China's Model of Free Economic Zones: Experiences and Prospects after over 20 Years

It is true that no FEZs in the world like in China have made so strong impact on national economic development and reform. Their existing condition, however, has been changed since the middle 1990s. Chinese FEZs have to face the new challenges and problems. This study discussed and prospected the transformation and further development of Chinese FEZs in the 21st century as well as their significance for the transformation of FEZs in other country based on the analyzing of the indicators such as the role, policy, industrial sectors, administration, development model, spatial structure, and location in this study. DOI: http://dx.doi.org/10.5564/mjia.v0i12.95 Mongolian Journal of International Affairs No.12 2005: 65-8

The Theory and Practice of Free Economic Zones : A Case Study of Tianjin, People's Republic of China

Diese Dissertation erörtert die Entwicklung und Struktur von Freiwirtschaftszonen auf internationaler, nationaler und lokaler Ebene. Sie besteht aus 3 Teilen: In Teil A wird zunächst die weltwirtschaftliche Integration und ihr Verhältnis zu Freiwirtschaftszonen dargestellt, um ihre dominierende Rolle in der Weltwirtschaft und ihrem Entwicklungstrend zu erläutern. Ein strukturelles und räumliches Entwicklungsmodell für Freiwirtschaftszonen auf internationaler Ebene wird herausgearbeitet auf Grund einer allgemeinen Definition, eines Faktorensystems und einer systematischen Typisierung von Freiwirtschaftszonen, was die früheren Studien ergänzt und ein nützliches Beispiel chinesischer Freiwirtschaftszonen zur Verfügung stellt. In Teil B steht die nationale Ebene im Mittelpunkt. Die Notwendigkeit zur Errichtung von Freiwirtschaftszonen in China wird am besten in einem Rückblick auf die wirtschaftliche und regionale Entwicklungspolitik Chinas seit 1949/50 dargestellt, unter besonderer Berücksichtigung des Zeitraums seit 1978. Das Entstehen und die allgemeinen Charakteristika der chinesischen Freiwirtschaftszonen wird auf der Grundlage von Hauptfaktoren und einem Vergleich mit Freiwirtschaftszonen weltweit dargestellt. Im Ergebnis stellt dieser Teil 20 Jahre Erfahrung Chinas mit Freiwirtschaftszonen und ihrer Entwicklungsmöglichkeiten dar. Teil C gibt einen kurzen historischen Überblick der urbanen und wirtschaftlichen Entwicklung Tjanjins während der letzten 100 Jahre wieder. Dies liefert den Hintergrund für das Verständnis der wirtschaftlichen und politischen Situation, die zur Gründung von TEDA (Tianjin Economic and Technological Development Area) und ihrer Entwicklung seit 1984 führte. Hier werden die Erfolge und Probleme von TEDA bis 2000 bewertet. Aus dieser Bewertung werden einige Konzepte entwickelt. Zum Schluss werden die empirischen Auswirkungen von TEDA auf die Freiwirtschaftszonen der Welt erörtert. Die Erfahrungen mit TEDA könnten eine Beitrag zur Weiterentwicklung von Theorie und Praxis von Freiwirtschaftszonen in China und der übrigen Welt sein

Identification of Autophagy-Related Gene 7 and Autophagic Cell Death in the Planarian Dugesia japonica

Planarians undergo continuous body size remodeling under starvation or during regeneration. This process likely involves autophagy and autophagic cell death, but this hypothesis is supported by few studies. To test this hypothesis, we cloned and characterized autophagy-related gene 7 (Atg7) from the planarian Dugesia japonica (DjAtg7). The full-length cDNA of DjAtg7 measures 2272 bp and includes a 2082-bp open reading frame encoding 693 amino acids with a molecular weight of 79.06 kDa. The deduced amino acid sequence of DjAtg7 contains a conserved ATP-binding site and a catalytic active site of an E1-like enzyme belonging to the ATG7 superfamily. DjAtg7 transcripts are mainly expressed in intestinal tissues of the intact animals. After amputation, DjAtg7 was highly expressed at the newly regenerated intestinal branch on days 3–7 of regeneration and in the old tissue of the distal intestinal branch on day 10 of regeneration. However, knockdown of DjAtg7 by RNAi did not affect planarian regeneration and did not block autophagosome formation, which indicates that autophagy is more complex than previously expected. Interestingly, TEM clearly confirmed that autophagy and autophagic cell death occurred in the old tissues of the newly regenerated planarians and clearly revealed that the dying cell released vesicles containing cellular cytoplasmic contents into the extracellular space. Therefore, the autophagy and autophagic cell death that occurred in the old tissue not only met the demand for body remodeling but also met the demand for energy supply during planarian regeneration. Collectively, our work contributes to the understanding of autophagy and autophagic cell death in planarian regeneration and body remodeling

Gaussian Boson Sampling with Pseudo-Photon-Number Resolving Detectors and Quantum Computational Advantage

