Miracle-dz/UniFAR-FTUs huggingface dataset:
Single image super-resolution using self-similarity and generalized nonlocal mean

In this paper, a super-resolution method based self-similarity and generalized nonlocal mean is proposed. The proposed method not only adopts the self-similarity of image to build a self-example training set but also exploits generalized nonlocal mean to improve the quality of the resultant image. In the proposed method, difference of Gaussians of the input low-resolution image is extracted firstly, and then a generalized nonlocal mean algorithm is proposed to estimate the missing high-frequency details of the low image. The experimental results show that the proposed algorithm has a good performance, and the high-resolution image generated by the proposed method is with better subjective and objective quality compared with other methods.
The Quest for Achieving Universal Social Protection in Nepal: Challenges and Opportunities

With the entry into the new millennium, social protection has emerged as a new priority for developing countries as well as international development institutions. Earlier, social protection programmes were considered unsuitable for developing countries, whereas recent years has seen a shift in the development paradigm with social protection policies now considered a key component of international poverty reduction strategies and a development instrument centred on the rights of the poor. Drawing from the experience of Nepal as a case study, this article seeks to examine the different approaches to social protection in the South Asian region, and also the challenges faced and issues remaining in providing a minimum level of social protection necessary for a decent living. The experience of Nepal is important because it marks a shift from social protection covering government pensioners only to one where the government is implementing a varied portfolio, despite high levels of poverty, political uncertainties, and low growth rates.
Kinetic and equilibrium binding studies of amsacrine-4-carboxamides: a class of asymmetrical DNA-intercalating agents which bind by threading through the DNA helix.

Detailed equilibrium and kinetic studies of the DNA interaction of the amsacrine-4-carboxamide class of compounds suggest that they bind by intercalating the acridine chromophore at near-maximal overlap with the base pairs, locating their two dissimilar side chains in specific grooves of the double helix. The first step is a fast bimolecular association to form an outside-bound complex (probably in the major groove). Insertion of the less bulky carboxamide side chain then occurs in a process governed largely by the rate of transient opening of the double helix by natural "breathing" motions and is followed by further monomolecular rearrangements to allow the carboxamide side chain to find its highest affinity binding sites in the minor groove. Dissociation of the complexes are much more ligand structure dependent, but also involve opening of the double helix to allow disengagement. Compounds of this type, which locate their two distinguishable side chains one in each DNA groove, form a unique class of DNA-binding ligand, with considerable potential for regiospecific delivery of reactive functionality to DNA. Although natural products which also have such specific binding modes are known (e.g. nogalamycin), the amsacrine-4-carboxamides discussed here are the first class of readily modified synthetic compounds with this property.
Sarcomere mechanics in striated muscles: from molecules to sarcomeres to cells.

Muscle contraction is commonly associated with the cross-bridge and sliding filament theories, which have received strong support from experiments conducted over the years in different laboratories. However, there are studies that cannot be readily explained by the theories, showing 1) a plateau of the force-length relation extended beyond optimal filament overlap, and forces produced at long sarcomere lengths that are higher than those predicted by the sliding filament theory; 2) passive forces at long sarcomere lengths that can be modulated by activation and Ca2+, which changes the force-length relation; and 3) an unexplained high force produced during and after stretch of activated muscle fibers. Some of these studies even propose "new theories of contraction. " While some of these observations deserve evaluation, many of these studies present data that lack a rigorous control and experiments that cannot be repeated in other laboratories. This article reviews these issues, looking into studies that have used intact and permeabilized fibers, myofibrils, isolated sarcomeres, and half-sarcomeres. A common mechanism associated with sarcomere and half-sarcomere length nonuniformities and a Ca2+-induced increase in the stiffness of titin is proposed to explain observations that derive from these studies.
Loss of profilin‐1 expression enhances breast cancer cell motility by Ena/VASP proteins

