The multi-level and multi-dimensional quantum wavelet packet transforms

© 2018, The Author(s). The classical wavelet packet transform has been widely applied in the information processing field. It implies that the quantum wavelet packet transform (QWPT) can play an important role in quantum information processing. In this paper, we design quantum circuits of a generalized tensor product (GTP) and a perfect shuffle permutation (PSP). Next, we propose multi-level and multi-dimensional (1D, 2D and 3D) QWPTs, including a Haar QWPT (HQWPT), a D4 QWPT (DQWPT) based on the periodization extension and their inverse transforms for the first time, and prove the correctness based on the GTP and PSP. Furthermore, we analyze the quantum costs and the time complexities of our proposed QWPTs and obtain precise results. The time complexities of HQWPTs is at most 6 on 2n elements, which illustrates high-efficiency of the proposed QWPTs. Simulation experiments demonstrate that the proposed QWPTs are correct and effective

Helicobacter pylori infection is associated with increased expression of macrophage migratory inhibitory factor - by epithelial cells, T cells, and macrophages - in gastric mucosa

The macrophage migratory inhibitory factor (MIF) plays a pivotal role in inflammatory and immune diseases; however, its role in gastrointestinal diseases has not been clarified. This study intended to determine the expression of MIF, by gastric epithelial cells, T cells, and macrophages, in Helicobacter pylori-induced gastritis. Sixty-four patients (30 males, 34 females; mean age, 47 years) referred for upper endoscopy were recruited. Biopsy specimens from the gastric antrum and corpus were obtained for (1) detection of H. pylori and histological examination, (2) single and double immunostaining to test for expression of MIF protein in epithelial cells, T cells, and macrophages, and (2) in situ hybridization for expression of MIF mRNA within the lamina propria. In mucosal specimens from each of the 2 sites, both the percentage of MIF + epithelial cells and the numbers of MIF mRNA+ inflammatory cells, MIF+ T cells, and MIF+ macrophages were significantly higher in H. pylori-positive patients than in H. pylori-negative patients. Overall, the percentage of MIF+ epithelial cells and the numbers of MIF mRNA+ cells, MIF+ T cells, and MIF+ macrophages were higher in the antrum than in the corpus. The percentage of MIF+ epithelial cells and the numbers of MIF mRNA+ cells, MIF+ T cells, and MIF+ macrophages increased in chronic gastritis, but, in the absence of H. pylori infection, this increase disappeared for all except MIF+ T cells. Therefore, H. pylori infection is associated with increased expression of the MIF protein and MIF mRNA in gastric epithelial and inflammatory cells; along with other cytokines, MIF may play a significant role in gastric inflammation related to H. pylori infection.published_or_final_versio

Expression of macrophage migration inhibitory factor in Helicobacter pylori-induced gastritis and peptic ulcer disease

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Role of CD56-expressing immature biliary epithelial cells in biliary atresia

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Observation of spectral enhancement in a soliton fiber laser with fiber Bragg grating

Author name used in this publication: L. M. ZhaoAuthor name used in this publication: C. LuAuthor name used in this publication: H. Y. TamAuthor name used in this publication: P. Shum2008-2009 > Academic research: refereed > Publication in refereed journalVersion of RecordPublishe

Nucleation of dislocations and their dynamics in layered oxide cathode materials during battery charging

Defects and their interactions in crystalline solids often underpin material properties and functionality as they are decisive for stability, result in enhanced diffusion, and act as a reservoir of vacancies. Recently, lithium-rich layered oxides have emerged among the leading candidates for the next-generation energy storage cathode material, delivering 50 % excess capacity over commercially used compounds. Oxygen-redox reactions are believed to be responsible for the excess capacity, however, voltage fading has prevented commercialization of these new materials. Despite extensive research the understanding of the mechanisms underpinning oxygen-redox reactions and voltage fade remain incomplete. Here, using operando three-dimensional Bragg coherent diffractive imaging, we directly observe nucleation of a mobile dislocation network in nanoparticles of lithium-rich layered oxide material. Surprisingly, we find that dislocations form more readily in the lithium-rich layered oxide material as compared with a conventional layered oxide material, suggesting a link between the defects and the anomalously high capacity in lithium-rich layered oxides. The formation of a network of partial dislocations dramatically alters the local lithium environment and contributes to the voltage fade. Based on our findings we design and demonstrate a method to recover the original high voltage functionality. Our findings reveal that the voltage fade in lithium-rich layered oxides is reversible and call for new paradigms for improved design of oxygen-redox active materials

Structural insight into SUMO chain recognition and manipulation by the ubiquitin ligase RNF4

The small ubiquitin-like modifier (SUMO) can form polymeric chains that are important signals in cellular processes such as meiosis, genome maintenance and stress response. The SUMO-targeted ubiquitin ligase RNF4 engages with SUMO chains on linked substrates and catalyses their ubiquitination, which targets substrates for proteasomal degradation. Here we use a segmental labelling approach combined with solution nuclear magnetic resonance (NMR) spectroscopy and biochemical characterization to reveal how RNF4 manipulates the conformation of the SUMO chain, thereby facilitating optimal delivery of the distal SUMO domain for ubiquitin transfer

Asiatic Acid Inhibits Liver Fibrosis by Blocking TGF-beta/Smad Signaling In Vivo and In Vitro

Liver fibrosis is a major cause of liver failure, but treatment remains ineffective. In the present study, we investigated the mechanisms and anti-hepatofibrotic activities of asiatic acid (AA) in a rat model of liver fibrosis induced by carbon tetrachloride (CCl4) and in vitro in TGF-beta1-stimulated rat hepatic stellate cell line (HSC-T6). Treatment with AA significantly attenuated CCl4-induced liver fibrosis and functional impairment in a dosage-dependent manner, including blockade of the activation of HSC as determined by inhibiting de novo alpha smooth muscle actin (a-SMA) and collagen matrix expression, and an increase in ALT and AST (all p<0.01). The hepatoprotective effects of AA on fibrosis were associated with upregulation of hepatic Smad7, an inhibitor of TGF-beta signaling, thereby blocking upregulation of TGF-beta1 and CTGF and the activation of TGF-beta/Smad signaling. The anti-fibrosis activity and mechanisms of AA were further detected in vitro in HSC-T6. Addition of AA significantly induced Smad7 expression by HSC-T6 cells, thereby inhibiting TGF-beta1-induced Smad2/3 activation, myofibroblast transformation, and collagen matrix expression in a dosage-dependent manner. In contrast, knockdown of Smad7 in HSC-T6 cells prevented AA-induced inhibition of HSC-T6 cell activation and fibrosis in response to TGF-beta1, revealing an essential role for Smad7 in AA-induced anti-fibrotic activities during liver fibrosis in vivo and in vitro. In conclusion, AA may be a novel therapeutic agent for liver fibrosis. Induction of Smad7-dependent inhibition of TGF-beta/Smad-mediated fibrogenesis may be a central mechanism by which AA protects liver from injury