GeohashTile: Vector Geographic Data Display Method Based on Geohash

© 2020 MDPI AG. All rights reserved. In the development of geographic information-based applications for mobile devices, achieving better access speed and visual effects is the main research aim. In this paper, we propose a new geographic data display method based on Geohash, namely GeohashTile, to improve the performance of traditional geographic data display methods in data indexing, data compression, and the projection of different granularities. First, we use the Geohash encoding system to represent coordinates, as well as to partition and index large-scale geographic data. The data compression and tile encoding is accomplished by Geohash. Second, to realize a direct conversion between Geohash and screen-pixel coordinates, we adopt the relative position projection method. Finally, we improve the calculation and rendering efficiency by using the intermediate result caching method. To evaluate the GeohashTile method, we have implemented the client and the server of the GeohashTile system, which is also evaluated in a real-world environment. The results show that Geohash encoding can accurately represent latitude and longitude coordinates in vector maps, while the GeohashTile framework has obvious advantages when requesting data volume and average load time compared to the state-of-the-art GeoTile system

BCCIP regulates homologous recombination by distinct domains and suppresses spontaneous DNA damage

Homologous recombination (HR) is critical for maintaining genome stability through precise repair of DNA double-strand breaks (DSBs) and restarting stalled or collapsed DNA replication forks. HR is regulated by many proteins through distinct mechanisms. Some proteins have direct enzymatic roles in HR reactions, while others act as accessory factors that regulate HR enzymatic activity or coordinate HR with other cellular processes such as the cell cycle. The breast cancer susceptibility gene BRCA2 encodes a critical accessory protein that interacts with the RAD51 recombinase and this interaction fluctuates during the cell cycle. We previously showed that a BRCA2- and p21-interacting protein, BCCIP, regulates BRCA2 and RAD51 nuclear focus formation, DSB-induced HR and cell cycle progression. However, it has not been clear whether BCCIP acts exclusively through BRCA2 to regulate HR and whether BCCIP also regulates the alternative DSB repair pathway, non-homologous end joining. In this study, we found that BCCIP fragments that interact with BRCA2 or with p21 each inhibit DSB repair by HR. We further show that transient down-regulation of BCCIP in human cells does not affect non-specific integration of transfected DNA, but significantly inhibits homology-directed gene targeting. Furthermore, human HT1080 cells with constitutive down-regulation of BCCIP display increased levels of spontaneous single-stranded DNA (ssDNA) and DSBs. These data indicate that multiple BCCIP domains are important for HR regulation, that BCCIP is unlikely to regulate non-homologous end joining, and that BCCIP plays a critical role in resolving spontaneous DNA damage

Intelligent Reflecting Surface Aided Power Control for Physical-Layer Broadcasting

Reconfigurable intelligent surface (RIS), a recently introduced technology for future wireless com-munication systems, enhances the spectral and energy efficiency by intelligently adjusting the propaga-tion conditions between a base station (BS) and mobile equipments (MEs). An RIS consists of manylow-cost passive reflecting elements to improve the quality of the received signal. In this paper, westudy the problem of power control at the BS for the RIS aided physical-layer broadcasting. Our goalis to minimize the transmit power at the BS by jointly designing the transmit beamforming at the BSand the phase shifts of the passive elements at the RIS. Furthermore, to help validate the proposedoptimization methods, we derive lower bounds to quantify the average transmit power at the BS as afunction of the number of MEs, the number of RIS elements, and the number of antennas at the BS.The simulation results demonstrated that the average transmit power at the BS is close to the lowerbound in an RIS aided system, and is significantly lower than the average transmit power in conventionalschemes without the RIS

Involvement of Caveolin-1 in Repair of DNA Damage through Both Homologous Recombination and Non-Homologous End Joining

Caveolin-1 (Cav-1), the major component of caveolae, is a 21-24 kDa integral membrane protein that interacts with a number of signaling molecules. By acting as a scaffolding protein, Cav-1 plays crucial roles in the regulation of various physiologic and patho-physiologic processes including oncogenic transformation and tumorigenesis, and tumor invasion and metastasis.In the present study we sought to explore the role of Cav-1 in response to DNA damage and the mechanism involved. We found that the level of Cav-1 was up-regulated rapidly in cells treated with ionizing radiation. The up-regulation of Cav-1 following DNA damage occurred only in cells expressing endogenous Cav-1, and was associated with the activation of DNA damage response pathways. Furthermore, we demonstrated that the expression of Cav-1 protected cells against DNA damage through modulating the activities of both the homologous recombination (HR) and non-homologous end joining (NHEJ) repair systems, as evidenced by the inhibitory effects of the Cav-1-targeted siRNA on cell survival, HR frequency, phosphorylation of DNA-dependent protein kinase (DNA-PK), and nuclear translocation of epidermal growth factor receptor (EGFR) following DNA damage, and by the stimulatory effect of the forced expression of Cav-1 on NHEJ frequency.Our results indicate that Cav-1 may play a critical role in sensing genotoxic stress and in orchestrating the response of cells to DNA damage through regulating the important molecules involved in maintaining genomic integrity