We previously showed that silencing profilin‐1 (Pfn1) expression increases breast cancer cell motility, but the underlying mechanisms have not been explored. Herein, we demonstrate that loss of Pfn1 expression leads to slower but more stable lamellipodial protrusion thereby enhancing the net protrusion rate and the overall motility of MDA‐MB‐231 breast cancer cells. Interestingly, MDA‐MB‐231 cells showed dramatic enrichment of VASP at their leading edge when Pfn1 expression was downregulated and this observation was also reproducible in other cell types including human mammary epithelial cells and vascular endothelial cells. We further demonstrate that Pfn1 downregulation results in a hyper‐motile phenotype of MDA‐MB‐231 cells in an Ena/VASP‐dependent mechanism. Pfn1‐depleted cells display a strong colocalization of VASP with lamellipodin (Lpd—a PI(3,4)P2‐binding protein that has been previously implicated in lamellipodial targeting of Ena/VASP) at the leading edge. Finally, inhibition of PI3‐kinase (important for generation of PI(3,4)P2) delocalizes VASP from the leading edge. This observation is consistent with a possible involvement of Lpd in enhanced membrane recruitment of VASP that results from loss of Pfn1 expression. Our findings for the first time highlight a possible mechanism of how reduced expression of a pro‐migratory molecule like Pfn1 could actually promote motility of breast cancer cells. J. Cell. Physiol. 219: 354–364, 2009. © 2008 Wiley‐Liss, Inc.
Integrated microfluidic systems for molecular diagnostics: A universal electrode platform for rapid diagnosis of urinary tract infections

Transforming microfluidics-based biosensing systems from laboratory research into clinical reality remains an elusive goal despite decades of intensive research. A fundamental obstacle in the development of fully automated microfluidic diagnostic systems is the lack of an effective strategy for combining multiple pumping, sample preparation, and detection modules into an integrated platform. In this article, we report a universal electrode approach, which incorporates dc electrolytic pumping, ac electrokinetic sample preparation, and electrochemical sensing based on a self-assembled monolayer (SAM) on a single microfluidic platform, to automate complicated molecular analysis procedures in nontraditional healthcare settings.
Sequential Ligand-Dependent Notch Signaling Activation Regulates Valve Primordium Formation and Morphogenesis.

RATIONALE The Notch signaling pathway is crucial for primitive cardiac valve formation by epithelial-mesenchymal transition, and NOTCH1 mutations cause bicuspid aortic valve; however, the temporal requirement for the various Notch ligands and receptors during valve ontogeny is poorly understood. OBJECTIVE The aim of this study is to determine the functional specificity of Notch in valve development. METHODS AND RESULTS Using cardiac-specific conditional targeted mutant mice, we find that endothelial/endocardial deletion of Mib1-Dll4-Notch1 signaling, possibly favored by Manic-Fringe, is specifically required for cardiac epithelial-mesenchymal transition. Mice lacking endocardial Jag1, Notch1, or RBPJ displayed enlarged valve cusps, bicuspid aortic valve, and septal defects, indicating that endocardial Jag1 to Notch1 signaling is required for post-epithelial-mesenchymal transition valvulogenesis. Valve dysmorphology was associated with increased mesenchyme proliferation, indicating that Jag1-Notch1 signaling restricts mesenchyme cell proliferation non-cell autonomously. Gene profiling revealed upregulated Bmp signaling in Jag1-mutant valves, providing a molecular basis for the hyperproliferative phenotype. Significantly, the negative regulator of mesenchyme proliferation, Hbegf, was markedly reduced in Jag1-mutant valves. Hbegf expression in embryonic endocardial cells could be readily activated through a RBPJ-binding site, identifying Hbegf as an endocardial Notch target. Accordingly, addition of soluble heparin-binding EGF-like growth factor to Jag1-mutant outflow tract explant cultures rescued the hyperproliferative phenotype. CONCLUSIONS During cardiac valve formation, Dll4-Notch1 signaling leads to epithelial-mesenchymal transition and cushion formation. Jag1-Notch1 signaling subsequently restrains Bmp-mediated valve mesenchyme proliferation by sustaining Hbegf-EGF receptor signaling. Our studies identify a mechanism of signaling cross talk during valve morphogenesis involved in the origin of congenital heart defects associated with reduced NOTCH function.
Vascular endothelial growth factor is efficiently synthesized in spite of low transfection efficiency of pSG5VEGF plasmids in vascular smooth muscle cells

