A Family of Maximum Margin Criterion for Adaptive Learning

In recent years, pattern analysis plays an important role in data mining and recognition, and many variants have been proposed to handle complicated scenarios. In the literature, it has been quite familiar with high dimensionality of data samples, but either such characteristics or large data have become usual sense in real-world applications. In this work, an improved maximum margin criterion (MMC) method is introduced firstly. With the new definition of MMC, several variants of MMC, including random MMC, layered MMC, 2D^2 MMC, are designed to make adaptive learning applicable. Particularly, the MMC network is developed to learn deep features of images in light of simple deep networks. Experimental results on a diversity of data sets demonstrate the discriminant ability of proposed MMC methods are compenent to be adopted in complicated application scenarios.Comment: 14 page

Conjugated polyelectrolyte nano field emission adlayers.

Here we report on a straightforward and rapid means of enhancing the field electron emission performance of nascent vertically aligned multi-walled carbon nanotubes by introducing a polar zwitterionic conjugated polyelectrolyte adlayer at the vacuum-emitter interface. We attribute the observed 66% decrease in turn-on electric field to the augmented emitter micro-morphology and shifted surface band structure. The composite emitters can be optically modulated by exploiting the absorption cross-section of the solution cast adlayer, which increases the local carrier concentration which broadens the effective electrostatic shape of the emitter during optical excitation. Assessment via scanning anode field emission microscopy reveals a 25% improvement in DC time stability, a significant reduction in long-term hysteresis shift, and a threefold increase in bandwidth during pulsed mode operation.Oppenheimer TrustThis is the final version of the article. It first appeared from the Royal Society of Chemistry via http://dx.doi.org/10.1039/c6nh00071

The Paleoproterozoic Chibaisong Mafic-Ultramafic Intrusion and Cu-Ni Deposit, North China Craton: SHRIMP Zircon U-Pband Re-Os Geochronology and Geodynamic Implications

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Unique Carboniferous-Permian tectonic-metallogenic framework of Northern Xinjiang (NW China): Constraints for the tectonics of the southern Paleoasian Domain

The late Paleozoic tectonic-metallogenic framework of North Xinjiang of the southern Paleoasian Domain was characterized by a serious of Carboniferous-Permian events, including: (1) late Carboniferous-Permian Chinese Altay island arc and its metamorphism, granulite in the Chinese Altay, radiolarian chert and high-pressure/ultra-high-pressure metamorphism; (2) late Carboniferous-early Permian adakites, Alaskan-type mafic-ultramafic complexes, and calc-alkaline magmatism, together with porphyry copper deposits, which occurred in the North Xinjiang; and (3) late Carboniferous ophiolite and island arc volcanic rocks located in the Tian Shan. Combined with the facts that there was no typical foreland basin, no typical collisional-type granitoid, and there were large amount of strike-slip faulting, it is suggested that in the Carboniferous-early Permian North Xinjiang was characterized by the coexistence of compression-extension-strike-slip structures with active magmatism and metallogeny. These phenomena all indicate that there were active margins during the late Carboniferous-early Permian, leading to the notion that the complicated accretionary orogeny along the southern Paleoasian Domain may have lasted to the latest Carboniferous-Permian.新疆北部晚古生代独特的构造一成矿作用以发育大量石炭纪一二叠纪构造一成矿事件为特征, 其中包括: (l) 发育于晚石炭世一二叠世的阿尔泰岛弧及其变质事件、阿尔泰麻粒岩与基性杂岩、西南天山放射虫硅质岩和高压一超高压一低压麻拉岩相变质事件; (2 )北疆发育的石炭纪(一二叠世)埃达克岩一高镁安山岩一富N d 玄武质岩组合、阿拉斯加型基性一超基性杂岩和大量的与俯冲相关的钙碱性岩浆活动与斑岩型铜矿床成矿作用; (3) 天山晚石炭世晚期蛇绿岩与岛弧火山岩等。结合北疆地区相关的前陆盆地发育不明显、碰撞型花岗岩欠发育与大量发育平行造山带大型走滑构造等现象, 可以认为新疆北部在石炭纪一二叠纪挤压一伸展一走滑并存, 岩浆活动与成矿作用活跃。这些新进展表明新疆北部在晚石炭世一二叠纪可能仍存在活动陆缘, 因此, 古亚洲洋构造域南部复杂增生造山作用最后延至晚石炭世晚期一二叠纪。published_or_final_versio

