The Butterfly Effect on the Agricultural Bank System at the Grass-Roots Level

The competition power of the Agricultural Bank of China has been dropping down for several years. The reason is that banks at the grass-roots level don’t think much of managing the subtle links. The paper uses the theory of butterfly effect in Chaos for reference to discusses the risks existed in the Agricultural Bank of China at the grass-roots level such as the credit risk, the incomplete internal control, the loose accounting system, the disorder market competitiveness, the brain drain, the weak service consciousness, the financial innovation lag and the unbalanced development. Finally eight pieces of advice are brought forward as the measures against the eight butterfly effects.the butterfly effect, the chaos, the Duffing-Holmes model, the agricultural bank system at the grass-roots level

Lymphotoxin-α Plays Only a Minor Role in Host Resistance to Respiratory Infection with Virulent Type A Francisella tularensis in Mice

This study examined the role of lymphotoxin (LT)-α in host defense against airborne infection with Francisella tularensis, a gram-negative facultative intracellular bacterium and the causative agent of tularemia. Following a low-dose aerosol infection with the highly virulent type A strain of F. tularensis, mice deficient in LTα (LTα−/−) consistently harbored approximately 10-fold fewer bacteria in their spleens at day 2 and 10-fold more bacteria in their lungs at day 4 than LTα+/+ mice. However, the mortality and median time to death were indistinguishable between the two mouse strains. In addition, the inflammatory responses to the infection, as reflected by the cytokine levels and leukocyte influx in the bronchoalveolar lavage fluid and histopathological analysis, were generally similar between LTα−/− and LTα+/+ mice. These data suggest that although LTα does not contribute significantly to the resistance and host responses of mice to airborne type A F. tularensis infection, it does play a subtle role in the multiplication/dissemination of F. tularensis

The influence of X-factor (trunk rotation) and experience on the quality of the badminton forehand smash

Sherpa Romeo green journal. Open access article. Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License 9CC BY-NC-ND 3.0) appliesNo existing studies of badminton technique have used full-body biomechanical modeling based on three dimensional (3D) motion capture to quantify the kinematics of the sport. The purposes of the current study were to: 1) quantitatively describe kinematic characteristics of the forehand smash using a 15-segment, full-body biomechanical model, 2) examine and compare kinematic differences between novice and skilled players with a focus on trunk rotation (the X-factor), and 3) through this comparison, identify principal parameters that contributed to the quality of the skill. Together, these findings have the potential to assist coaches and players in the teaching and learning of the forehand smash. Twenty-four participants were divided into two groups (novice, n = 10 and skilled, n = 14). A 10-camera VICON MX40 motion capture system (200 frames/s) was used to quantify full-body kinematics, racket movement and the flight of the shuttlecock. Results confirmed that skilled players utilized more trunk rotation than novices. In two ways, trunk rotation (the X-factor) was shown to be vital for maximizing the release speed of the shuttlecock – an important measure of the quality of the forehand smash. First, more trunk rotation invoked greater lengthening in the pectoralis major (PM) during the preparation phase of the stroke which helped generate an explosive muscle contraction. Second, larger range of motion (ROM) induced by trunk rotation facilitated a whip-like (proximal to distal) control sequence among the body segments responsible for increasing racket speed. These results suggest that training intended to increase the efficacy of this skill needs to focus on how the X-factor is incorporated into the kinematic chain of the arm and the racket.Ye

Research of the mechanism on miRNA193 in exosomes promotes cisplatin resistance in esophageal cancer cells.

