The Chinese People's Liberation Army, 1980-82: modernisation, strategy and politics

For some years China has played the role of a latent, de facto partner in the Western security alliance system, thereby contributing to world stability. Her capacity to tie down a high proportion of Soviet conventional forces and tactical nuclear weapons is one reason why the West should maintain good relations with China. It is a simple but vital truth that armies deployed in the Far East cannot simultaneously be used in the European theatre. Dr Ngok Lee has made an extensive study of the Chinese People's Liberation Army (PLA). He believes that economic constraints have forced China to depend on her own efforts even while seeking foreign technical help. As the same time, Sino-American differences over Taiwan have developed during the Reagan administration to a stage which probably prevents China from seeking US arms. Dr Lee analyses China's strategy for national defence ('People's War') under modern conditions as a defence doctrine based on a modification of Mao Zedong's military thought plus a political conscious people's army properly equipped and proficient in modern military thinking. The recently revitalised militia and its important logistical support for the PLA in turn constitute an integral part of the nation's security system. As an illustration he examines China's defence of the Northeast in the face of a possible Soviet conventional and/or nuclear attack. Finally, Dr Lee discusses politics in the PLA with a view to clarifying the complexities in China's implementation of her defence strategy. Such complexities exist despite the fall of Hua Guofeng and the predominance of Deng Xiaoping in the PLA as China continues to face entrenched Leftist influence, the political ills inherited from the Cultural Revolution and other problems arising from the fostering of the Four Modernisations

Designing an Effective Collaboration using Information Technology Towards World Class University

One of the challenges in achieving success in the global competition for the government is to set up higher education institutions to be able to become a World Class University (WCU). It is believed that to address this challenge they need effective collaboration for both internally and externally where information technology (IT) is set as an enabler. However, in fact, this research has found that it is still not utilized effectively although the need for the collaboration has clearly stated in the organization's strategic direction. This paper aims to increase such an effective collaboration model for higher education in Indonesia towards WCU. By using one of reputable state Islamic universities in Indonesia as research object, UIN Maliki Malang, which consist of more than 17,000 students and staffs, this paper proposing a collaboration architecture model equipped with suitable supporting tools. As approaching methods, we use business model design and transformation by mapping study object's business strategic programs into proven collaborative model and their strategic planning of IS/IT. The result of the analysis conducted in the research shows that the majority of the strategic direction of UIN Maliki Malang requires collaboration using information technology both internally and externally. Additionally, UIN Maliki Malang also has facilitated by several collaborations tools within the organization. However, they still need a formal collaboration architecture model to achieve their strategic direction goals effectively. Thus, through the achievement of collaboration effectiveness using information technology, the achievement of a world class university can be realized

A novel Hsp90 inhibitor AT13387 induces senescence in EBV-positive nasopharyngeal carcinoma cells and suppresses tumor formation

Background: Nasopharyngeal carcinoma (NPC) is an epithelial malignancy strongly associated with Epstein-Barr virus (EBV). AT13387 is a novel heat shock protein 90 (Hsp90) inhibitor, which inhibits the chaperone function of Hsp90 and reduces expression of Hsp90-dependent client oncoproteins. This study aimed to evaluate both the in vitro and in vivo antitumor effects of AT13387 in the EBV-positive NPC cell line C666-1.Results: Our results showed that AT13387 inhibited C666-1 cell growth and induced cellular senescence with the downregulation of multiple Hsp90 client oncoproteins EGFR, AKT, CDK4, and restored the protein expression of negative cell cycle regulator p27. We also studied the ability of AT13387 to restore p27 expression by downregulation of AKT and the p27 ubiquitin mediator, Skp2, using AKT inhibitor and Skp2 siRNA. In the functional study, AT13387 inhibited cell migration with downregulation of a cell migration regulator, HDAC6, and increased the acetylation and stabilization of α-tubulin. We also examined the effect of AT13387 on putative cancer stem cells (CSC) by 3-D tumor sphere formation assay. AT13387 effectively reduced both the number and size of C666-1 tumor spheres with decreased expression of NPC CSC-like markers CD44 and SOX2. In the in vivo study, AT13387 significantly suppressed tumor formation in C666-1 NPC xenografts.Conclusion: AT13387 suppressed cell growth, cell migration, tumor sphere formation and induced cellular senescence on EBV-positive NPC cell line C666-1. Also, the antitumor effect of AT13387 was demonstrated in an in vivo model. This study provided experimental evidence for the preclinical value of using AT13387 as an effective antitumor agent in treatment of NPC. © 2013 Chan et al.; licensee BioMed Central Ltd.published_or_final_versio

Validation of the psychometric properties of the health-promoting lifestyle profile in a sample of Taiwanese women

PURPOSE: To examine the preliminary psychometric properties of the Chinese health-promoting lifestyle profile II (HPLP II) among Taiwanese women. METHODS: We conducted a secondary analysis of cross-sectional data from 137 middle-aged women in southern Taiwan. HPLP II reliability was estimated with Cronbach's alpha coefficient, and concurrent validity was estimated with Pearson's correlation between the HPLP II, the World Health Organization's abbreviated Quality of Life assessment (WHOQOL-BREF), perceived health, and demographic variables. Confirmatory factor analysis (CFA) evaluated construct validity. RESULTS: Initial CFA using a six-factor measurement model aligned with the original HPLP II, excepting the factor loading of one subsequently excluded item. CFA of the revised 51-item HPLP II yielded a good estimate of fit. Correlations between the revised instrument and the six subscales were acceptable >0.7. The Cronbach's alpha coefficient surpassed 0.7 for the revised instrument and six subscales ranged from 0.71 to 0.91. The relationships between the 51-item instrument, perceived health, WHOQOL-BREF domain scores, and demographic variables were also significantly positive. CONCLUSIONS: The revised HPLP II scale is appropriate to measure the health-promoting lifestyles of Taiwanese women.published_or_final_versionSpringer Open Choice, 21 Feb 201