Lack of association between the GRP78 polymorphisms in the promoter and 3' UTR and susceptibility to chronic HBV infection in a Chinese Han population

<p>Abstract</p> <p>Background</p> <p>Hepatitis B virus (HBV) infection causes large amount of unfolding or false-folding protein accumulation in the endoplasmic reticulum (ER), which in turn induces the expression of glucose-regulated protein 78 (GRP78). The aim in the present study was to analyse the potential association between GRP78 single-nucleotide polymorphisms (SNPs) and the risk of HBV infection.</p> <p>Methods</p> <p>The associations between seven common <it>GRP78 </it>polymorphisms in the promoter (rs391957, rs17840762, rs17840761, rs11355458) and in the 3' untranslated region (UTR) (rs16927997, rs1140763, rs12009) and possible risk of chronic HBV infection were assessed in a case-control study. 496 cases and 539 individually matched healthy controls were genotyped.</p> <p>Results</p> <p>Overall, no associations were observed in genotypic analyses. In addition, haplotypes and diplotypes combining those SNPs in the promoter or in the 3' UTR in high linkage disequilibrium (LD) were also not associated with HBV risk.</p> <p>Conclusion</p> <p>These observations do not support a role for <it>GRP78 </it>polymorphisms in HBV infection in a predominantly Chinese Han population.</p

Suppression of liver tumor growth and metastasis by adiponectin in nude mice through inhibition of tumor angiogenesis and downregulation of rho kinase/IFN-inducible protein 10/matrix metalloproteinase 9 signaling

Purpose: We aimed to investigate the effects of adiponectin on liver cancer growth and metastasis and explore the underlying mechanisms. Experimental Design: An orthotopic liver tumor nude mice model with distant metastatic potential was applied. Either Ad-adiponectin (1 × 10 8; treatment group) or Ad-luciferase (control group) was injected via portal vein after tumor implantation. Tumor growth and metastasis were monitored by Xenogen In vivo Imaging System. Hepatic stellate cell activation by α-smooth muscle actin staining, microvessel density by CD34 staining, macrophage infiltration in tumor tissue, and cell signaling leading to invasion, migration [Rho kinase (ROCK), IFN-inducible protein 10 (IP10), and matrix metalloproteinase 9], and angiogenesis [vascular endothelial growth factor (VEGF) and angiopoietin 1] were also compared. Tumor-nontumor margin was examined under electron microscopy. Direct effects of adiponectin on liver cancer cells and endothelial cells were further investigated by a series of functional studies. Results: Tumor growth was significantly inhibited by adiponectin treatment, accompanied by a lower incidence of lung metastasis. Hepatic stellate cell activation and macrophage infiltration in the liver tumors were suppressed by adiponectin treatment, along with decreased microvessel density. The treatment group had less Ki-67-positive tumor cells and downregulated protein expression of ROCK1, proline-rich tyrosine kinase 2, and VEGF. Tumor vascular endothelial cell damage was found in the treatment group under electron microscopy. In vitro functional study showed that adiponectin not only downregulated the ROCK/IP10/VEGF signaling pathway but also inhibited the formation of lamellipodia, which contribute to cell migration. Conclusion: Adiponectin treatment significantly inhibited liver tumor growth and metastasis by suppression of tumor angiogenesis and downregulation of the ROCK/IP10/matrix metalloproteinase 9 pathway. ©2010 AACR.postprin

A 10-year study reveals clinical and laboratory evidence for the 'semi-invasive' properties of chronic pulmonary aspergillosis

