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過去以國際合資事業為焦點的研究已普遍受到重視，然而從雙方母公司的配適觀點及環境衝擊，探討國際合資事業不穩定性之研究則付之闕如。本研究旨在探討夥伴配適性及環境衝擊如何影響國際合資事業的不穩定性及績效，並提出四項研究假說。透過台灣與捷克之國營事業成立的國際合資事業為個案研究對象，本研究自雙方意圖合資至該合資事業成立以來之十年間(1995-2005)，依時間演化時程切割為33個事件階段，探討各事件階段序列之變化，以驗證研究假說。研究結果發現：(1)當國際合資事業夥伴間配適性越愈高時，其國際合資事業穩定性愈高；(2)當國際合資事業認知的環境衝擊程度越愈高時，則國際合資事業不穩定性愈高；(3)當國際合資事業夥伴問配適性越愈高時，其國際合資事業績效愈佳；以及(4)當國際合資事業不穩定性越愈高時，將導致合資事業績效不佳的狀況。最後提出相關建議供未來研究及管理實務運作參考。

The enterotoxins produced by enterotoxigenic Escherichia coli (ETEC) cells include heat labile (LT) and heat stable toxins (ST). These toxins cause diarrheal in humans and domestic animals. In this study, we combined LT I and ST II gene specific PCR primers into a multiplex PCR systemand used this system for the simultaneous detection of LT I and ST II ETEC cells in tap water and environmental waters. Using Chromocult coliform agar (CCA), we found that tap water and underground water were contaminated with 0-10 0 CFU/ml of E. coli and coliform cells while the waters from four rivers near Taichung City were contaminated with 10 2 - 10 4 CFU/ml of E. coli and coliform cells. Furthermore, three of the four river waters were contaminated with LT I/ST II ETEC cells. The high levels of microfloral contamination in these river waters near an urban area should be attended to urgently.

Colorectal cancer（CRC） is the second most common cancer in women and the third most common in men globally. CRC arises from one or a combination of chromosomal instability, Cp G island methylator phenotype, and microsatellite instability. Genetic instability is usually caused by aneuploidy and loss of heterozygosity. Mutations in the tumor suppressor or cell cycle genes may also lead to cellular transformation. Similarly, epigenetic and/or genetic alterations resulting in impaired cellular pathways, such as DNA repair mechanism, may lead to microsatellite instability and mutator phenotype. Non-coding RNAs, more importantly micro RNAs and long non-coding RNAs have also been implicated at various CRC stages. Understanding the specific mechanisms of tumorigenesis and the underlying genetic and epigenetic traits is critical in comprehending the disease phenotype. This paper reviews these mechanisms along with the roles of various non-coding RNAs in CRCs.

Inertial fusion energy （IFE） has been considered a promising, nearly inexhaustible source of sustainable carbon-free power for the world＇s energy future. It has long been recognized that the control of hydrodynamic instabilities is of critical importance for ignition and high-gain in the inertial-confinement fusion （ICF） hot-spot ignition scheme. In this mini-review, we summarize the progress of theoretical and simulation research of hydrodynamic instabilities in the ICF central hot-spot implosion in our group over the past decade. In order to obtain sufficient understanding of the growth of hydrodynamic instabilities in ICF, we first decompose the problem into different stages according to the implosion physics processes. The decomposed essential physics pro- cesses that are associated with ICF implosions, such as Rayleigh-Taylor instability （RTI）, Richtmyer-Meshkov instability （RMI）, Kelvin-Helmholtz instability （KHI）, convergent geometry effects, as well as perturbation feed-through are reviewed. Analyti- cal models in planar, cylindrical, and spherical geometries have been established to study different physical aspects, including density-gradient, interface-coupling, geometry, and convergent effects. The influence of ablation in the presence of preheating on the RTI has been extensively studied by numerical simulations. The KHI considering the ablation effect has been discussed in detail for the first time. A series of single-mode ablative RTI experiments has been performed on the Shenguang-II laser facility. The theoretical and simulation research provides us the physical insights of linear and weakly nonlinear growths, and nonlinear evolutions of the hydrodynamic instabilities in ICF implosions, which has directly supported the research of ICF ignition target design. The ICF hot-spot ignition implosion design that uses several controlling features, based on our current understanding of hydrodynamic instabilities, to address shell implosion stability, has been briefly described, several of which are novel.