Mechanisms of iron- and O2-sensing by the [4Fe-4S] cluster of the global iron regulator RirA

RirA is a global regulator of iron homeostasis in Rhizobium and related α-proteobacteria. In its [4Fe-4S] cluster-bound form it represses iron uptake by binding to IRO Box sequences upstream of RirA-regulated genes. Under low iron and/or aerobic conditions, [4Fe-4S] RirA undergoes cluster conversion/degradation to apo-RirA, which can no longer bind IRO Box sequences. Here, we apply time-resolved mass spectrometry and electron paramagnetic resonance spectroscopy to determine how the RirA cluster senses iron and O2. The data indicate that the key iron-sensing step is the O2-independent, reversible dissociation of Fe2+ from [4Fe-4S]2+ to form [3Fe-4S]0. The dissociation constant for this process was determined as Kd = ~3 µM, which is consistent with the sensing of ‘free’ iron in the cytoplasm. O2-sensing occurs through enhanced cluster degradation under aerobic conditions, via O2-mediated oxidation of the [3Fe-4S]0 intermediate to form [3Fe-4S]1+. This work provides a detailed mechanistic/functional view of an iron-responsive regulator

Sensing iron availability via the fragile [4Fe-4S] cluster of the bacterial transcriptional repressor RirA

Rhizobial iron regulator A (RirA) is a global regulator of iron homeostasis in many nitrogen-fixing Rhizobia and related species of α-proteobacteria. It belongs to the widespread Rrf2 super-family of transcriptional regulators and features three conserved Cys residues that characterise the binding of an iron–sulfur cluster in other Rrf2 family regulators. Here we report biophysical studies demonstrating that RirA contains a [4Fe–4S] cluster, and that this form of the protein binds RirA-regulated DNA, consistent with its function as a repressor of expression of many genes involved in iron uptake. Under low iron conditions, [4Fe–4S] RirA undergoes a cluster conversion reaction resulting in a [2Fe–2S] form, which exhibits much lower affinity for DNA. Under prolonged low iron conditions, the [2Fe–2S] cluster degrades to apo-RirA, which does not bind DNA and can no longer function as a repressor of the cell's iron-uptake machinery. [4Fe–4S] RirA was also found to be sensitive to O2, suggesting that both iron and O2 are important signals for iron metabolism. Consistent with this, in vivo data showed that expression of RirA-regulated genes is also affected by O2. These data lead us to propose a novel regulatory model for iron homeostasis, in which RirA senses iron via the incorporation of a fragile iron–sulfur cluster that is sensitive to iron and O2 concentrations

VEGF and Angiopoietin-1 Exert Opposing Effects on Cell Junctions by Regulating the Rho GEF Syx

Vascular endothelial growth factor (VEGF) and Ang1 (Angiopoietin-1) have opposing effects on vascular permeability, but the molecular basis of these effects is not fully known. We report in this paper that VEGF and Ang1 regulate endothelial cell (EC) junctions by determining the localization of the RhoA-specific guanine nucleotide exchange factor Syx. Syx was recruited to junctions by members of the Crumbs polarity complex and promoted junction integrity by activating Diaphanous. VEGF caused translocation of Syx from cell junctions, promoting junction disassembly, whereas Ang1 maintained Syx at the junctions, inducing junction stabilization. The VEGF-induced translocation of Syx from EC junctions was caused by PKD1 (protein kinase D1)-mediated phosphorylation of Syx at Ser806, which reduced Syx association to its junctional anchors. In support of the pivotal role of Syx in regulating EC junctions, syx−/− mice had defective junctions, resulting in vascular leakiness, edema, and impaired heart function

MicroRNA profiling study reveals MIR-150 in association with metastasis in nasopharyngeal carcinoma

© 2017 The Author(s). MicroRNAs (miRNAs) are small non-coding RNAs that play a crucial role in pathogenesis of human cancers. Several miRNAs have been shown to involve in nasopharyngeal carcinoma (NPC) pathogenesis through alteration of gene networks. A global view of the miRNA expression profile of clinical specimens would be the best way to screen out the possible miRNA candidates that may be involved in disease pathogenesis. In this study, we investigated the expression profiles of miRNA in formalin-fixed paraffin-embedded tissues from patients with undifferentiated NPC versus non-NPC controls using a miRNA real-time PCR platform, which covered a total of 95 cancer-related miRNAs. Hierarchical cluster analysis revealed that NPC and non-NPC controls were clearly segregated. Promisingly, 10 miRNA candidates were differentially expressed. Among them, 9 miRNAs were significantly up-regulated of which miR-205 and miR-196a showed the most up-regulated in NPC with the highest incidence percentage of 94.1% and 88.2%, respectively, while the unique down-regulated miR-150 was further validated in patient sera. Finally, the in vitro gain-of-function and loss-of-function assays revealed that miR-150 can modulate the epithelial-mesenchymal-transition property in NPC/HK-1 cells and led to the cell motility and invasion. miR-150 may be a potential biomarker for NPC and plays a critical role in NPC tumourigenesis.Link_to_subscribed_fulltex