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Anti-epileptic effect of Ganoderma lucidum polysaccharides by inhibition of intracellular calcium accumulation and stimulation of expression of CaMKII a in epileptic hippocampal neurons

Purpose: To investigate the mechanism of the anti-epileptic effect of Ganoderma lucidum polysaccharides (GLP), the changes of intracellular calcium and CaMK II a expression in a model of epileptic neurons were investigated. Method: Primary hippocampal neurons were divided into: 1) Control group, neurons were cultured with Neurobasal medium, for 3 hours; 2) Model group I: neurons were incubated with Mg2+ free medium for 3 hours; 3) Model group II: neurons were incubated with Mg2+ free medium for 3 hours then cultured with the normal medium for a further 3 hours; 4) GLP group I: neurons were incubated with Mg2+ free medium containing GLP (0.375 mg/ml) for 3 hours; 5) GLP group II: neurons were incubated with Mg2+ free medium for 3 hours then cultured with a normal culture medium containing GLP for a further 3 hours. The CaMK II a protein expression was assessed by Western-blot. Ca2+ turnover in neurons was assessed using Fluo-3/AM which was added into the replacement medium and Ca2+ turnover was observed under a laser scanning confocal microscope. Results: The CaMK II a expression in the model groups was less than in the control groups, however, in the GLP groups, it was higher than that observed in the model group. Ca2+ fluorescence intensity in GLP group I was significantly lower than that in model group I after 30 seconds, while in GLP group II, it was reduced significantly compared to model group II after 5 minutes. Conclusion: GLP may inhibit calcium overload and promote CaMK II a expression to protect epileptic neuron

Humanized mice efficiently engrafted with fetal hepatoblasts and syngeneic immune cells develop human monocytes and NK cells

Human liver chimeric mice are useful models of human hepatitis virus infection, including hepatitis B and C virus infections. Independently, immunodeficient mice reconstituted with CD34(+) hematopoietic stem cells (HSC) derived from fetal liver reliably develop human T and B lymphocytes. Combining these systems has long been hampered by inefficient liver reconstitution of human fetal hepatoblasts. Our study aimed to enhance hepatoblast engraftment in order to create a mouse model with syngeneic human liver and immune cells.The effects of human oncostatin-M administration on fetal hepatoblast engraftment into immunodeficient fah(-/-) mice was tested. Mice were then transplanted with syngeneic human hepatoblasts and HSC after which human leukocyte chimerism and functionality were analyzed by flow cytometry, and mice were challenged with HBV.Addition of human oncostatin-M enhanced human hepatoblast engraftment in immunodeficient fah(-/-) mice by 5-100 fold. In contrast to mice singly engrafted with HSC, which predominantly developed human T and B lymphocytes, mice co-transplanted with syngeneic hepatoblasts also contained physiological levels of human monocytes and natural killer cells. Upon infection with HBV, these mice displayed rapid and sustained viremia.Our study provides a new mouse model with improved human fetal hepatoblast engraftment and an expanded human immune cell repertoire. With further improvements, this model may become useful for studying human immunity against viral hepatitis.Important human pathogens such as hepatitis B virus, hepatitis C virus and human immunodeficiency virus only infect human cells which complicates the development of mouse models for the study of these pathogens. One way to make mice permissive for human pathogens is the transplantation of human cells into immune-compromised mice. For instance, the transplantation of human liver cells will allow the infection of these so-called liver chimeric mice with hepatitis B virus and hepatitis C virus. The co-transplantation of human immune cells into liver chimeric mice will further allow the study of human immune responses to hepatitis B virus or hepatitis C virus. However, for immunological studies it will be crucial that the transplanted human liver and immune cells are derived from the same human donor. In our study we describe the efficient engraftment of human fetal liver cells and immune cells derived from the same donor into mice. We show that liver co-engraftment resulted in an expanded human immune cell repertoire, including monocytes and natural killer cells in the liver. We further demonstrate that these mice could be infected with hepatitis B virus, which lead to an expansion of natural killer cells. In conclusion we have developed a new mouse model that could be useful to study human immune responses to human liver pathogens