The limitation of lipotransfection with plasmid vectors is its low efficiency and the short-term expression of introduced genes. This is particularly important when the synthesis of high amounts of therapeutic products is required. However, growth factors with paracrine action overcome this problem. The aim of our study was to check whether the amounts of vascular endothelial growth factor (VEGF) generated after plasmid lipotransfection into vascular smooth muscle cells (VSMC) can be sufficient to stimulate endothelial cell proliferation. Two plasmids, pSG5-VEGF121 and pSG5-VEGF165, harboring human VEGF121 and VEGF165 iso-forms were constructed and lipotransfected into COS-7 cells or to rat VSMC. The transfection efficiency, estimated by the expression of control, b-galactosidase gene, was about 50% in COS- 7 but rarely exceeded 5% in VSMC. However, despite this, the smooth muscle cells generated high amounts of VEGF protein, up to 3 ng/ml medium. The biological activity of this VEGF was confirmed by enhanced proliferation of human umbilical vein and coronary artery endothelial cells, stimulated with conditioned media of pSG5-VEGF transfected cells. Thus, the low transfection efficiency does not preclude the generation of high amounts of VEGF by VSMC. After reaching the maximum at about 48 h after transfection, the generation of VEGF decreased in the following days. Such a situation may be sufficient for the gene therapy of restenosis when the long-term expression of therapeutic gene(s) is not necessary. Thus, we suggest that the pSG5-VEGF121 and pSG5-VEGF165 plasmids can be used for therapeutic application.
Effects of adding P38 mitogen-activated protein-kinase inhibitor to celsior solution in canine heart transplantation from non–heart-beating donors

Background. The activation of p38 mitogen-activated protein kinase (MAPK) plays an important role in ischemia-reperfusion injury. This study evaluated the effects of p38 MAPK inhibition using FR167653, a novel p38 MAPK inhibitor, as an additive to Celsior solution in canine heart transplantation from non–heart-beating donors (NHBDs). Methods. Donor hearts were left in situ for 20 minutes after cardiac arrest, which was induced by rapid exsanguination. Twelve donor-recipient pairs of mongrel dogs were divided into two groups: the control and FR167653 (FR) groups (n=6 each). In both groups, the grafts were subjected to coronary flushing and immersed in Celsior solution for 4 hours with or without FR167653. Orthotopic heart transplantation was then performed. Cardiac output (CO), left ventricular pressure (LVP), and end-systolic maximal elastance (Emax) were measured 2 hours after weaning from cardiopulmonary bypass (CPB), and the hearts were then harvested for histopathologic study. The activation of p38 MAPK was evaluated in another 20 mongrel dogs. Results. In the FR group, CO, LVP recovery rate, and Emax were significantly (P <0.05) higher 2 hours after weaning from CPB, histopathologic damage was attenuated, and the activation of p38 MAPK was significantly (P <0.05) inhibited 10 minutes after reperfusion compared with the control group. Conclusions. The addition of FR167653 to Celsior solution improved heart-graft viability, probably by way of the inhibition of p38 MAPK activation, which may attenuate ischemia-reperfusion injury in heart transplantation from NHBDs.
Navigating Institutional Complexity: The Production of Risk Culture in the Financial Sector