PURPOSE:Chemotherapy resistance of esophageal cancer is a key factor affecting the postoperative treatment of esophageal cancer. Among the media that transmit signals between cells, the exosomes secreted by tumor cells mediate information transmission between tumor cells, which can make sensitive cells obtain resistance. Although some cellular exosomes play an important role in tumor's acquired drug resistance, the related action mechanism is still not explored specifically. METHODS:To elucidate this process, we constructed a cisplatin-resistant esophageal cancer cell line, and proved that exosomes conferring cellular resistance in esophageal cancer can promote cisplatin resistance in sensitive cells. Through high-throughput sequencing analysis of the exosome and of cells after stimulation by exosomes, we determined that the miRNA193 in exosomes conferring cellular resistance played a key role in sensitive cells acquiring resistance to cisplatin. In vitro experiments showed that miRNA193 can regulate the cell cycle of esophageal cancer cells and inhibit apoptosis, so that sensitive cells can acquire resistance to cisplatin. An in vivo experiment proved that miRNA193 can promote tumor proliferation through the exosomes, and provide sensitive cells with slight resistance to cisplatin. RESULTS:Small RNA sequencing of exosomes showed that exosomes in drug-resistant cells have 189 up-regulated and 304 down-regulated miRNAs; transcriptome results showed that drug-sensitive cells treated with drug-resistant cellular exosomes have 3446 high-expression and 1709 low-expression genes; correlation analysis showed that drug-resistant cellular exosomes mainly affect the drug resistance of sensitive cells through paths such as cytokine-cytokine receptor interaction, and the VEGF and Jak-STAT signaling pathways; miRNA193, one of the high-expression miRNAs in drug-resistant cellular exosomes, can promote drug resistance by removing cisplatin's inhibition of the cell cycle of sensitive cells. CONCLUSION:Sensitive cells can become resistant to cisplatin through acquired drug-resistant cellular exosomes, and miRNA193 can make tumor cells acquire cisplatin resistance by regulating the cell cycle

Generation of induced pluripotent stem cell line (ZZUi0012-A) from a patient with Fahr's disease caused by a novel mutation in SLC20A2 gene

Several SLC20A2 mutations have been implicated as potential causes of Fahr's disease, a subtype of primary familial brain calcification (PFBC), but very few patient-derived induced pluripotent stem cell (iPSC) models have been established. We have identified a novel SLC20A2 mutation in a family with Fahr's disease. We subsequently obtained dermal fibroblasts from a patient in this family. These fibroblasts were successfully transformed into iPSCs by employing episomal plasmids expressing OCT3/4, SOX2, KLF4, LIN28, and L-MYC. Our approach offers a resource and a platform for further research into the mechanism of Fahr's disease and could facilitate development and screening of pharmaceutical and gene therapies

Silicone oil-based solar-thermal fluids dispersed with PDMS-modified Fe3O4@graphene hybrid nanoparticles

One of the most challenging problems that limit the practical application of carbon-based photothermal nanofluids is their poor dispersion stability and tendency to form aggregation. Herein, by using Fe3O4@graphene hybrid nanoparticles as a model system, we proposed a new method to prepare stably dispersed silicone oil-based solar-thermal nanofluids that can operate at high temperatures than water-based fluids. The introduction of Fe3O4 nanoparticles between graphene nanosheets not only physically increases the inter-plane distance of the graphene nanosheet but also provides numerous anchoring points for surface modification. Phosphate-terminated polydimethylsiloxane chains, which have high compatibility with the silicone oil base fluids and high-temperature stability, were synthesized and utilized to modify the Fe3O4 nanoparticle surfaces. The attached chains create steric hindrance and effectively screen the strong inter-plane van der Waals attraction between graphene sheets. Dispersion stability of the nanofluids with different concentrations of surface-modified hybrid nanoparticles and heated under different temperatures was investigated. We have demonstrated that such fluids could maintain stable dispersion under a heating temperature up to 150 °C depending on the concentration of the hybrid nanoparticles. The resultant nanofluids maintained stable dispersion after repeated heating and were employed for consistent direct solar-thermal energy harvesting at 100 °C. Keywords: Silicone oil, Graphene, Nanofluid, Dispersion, Solar-thermal energ

