interpreted with caution.
IKKβ Regulates the Repair of DNA Double-Strand Breaks Induced by Ionizing Radiation in MCF-7 Breast Cancer Cells
Lixian Wu,Lijian Shao,Ningfei An,Junru Wang,Senthil Pazhanisamy,Wei Feng,Martin Hauer-Jensen,Shigeki Miyamoto,Daohong Zhou
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0018447
Abstract: Activation of the IKK-NFκB pathway increases the resistance of cancer cells to ionizing radiation (IR). This effect has been largely attributed to the induction of anti-apoptotic proteins by NFκB. Since efficient repair of DNA double strand breaks (DSBs) is required for the clonogenic survival of irradiated cells, we investigated if activation of the IKK-NFκB pathway also regulates DSB repair to promote cell survival after IR. We found that inhibition of the IKK-NFκB pathway with a specific IKKβ inhibitor significantly reduced the repair of IR-induced DSBs in MCF-7 cells. The repair of DSBs was also significantly inhibited by silencing IKKβ expression with IKKβ shRNA. However, down-regulation of IKKα expression with IKKα shRNA had no significant effect on the repair of IR-induced DSBs. Similar findings were also observed in IKKα and/or IKKβ knockout mouse embryonic fibroblasts (MEFs). More importantly, inhibition of IKKβ with an inhibitor or down-regulation of IKKβ with IKKβ shRNA sensitized MCF-7 cells to IR-induced clonogenic cell death. DSB repair function and resistance to IR were completely restored by IKKβ reconstitution in IKKβ-knockdown MCF-7 cells. These findings demonstrate that IKKβ can regulate the repair of DSBs, a previously undescribed and important IKKβ kinase function; and inhibition of DSB repair may contribute to cance cell radiosensitization induced by IKKβ inhibition. As such, specific inhibition of IKKβ may represents a more effective approach to sensitize cancer cells to radiotherapy.
A Novel Cationic Microbubble Coated with Stearic Acid-Modified Polyethylenimine to Enhance DNA Loading and Gene Delivery by Ultrasound
Qiaofeng Jin, Zhiyong Wang, Fei Yan, Zhiting Deng, Fei Ni, Junru Wu, Robin Shandas, Xin Liu, Hairong Zheng
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0076544
Abstract: A novel cationic microbubble (MB) for improvement of the DNA loading capacity and the ultrasound-mediated gene delivery efficiency has been developed; it has been prepared with commercial lipids and a stearic acid modified polyethylenimine 600 (Stearic-PEI600) polymer synthesized via acylation reaction of branched PEI600 and stearic acid mediated by N, N'-carbonyldiimidazole (CDI). The MBs’ concentration, size distribution, stability and zeta potential (ζ-potential) were measured and the DNA loading capacity was examined as a function of the amount of Stearic-PEI600. The gene transfection efficiency and cytotoxicity were also examined using breast cancer MCF-7 cells via the reporter plasmid pCMV-Luc, encoding the firefly luciferase gene. The results showed that the Stearic-PEI600 polymer caused a significant increase in magnitude of ζ-potential of MBs. The addition of DNA into cationic MBs can shift ζ-potentials from positive to negative values. The DNA loading capacity of the MBs grew linearly from (5±0.2) ×10?3 pg/μm2 to (20±1.8) ×10?3 pg/μm2 when Stearic-PEI600 was increased from 5 mol% to 30 mol%. Transfection of MCF-7 cells using 5% PEI600 MBs plus ultrasound exposure yielded 5.76±2.58×103 p/s/cm2/sr average radiance intensity, was 8.97- and 7.53-fold higher than those treated with plain MBs plus ultrasound (6.41±5.82) ×102 p/s/cm2/sr, (P<0.01) and PEI600 MBs without ultrasound (7.65±6.18) ×102 p/s/cm2/sr, (P<0.01), respectively. However, the PEI600 MBs showed slightly higher cytotoxicity than plain MBs. The cells treated with PEI600-MBs and plain MBs plus ultrasound showed 59.5±6.1% and 71.4±7.1% cell viability, respectively. In conclusion, our study demonstrated that the novel cationic MBs were able to increase DNA loading capacity and gene transfection efficiency and could be potentially applied in targeted gene delivery and therapy.
C/EBPδ Deficiency Sensitizes Mice to Ionizing Radiation-Induced Hematopoietic and Intestinal Injury
Snehalata A. Pawar, Lijian Shao, Jianhui Chang, Wenze Wang, Rupak Pathak, Xiaoyan Zhu, Junru Wang, Howard Hendrickson, Marjan Boerma, Esta Sterneck, Daohong Zhou, Martin Hauer-Jensen
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0094967
Abstract: Knowledge of the mechanisms involved in the radiation response is critical for developing interventions to mitigate radiation-induced injury to normal tissues. Exposure to radiation leads to increased oxidative stress, DNA-damage, genomic instability and inflammation. The transcription factor CCAAT/enhancer binding protein delta (Cebpd; C/EBPδ is implicated in regulation of these same processes, but its role in radiation response is not known. We investigated the role of C/EBPδ in radiation-induced hematopoietic and intestinal injury using a Cebpd knockout mouse model. Cebpd?/? mice showed increased lethality at 7.4 and 8.5 Gy total-body irradiation (TBI), compared to Cebpd+/+ mice. Two weeks after a 6 Gy dose of TBI, Cebpd?/? mice showed decreased recovery of white blood cells, neutrophils, platelets, myeloid cells and bone marrow mononuclear cells, decreased colony-forming ability of bone marrow progenitor cells, and increased apoptosis of hematopoietic progenitor and stem cells compared to Cebpd+/+ controls. Cebpd?/? mice exhibited a significant dose-dependent decrease in intestinal crypt survival and in plasma citrulline levels compared to Cebpd+/+ mice after exposure to radiation. This was accompanied by significantly decreased expression of γ-H2AX in Cebpd?/? intestinal crypts and villi at 1 h post-TBI, increased mitotic index at 24 h post-TBI, and increase in apoptosis in intestinal crypts and stromal cells of Cebpd?/? compared to Cebpd+/+ mice at 4 h post-irradiation. This study uncovers a novel biological function for C/EBPδ in promoting the response to radiation-induced DNA-damage and in protecting hematopoietic and intestinal tissues from radiation-induced injury.
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