Following the financial crisis, financial sector organizations faced increased pressures to reform their ‘risk cultures’. In this paper, we argue that the emergence of regulatory and managerial attention to risk culture is symptomatic of pressures to redefine the fundamental ends of financial institutions and to rebalance the pre-crisis emphasis on a logic of opportunity and risk-taking with a logic of precaution and risk control. Based on the analysis of normative practitioner texts and on extended contact with regulators, advisers and corporate actors in the UK financial sector over four years, we show how this initial complexity of ends is translated into uncertainty and conflict about the means through which risk culture might become an object amenable to intervention. On this basis, we contribute to the growing literature on ‘institutional complexity’ by showing how organizational actors address conflicting pressures about both ends and means, and by discussing some key implications of their simplification strategies. Our analysis also contributes to recent studies of ‘means-ends decoupling’, showing how means, ends and the object of intervention itself – risk culture – co-evolve as they are reconstructed by organizational actors via their everyday practices.
Exchange Rate and Trade Balance in Zambia: An Empirical Investigation of the J-Curve Effect

Trade balance is one of the main factors affecting the balance of payments position. This study examined the relationship between exchange rate and trade balance in Zambia, both in the short run and long run using quarterly data from 1998:1 to 2009:4. The study investigated how trade balance responds to exchange rate changes over time and if the J-curve exists for Zambia. The elasticity approach to the balance of payments was the theoretical framework applied in this study. The elasticity approach contends that there is a long term relationship between exchange rate and trade balance, though disequilibrium may exist in the short run. A number of studies done in the past have shown that the relationship between exchange rate and trade balance varies across countries. Predictions about effects of exchange rate changes on the balance of trade may be affected by a number of factors. Apart from behavior of economic agents, macroeconomic and structural conditions that exist in a country may affect the responsiveness of imports and exports to exchange rate changes. Cointegration, Vector Error Correction modeling and Impulse Response Functions are the time series econometric methods applied in this study. The empirical results have shown that there is a long term equilibrium relationship between exchange rate and trade balance. Depreciation of the exchange rate is effective in improving the Zambian trade balance in the long run. However, in the short run the trade balance initially deteriorates but eventually improves over the long run. Therefore, the response of trade balance to exchange rate appears to follow the J-Curve. The Marshal-Lerner condition for depreciation to improve trade balance is met in the long run, but not in the short run. The Granger causality results have shown that causality runs from exchange rate to trade balance and not the other way round. Therefore, exchange rate may be used to influence and provide information about trade balance developments in Zambia. Policies that ensure stability and competitiveness of exchange rate should be promoted as one of the ways of strengthening the external balance position.
Model predictive control method to reduce common-mode voltage and balance the neutral-point voltage in three-level T-type inverter

The three-level T-type inverter has outstanding performances and better in the switching device selection than a two-level inverter. However, the problem of common-mode voltages and neutral-point potential (NP) unbalance is generated. This paper proposes a model predictive control method for reducing the common mode voltage and balancing the neutral-point potential (NP). Based on the relationship between the switching states and common-mode voltage (CMV), the 19 voltage switching vectors are adopted to reduce the CMV. In addition, the P-type and N-type small vectors are selected to control the NP balance. Without utilizing the redundancy zero and small vectors, the common-mode voltage controlled by the proposed MPC algorithms can be restricted within ±Vdc/6. Furthermore, the proposed technique can balance the DC-link voltage with reduced CMV. The proposed method has been verified by the lab experiment.
Constructing the ideal river: the 19th century origins of the first international organizations

For decades, International Relations scholars have debated the role and efficacy of international institutions in advancing international cooperation. However, scholarship that takes institutions seriously often adopts the functionalist assumption that international organizations are created as technocratic bodies to facilitate the division of economic goods. My dissertation examines the first international organizations created in the 19th century to manage international rivers (specifically the Rhine, the Danube and the Congo Rivers) and puts forward two strands of argumentation that challenges this functionalist, rationalist and technocratic view of institutional creation. First, I examine the broad social construction of the international river as an untamed space to be disciplined and redefined as a useful economic entity. In the mid-18th century, Frederick the Great wrote in a letter to Voltaire, “whoever improves the soil, cultivates land lying waste and drains swamps is making conquests from barbarism”. Here, Fredrick declared war against the barbarism and chaos of untamed nature; his battles were fought by cartographers, surveyors, engineers and statisticians to establish control over the wild world of reeds and marshes. Following from this conception of nature, 19th century international cooperation along transboundary rivers also aimed to maximize the economic utility of the river—to straighten and deepen the river to create a more efficient economic highway—which also tamed the anarchic dangers of unregulated river politics. Second, I investigate the construction the international river’s meaning at three 19th century critical junctures in European politics—the 1815 Congress of Vienna, the 1856 Peace of Paris, and the 1885 Berlin Conference. I trace how competing meanings of the transboundary river coexisted at each juncture to complicate cooperation and shape the institutional beginnings of each river commission. In doing so, I contend that these international river commissions should be seen as contingent political formations born of specific European configurations of power, rather than as a straightforward progression towards a generalizable model institution that would eventually banish international conflict.
Cross‐talk between the epidermal growth factor‐like repeats/fibronectin 6–8 repeats domains of Tenascin‐R and microglia modulates neural stem/progenitor cell proliferation and differentiation