Both gene deletion and promoter hyper-methylation contribute to the down-regulation of ZAC/PLAGL1 gene in gastric adenocarcinomas: A case control study

Background and objective: Pleiomorphic adenoma gene-like 1 (PLAGL1, also known as LOT1 and ZAC) is a zinc-finger nuclear transcription factor, which possesses antiproliferative effects and is frequently epigenetically silenced during tumorigenesis. PLAGL1 gene is located on 6q24-25, a chromosomal region that is frequently deleted in various kinds of cancers. Both promoter hyper-methylation and loss of heterozygosity may lead to the down-regulation of PLAGL1 in human somatic cancers. Here we aimed to investigate the abnormalities of PLAGL1 in gastric cancers. Methods: We collected 153 case-matched gastric adenocarcinoma (GAC) cases. Quantitative real-time PCR method was applied to evaluate the expression levels as well as gene copy numbers of PLAGL1 in the collected samples. Methylation-specific PCR (MSP) assay was performed to analyze the methylation status of PLAGL1 P1 promoter. Results: Decreased expression of PLAGL1 mRNA was observed in GAC tissues, especially in advanced GACs. Copy number decrease of PLAGL1 gene in GACs was observed in 9.15% (19 out of 153) of the GAC samples and was closely correlated with gene expression. Methylation status of PLAGL1 promoter in GAC tissues was higher than in normal controls, which was inversely correlated with the expression levels of PLAGL1 mRNA. Conclusion: DNA deletion and promoter hyper-methylation both contribute to the downregulation of PLAGL1 in GACs. (C) 2013 Published by Elsevier Masson SAS

Linc00210 drives Wnt/β-catenin signaling activation and liver tumor progression through CTNNBIP1-dependent manner

Abstract Background Liver tumor initiating cells (TICs) have self-renewal and differentiation properties, accounting for tumor initiation, metastasis and drug resistance. Long noncoding RNAs are involved in many physiological and pathological processes, including tumorigenesis. DNA copy number alterations (CNA) participate in tumor formation and progression, while the CNA of lncRNAs and their roles are largely unknown. Methods LncRNA CNA was determined by microarray analyses, realtime PCR and DNA FISH. Liver TICs were enriched by surface marker CD133 and oncosphere formation. TIC self-renewal was analyzed by oncosphere formation, tumor initiation and propagation. CRISPRi and ASO were used for lncRNA loss of function. RNA pulldown, western blot and double FISH were used to identify the interaction between lncRNA and CTNNBIP1. Results Using transcriptome microarray analysis, we identified a frequently amplified long noncoding RNA in liver cancer termed linc00210, which was highly expressed in liver cancer and liver TICs. Linc00210 copy number gain is associated with its high expression in liver cancer and liver TICs. Linc00210 promoted self-renewal and tumor initiating capacity of liver TICs through Wnt/β-catenin signaling. Linc00210 interacted with CTNNBIP1 and blocked its inhibitory role in Wnt/β-catenin activation. Linc00210 silencing cells showed enhanced interaction of β-catenin and CTNNBIP1, and impaired interaction of β-catenin and TCF/LEF components. We also confirmed linc00210 copy number gain using primary hepatocellular carcinoma (HCC) samples, and found the correlation between linc00210 CNA and Wnt/β-catenin activation. Of interest, linc00210, CTNNBIP1 and Wnt/β-catenin signaling targeting can efficiently inhibit tumor growth and progression, and liver TIC propagation. Conclusion With copy-number gain in liver TICs, linc00210 is highly expressed along with liver tumorigenesis. Linc00210 drives the self-renewal and propagation of liver TICs through activating Wnt/β-catenin signaling. Linc00210 interacts with CTNNBIP1 and blocks the combination between CTNNBIP1 and β-catenin, driving the activation of Wnt/β-catenin signaling. Linc00210-CTNNBIP1-Wnt/β-catenin axis can be targeted for liver TIC elimination