842 research outputs found
Get the permission for paper publication--UTiris--Author Siming Zheng--2019-11-10
No full textRequesting the permission for paper publication.Author Siming ZhengWritten date: 2019-11-10</div
A possible link between the Galactic center HESS source and Sagittarius A*
No full textD. R. Ballantyne, Fulvio Melia, Siming Liu, and
Roland M. Crocke
An Efficient Implementation of Lattice Staggered Multicarrier Faster-Than-Nyquist Signaling
No full textIn this letter, we investigate the lattice staggered multicarrier faster-than-Nyquist (MFTN) signaling. Specifically, we consider the time-frequency packing and optimal hexagonal lattice over additive white Gaussian noise channels. First, an efficient implementation of the lattice staggered MFTN based on the fast Fourier transform algorithm is proposed, and we show that the modulation and demodulation complexity could be substantially reduced. Furthermore, we consider, at the receiver, a low-complexity symbol-by-symbol detector. Our practical spectral efficiency and bit-error-rate performance investigation demonstrate that the MFTN with optimal hexagonal lattice outperforms the conventional rectangular lattice
Lipid-based DNA/siRNA transfection agents disrupt neuronal bioenergetics and mitophagy
No full textA multitude of natural and artificial compounds have been recognized to modulate autophagy, providing direct or, through associated pathways, indirect entry points to activation and inhibition. While these pharmacological tools are extremely useful in the study of autophagy, their abundance also suggests the potential presence of unidentified autophagic modulators that may interfere with experimental designs if applied unknowingly. Here, we report unanticipated effects on autophagy and bioenergetics in neuronal progenitor cells (NPCs) incubated with the widely used lipid-based transfection reagent lipofectamine (LF), which induced mitochondria depolarization followed by disruption of electron transport. When NPCs were exposed to LF for 5 h followed by 24, 48, and 72 h in LF-free media, an immediate increase in mitochondrial ROS production and nitrotyrosine formation was observed. These events were accompanied by disrupted mitophagy (accumulation of dysfunctional and damaged mitochondria, and of LC3II and p62), in an mTOR- and AMPK-independent manner, and despite the increased mitochondrial PINK1 (PTEN-inducible kinase 1) localization. Evidence supported a role for a p53-mediated abrogation of parkin translocation and/or abrogation of membrane fusion between autophagosome and lysosomes. While most of the outcomes were LF-specific, only two were shared by OptiMEM exposure (with no serum and reduced glucose levels) albeit at lower extents. Taken together, our findings show that the use of transfection reagents requires critical evaluation with respect to consequences for overall cellular health, particularly in experiments designed to address autophagy-inducing effects and/or energy stress.</jats:p
Optimal multicarrier faster-than-Nyquist signaling under symbol-by-symbol detection
No full textWe consider the multicarrier faster-than-Nyquist (MFTN) signaling under low complexity symbol-by-symbol detection, where the lattice structure and time-frequency spacing play key roles in determining the system performance. Specifically, the energy of intersymbol interference (ISI) and intercarrier interference (ICI) introduced by time-frequency packing is taken as a figure of merit. In this regard, we firstly prove the asymptotical equivalence of the hexagonal MFTN and conventional rectangular MFTN signaling systems when the time packing factor is small enough, and we also reveal the potential benefit of hexagonal MFTN with respect to conventional rectangular MFTN for moderate time-frequency spacing. Then, an optimal MFTN signaling scheme under the given signaling efficiency is proposed. By jointly optimizing the lattice structure and time-frequency spacing to minimize the interference energy, we show that the optimal time-frequency spacing can be accurately obtained with substantially reduced complexity than conventional exhaustive search scheme. Finally, we demonstrate that there is a good match between minimizing the interference energy and maximizing the achievable spectral efficiency, which is also considered to be an important figure for MFTN signaling system. Our theoretical analysis and numerical results validate that the proposed scheme outperforms conventional MFTN signaling system
Author Siming Zheng-Experimental Iris Images--IRIS V.1
No full textUniversity of Tehran IRIS (UTIRIS) image repository is the first iris biometric databank registered in two distinct sessions of Visible Wavelength (VW) and Near InfraRed (NIR) imaging during 24-27th of June 2007
Differential Reactivity of Metal Binding Domains of Copper ATPases towards Cisplatin and Colocalization of Copper and Platinum
No full textThe Menkes (MNK) and Wilson (WLN) disease proteins are two P-type ATPases responsible for active Cu efflux. These ATPases are also associated with resistance to cisplatin. In this work, different metal-binding domains (MBDs) of ATPases (9 out of 12 domains) were compared based on their reactivity towards cisplatin. The reaction rates of the MBDs can be largely different; the reaction of MNK6 is about six times faster than that of WLN2. Copper coordination favors the platination of the MBDs to different extents. The rate of platination was generally greater for holo-MBDs than for apo-MBDS (particularly in the case of WLN4 and WLN2); however, it was negligibly affected in the case of MNK6. Interestingly, the platinum binding weakens the CuI coordination, but does not expel the copper ion from MBDs. The latter results nicely explain the inhibitory effect of Cu upon the cisplatin translocation promoted by Cu-ATPases and can help in understanding how copper levels can modulate the sensitivity of cancer cells to platinum chemotherapy
Tetrathiomolybdate inhibits the reaction of cisplatin with human copper chaperone Atox1
No full textCisplatin is a widely used anticancer drug in clinic, and ammonium tetrathiomolybdate ([(NH 4 ) 2 MoS 4 ], TM) is a copper chelator used in clinic for the treatment of Wilson's disease. Recently, TM has been found to enhance the therapeutic effect of cisplatin; however, the origin of this effect is not clear. Here we found that TM can inhibit the reaction of cisplatin with Cu-Atox1 and prevent the protein unfolding and aggregation induced by cisplatin. Although Ag(i) binds to Atox1 in a way similar to Cu(i)-Atox1, TM does not prevent the reaction of Ag-Atox1 with cisplatin. This result indicates that the formation of a Mo-centered trimeric protein cluster in the TM-Cu-Atox1 system plays a role in the inhibitory effect. This work provides new insights into the mechanism by which TM enhances the cytotoxic efficacy of cisplatin and helps to circumvent cisplatin resistance of tumor cells
Cisplatin reacts with histone H1 and the adduct forms a ternary complex with DNA
No full textCisplatin is an anticancer drug widely used in clinics; it induces the apoptosis of cancer cells by targeting DNA. However, its interaction with proteins has been found to be crucial in modulating the pre and post-target activity. Nuclear DNA is tightly assembled with histone proteins to form nucleosomes in chromatin; this can impede the drug to access DNA. On the other hand, the linker histone H1 is considered 'the gate to nucleosomal DNA' due to its exposed location and dynamic conformation; therefore, this protein can influence the platination of DNA. In this study, we performed a reaction of cisplatin with histone H1 and investigated the interaction of the H1/cisplatin adduct with DNA. The reactions were conducted on the N-terminal domains of H1.4 (sequence 1-90, H1 N90 ) and H1.0 (sequence 1-7, H1 N7 ). The results show that H1 readily reacts with cisplatin and generates bidentate and tridentate adducts, with methionine and glutamate residues as the preferential binding sites. Chromatographic and NMR analyses show that the platination rate of H1 is slightly higher than that of DNA and the platinated H1 can form H1-cisplatin-DNA ternary complexes. Interestingly, cisplatin is more prone to form H1-Pt-DNA ternary complexes than trans-oriented platinum agents. The formation of H1-cisplatin-DNA ternary complexes and their preference for cis- over trans-oriented platinum agents suggest an important role of histone H1 in the mechanism of action of cisplatin
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