Mounting evidence has demonstrated that the microenvironment of stem/progenitor cells plays an important role in their proliferation and commitment to their fate. However, it remains unclear how all elements, such as astrocytes, microglia, extracellular matrix molecules, soluble factors, and their cross‐talk interactions in the microenvironments, affect neural stem/progenitor cell fate. This work explored the influences of cross‐talk between Tenascin‐R (TN‐R) and microglia on neural stem/progenitor cell proliferation and differentiation. Our results show that microglia triggered by TN‐R distinct domains EGF‐like repeats (EGFL) and fibronectin 6–8 repeats (FN6–8) significantly enhanced the proliferation of neural stem/progenitor cells and also obviously induced the differentiation into neurons but not oligodendrocytes. Neurite processes of neurons generated from neural progenitor cells were promoted by both EGFL and FN6–8 domains‐activated microglia. Microglia triggered by EGFL and FN6–8 secreted brain‐derived neurotrophic factor (BDNF) and transforming growth factor‐β (TGF‐β); interestingly, FN6–8 could activate microglia to secrete nerve growth factor in addition to BDNF and TGF‐β, but EGFL domain could not. All these data implied that the cross‐talk between TN‐R distinct domains EGFL/FN6–8 and microglia promoted neural stem/progenitor cell proliferation and induced their differentiation into neurons. © 2007 Wiley‐Liss, Inc.
Automatic text categorization based on angle distribution

In order to improve the performance of Chinese text categorization, a new Chinese text categorization method based on angle distribution is presented. The new method describes the text with a more precise model and proposed a new categorization algorithm by employing angle distribution. Simulation results on open Chinese text collection show that the precision and recall of most classes have been increased with reference to the classical method, and the macro average of precision and recall are both about 72 percents, which certificating the effectiveness and feasibility of the angle distribution-based algorithm.
BDNF and glucocorticoids regulate corticotrophin-releasing hormone (CRH) homeostasis in the hypothalamus

Regulation of the hypothalamic–pituitary–adrenal (HPA) axis is critical for adaptation to environmental changes. The principle regulator of the HPA axis is corticotrophin-releasing hormone (CRH), which is made in the parventricular nucleus and is an important target of negative feedback by glucocorticoids. However, the molecular mechanisms that regulate CRH are not fully understood. Disruption of normal HPA axis activity is a major risk factor of neuropsychiatric disorders in which decreased expression of the glucocorticoid receptor (GR) has been documented. To investigate the role of the GR in CRH neurons, we have targeted the deletion of the GR, specifically in the parventricular nucleus. Impairment of GR function in the parventricular nucleus resulted in an enhancement of CRH expression and an up-regulation of hypothalamic levels of BDNF and disinhibition of the HPA axis. BDNF is a stress and activity-dependent factor involved in many activities modulated by the HPA axis. Significantly, ectopic expression of BDNF in vivo increased CRH, whereas reduced expression of BDNF, or its receptor TrkB, decreased CRH expression and normal HPA functions. We find the differential regulation of CRH relies upon the cAMP response-element binding protein coactivator CRTC2, which serves as a switch for BDNF and glucocorticoids to direct the expression of CRH.