In January 2013, a severe fog and haze event （FHE） of strong intensity, long duration, and extensive coverage occurred in eastern China. The present study investigates meteorological conditions for this FHE by diagnosing both its atmospheric back- ground fields and daily evolution in January 2013. The results show that a weak East Asian winter monsoon existed in January 2013. Over eastern China, the anomalous southerly winds in the middle and lower troposphere are favorable for more water vapor transported to eastern China. An anomalous high at 500 hPa suppresses convection. The weakened surface winds are favorable for the fog and haze concentrating in eastern China. The reduction of the vertical shear of horizontal winds weakens the synoptic disturbances and vertical mixing of atmosphere. The anomalous inversion in near-surface increases the stability of surface air. All these meteorological background fields in January 2013 were conducive to the maintenance and development of fog and haze over eastern China. The diagnosis of the daily evolution of the FHE shows that the surface wind velocity and the vertical shear of horizontal winds in the middle and lower troposphere can exert dynamic effects on fog and haze. The larger （smaller） they are, the weaker （stronger） the fog and haze are. The thermodynamic effects include stratification instabil- ity in middle and lower troposphere and the inversion and dew-point deficit in near-surface. The larger （smaller） the stratifica- tion instability and the inversion are, the stronger （weaker） the fog and haze are. Meanwhile, the smaller （larger） the dewpoint deficit is, the stronger （weaker） the fog and haze are. Based on the meteorological factors, a multi-variate linear regression model is set up. The model results show that the dynamic and thermodynamic effects on the variance of the fog and haze evo- lution are almost the same. The contribution of the meteorological factors to the variance of the daily fog and haze evolution reaches 0.68, which explains more than 2/3 of the variance.

Understanding of the mechanism of colorectal carcinogenesis has been gaining momentum for some years on account of its high incidence and impact on the lives of individuals affected. Different genetic abnormalities have been found in colorectal cancers from different sites. For example, proximal colon cancer is usually related to the nucleotide instability pathway, as microsatellite instability （MSI）. However, distal colon cancer is usually associated with specific chromosomal instability （CIN）. The development of cancer at the rectum, though similar to that at the colon, displays its own unique features. These differences might be partially attributed to different embryological development and physiological circumstances. Environmental factors such as diet and alcohol intake also differ in their role in the development of tumors in the three segments, proximal colon, distal colon, and rectum. ＂Proximal shift＂ of colon cancer has been known for some time, and survival rates of colorectal cancer are higher when rectal cancers are excluded, both of which emphasize the three different segments of coloreetal cancer and their different properties. Meanwhile, colonic and rectal cancers are distinctive therapeutic entities. The concept of three entities of coloreetal cancer may be important in designing clinical trails or therapeutic strategies. However, the dispute about the inconsistency of data coneerning the site-specific mechanism of eolorectal carcinoma does exist, and more evidence about molecular events of carcinogenesis and targeted therapy needs to be collected to definitely confirm the conception.

Tumor suppressor PTEN regulates cellular activities and controls genome stability through multiple mechanisms. In this study, we report that PTEN is necessary for the protection of DNA replication forks against replication stress. We show that deletion of PTEN leads to replication fork collapse and chromosomal instability upon fork stalling following nucleotide depletion induced by hydroxyurea. PTEN is physically associated with replication protein A 1 （RPA1） via the RPA1 C-terminal domain. STORM and iPOND reveal that PTEN is localized at replication sites and promotes RPA1 accumulation on replication forks. PTEN recruits the deubiquitinase OTUB1 to mediate RPA1 deubiquitination. RPA1 deletion confers a phenotype like that observed in PTEN knockout cells with stalling of rep- lication forks. Expression of PTEN and RPA1 shows strong correlation in colorectal cancer. Heterozygous disruption of RPA1 promotes tumorigenesis in mice. These results demonstrate that PTEN is essential for DNA replication fork protection. We propose that RPA1 is a target of PTEN function in fork protection and that PTEN maintains genome stability through regulation of DNA replication.