We report new Gaussian boson sampling experiments with pseudo-photon-number-resolving detection, which register up to 255 photon-click events. We consider partial photon distinguishability and develop a more complete model for characterization of the noisy Gaussian boson sampling. In the quantum computational advantage regime, we use Bayesian tests and correlation function analysis to validate the samples against all current classical mockups. Estimating with the best classical algorithms to date, generating a single ideal sample from the same distribution on the supercomputer Frontier would take ~ 600 years using exact methods, whereas our quantum computer, Jiuzhang 3.0, takes only 1.27 us to produce a sample. Generating the hardest sample from the experiment using an exact algorithm would take Frontier ~ 3.1*10^10 years.Comment: submitted on 10 Apri

Germline variation at 8q24 and prostate cancer risk in men of European ancestry

Chromosome 8q24 is a susceptibility locus for multiple cancers, including prostate cancer. Here we combine genetic data across the 8q24 susceptibility region from 71,535 prostate cancer cases and 52,935 controls of European ancestry to define the overall contribution of germline variation at 8q24 to prostate cancer risk. We identify 12 independent risk signals for prostate cancer (p < 4.28 × 10−15), including three risk variants that have yet to be reported. From a polygenic risk score (PRS) model, derived to assess the cumulative effect of risk variants at 8q24, men in the top 1% of the PRS have a 4-fold (95%CI = 3.62–4.40) greater risk compared to the population average. These 12 variants account for ~25% of what can be currently explained of the familial risk of prostate cancer by known genetic risk factors. These findings highlight the overwhelming contribution of germline variation at 8q24 on prostate cancer risk which has implications for population risk stratification

Fine-mapping of prostate cancer susceptibility loci in a large meta-analysis identifies candidate causal variants

Prostate cancer is a polygenic disease with a large heritable component. A number of common, low-penetrance prostate cancer risk loci have been identified through GWAS. Here we apply the Bayesian multivariate variable selection algorithm JAM to fine-map 84 prostate cancer susceptibility loci, using summary data from a large European ancestry meta-analysis. We observe evidence for multiple independent signals at 12 regions and 99 risk signals overall. Only 15 original GWAS tag SNPs remain among the catalogue of candidate variants identified; the remainder are replaced by more likely candidates. Biological annotation of our credible set of variants indicates significant enrichment within promoter and enhancer elements, and transcription factor-binding sites, including AR, ERG and FOXA1. In 40 regions at least one variant is colocalised with an eQTL in prostate cancer tissue. The refined set of candidate variants substantially increase the proportion of familial relative risk explained by these known susceptibility regions, which highlights the importance of fine-mapping studies and has implications for clinical risk profiling. © 2018 The Author(s).Prostate cancer is a polygenic disease with a large heritable component. A number of common, low-penetrance prostate cancer risk loci have been identified through GWAS. Here we apply the Bayesian multivariate variable selection algorithm JAM to fine-map 84 prostate cancer susceptibility loci, using summary data from a large European ancestry meta-analysis. We observe evidence for multiple independent signals at 12 regions and 99 risk signals overall. Only 15 original GWAS tag SNPs remain among the catalogue of candidate variants identified; the remainder are replaced by more likely candidates. Biological annotation of our credible set of variants indicates significant enrichment within promoter and enhancer elements, and transcription factor-binding sites, including AR, ERG and FOXA1. In 40 regions at least one variant is colocalised with an eQTL in prostate cancer tissue. The refined set of candidate variants substantially increase the proportion of familial relative risk explained by these known susceptibility regions, which highlights the importance of fine-mapping studies and has implications for clinical risk profiling. © 2018 The Author(s).Peer reviewe

Djhsp60 Is Required for Planarian Regeneration and Homeostasis

HSP60, a well-known mitochondrial chaperone, is essential for mitochondrial homeostasis. HSP60 deficiency causes dysfunction of the mitochondria and is lethal to animal survival. Here, we used freshwater planarian as a model system to investigate and uncover the roles of HSP60 in tissue regeneration and homeostasis. HSP60 protein is present in all types of cells in planarians, but it is relatively rich in stem cells and head neural cells. Knockdown of HSP60 by RNAi causes head regression and the loss of regenerating abilities, which is related to decrease in mitotic cells and inhibition of stem cell-related genes. RNAi-HSP60 disrupts the structure of the mitochondria and inhibits the mitochondrial-related genes, which mainly occur in intestinal tissues. RNAi-HSP60 also damages the integrity of intestinal tissues and downregulates intestine-expressed genes. More interestingly, RNAi-HSP60 upregulates the expression of the cathepsin L-like gene, which may be the reason for head regression and necrotic-like cell death. Taking these points together, we propose a model illustrating the relationship between neoblasts and intestinal cells, and also highlight the essential role of the intestinal system in planarian regeneration and tissue homeostasis