DNA double-strand breaks （DSBs） are traditionally associated with cancer through their abilities to cause chro- mosomal instabilities or gene mutations. Here we report a new class of self-inflicted DNA DSBs that can drive tumor growth irrespective of their effects on genomic stability. We discover a mechanism through which cancer cells cause DSBs in their own genome spontaneously independent of reactive oxygen species or replication stress. In this mech- anism, low-level cytochrome c leakage from the mitochondria leads to sublethal activation of apoptotic caspases and nucleases, which causes DNA DSBs. In response to these spontaneous DNA DSBs, ATM, a key factor involved in DNA damage response, is constitutively activated. Activated ATM leads to activation of transcription factors NF- KB and STAT3, known drivers of tumor growth. Moreover, self-inflicted DNA DSB formation and ATM activation are important in sustaining the sternness of patient-derived glioma cells. In human tumor tissues, elevated levels of activated ATM correlate with poor patient survival. Self-inflicted DNA DSBs therefore are functionally important for maintaining the malignancy of cancer cells.

Comprehensive understanding of the structural/morphology stability of ultrathin （diameter 〈 10 nm） gold nanowires under real service conditions （such as under Joule heating） is a prerequisite for the reliable implementation of these emerging building blocks into functional nanoelectronics and mechatronics systems. Here, by using the in situ transmission electron microscopy （TEM） technique, we discovered that the Rayleigh instability phenomenon exists in ultrathin gold nanowires upon moderate heating. Through the controlled electron beam irradiation-induced heating mechanism （with 〈 100 ~C temperature rise）, we further quantified the effect of electron beam intensity and its dependence on Rayleigh instability in altering the geometry and morphology of the ultrathin gold nanowires. Moreover, in situ high-resolution TEM （HRTEM） observations revealed surface atomic diffusion process to be the dominating mechanism for the morphology evolution processes. Our results, with unprecedented details on the atomic-scale picture of Rayleigh instability and its underlying physics, provide critical insights on the thermal/structural stability of gold nanostructures down to a sub-10 nm level which may pave the way for their interconnect applications in future ultra- large-scale integrated ciroaits.

Subtelomeres consist of sequences adjacent to telomeres and contain genes involved in important cellular functions, as subtelomere instability is associated with several human diseases. Balancing between subtelomere stability and plasticity is particularly important for Trypanosoma bruce/, a protozoan parasite that causes human African trypanosomiasis. T. bruce/regularly switches its major variant surface antigen, variant surface glycoprotein （VSG）, to evade the host immune response, and VSGs are expressed exclusively from subtelomeres in a strictly monoallelic fashion. Telomere proteins are important for protecting chromosome ends from illegitimate DNA processes. However, whether they contribute to subtelomere integrity and stability has not been well studied. We have identified a novel T. bruce/telomere protein, T. bruce/TRF-Interacting Factor 2 （TbTIF2）, as a functional homolog of mammalian TIN2. A transient depletion of TbTIF2 led to an elevated VSG switching frequency and an increased amount of DNA double-strand breaks （DSBs） in both active and silent subtelomeric bloodstream form expression sites （BESs）. Therefore, TbTIF2 plays an important role in VSG switching regulation and is important for subtelomere integrity and stability. TbTIF2 depletion increased the association of TbRAD51 with the telomeric and subtelomeric chromatin, and TbRAD51 deletion further increased subtelomeric DSBs in TbTIF2-depleted cells, suggesting that TbRAD51-mediated DSB repair is the underlying mechanism of subsequent VSG switching. Surprisingly, significantly more TbRAD51 associated with the active BES than with the silent BESs upon TbTIF2 depletion, and TbRAD51 deletion induced much more DSBs in the active BES than in the silent BESs in TbTIF2- depleted cells, suggesting that TbRAD51 preferentially repairs DSBs in the active BES.