Effects of Weaning by Surrogate Mothers (ACI) on Tumor Development in SD Rats Treatedwith Methylnitrosourea (MNU) and/or N-Methyl-N-nitro-N-nitrosoguanidine (MNNG)

In this experiment, MNU was administered, followed by MNNG, to assess effects ofsurrogate mothering on tumor. One or two day old male SD pups were treated with or without30mg/kg body weight of methylnitrosourea (MNU) and nursed by SD or ACI surrogate mothersfor 5 weeks. When 6-weeks-old they were then treated with 100ppmN-methyl-N-nitro-N-nitrosoguanidine (MNNG) or tap water for 16 weeks. The tumor incidencein the MNNG alone group was significantly lower than with MNU alone or MNU+MNNG (p<0.01).Kidney or nerve tumors mainly developed in the MNU group, gastric tumors in the MNNG group,and the two combined in the MNU+MNNG group. The incidence and mean number of tumors didnot significantly differ between the two weaning groups. However, mean survival time withthe ACI surrogate mothers after treatment with MNU was increased as compared with the SDmother group. Cumulative development of tumors in the ACI surrogate mother group was alsodelayed (p<0.05). Similar results were obtained with MNU+MNNG and MNNG alone. The presentexperiment suggested that tumor induction might be effected by components of the mother'smilk

Regulation of MUTYH, a DNA Repair Enzyme, in Renal Proximal Tubular Epithelial Cells

MUTYH is a DNA repair enzyme that initiates a base excision repair (BER) by recognizing and removing 8-Oxoguanine (8-oxoG) and its paired adenine. We demonstrated that both TGF-β1 and H2O2 treatment led to an increased 8-oxoG in cultured human proximal tubule epithelial (HK-2) cells, while the former induced epithelial-mesenchymal transition and the latter caused cell apoptosis. Without stimulation, HK-2 cells showed MUTYH expression in mitochondria. TGF-β1 triggered a transient upregulation of mitochondrial MUTYH and induced the expression of nuclear isoforms, while H2O2 showed no role on MUTYH expression. Ureteral obstruction (UUO) mice exhibited high 8-oxoG reactivity with tubulointerstitial lesions. After obstruction, the MUTYH expression was increased only in tubules at day 3 and decreased with obvious tubular atrophy at day 10. Particularly, MUTYH was primarily located in normal tubular cytoplasm with a dominant mitochondrial form. A few cells with nuclear MUTYH expression were observed in the fibrotic interstitium. We confirmed that increased MUTYH expression was upregulated and positively correlated with the severity of kidney fibrosis. Thus, renal fibrosis caused a cell-type-specific and time-dependent response of oxidative DNA repairs, even within the same tissues. It suggests that intervention of MUTYH might be effective for therapies

Requirement of Mouse BCCIP for Neural Development and Progenitor Proliferation

Multiple DNA repair pathways are involved in the orderly development of neural systems at distinct stages. The homologous recombination (HR) pathway is required to resolve stalled replication forks and critical for the proliferation of progenitor cells during neural development. BCCIP is a BRCA2 and CDKN1A interacting protein implicated in HR and inhibition of DNA replication stress. In this study, we determined the role of BCCIP in neural development using a conditional BCCIP knock-down mouse model. BCCIP deficiency impaired embryonic and postnatal neural development, causing severe ataxia, cerebral and cerebellar defects, and microcephaly. These development defects are associated with spontaneous DNA damage and subsequent cell death in the proliferative cell populations of the neural system during embryogenesis. With in vitro neural spheroid cultures, BCCIP deficiency impaired neural progenitor's self-renewal capability, and spontaneously activated p53. These data suggest that BCCIP and its anti-replication stress functions are essential for normal neural development by maintaining an orderly proliferation of neural progenitors

Fabrication of Au/Pd alloy nanoparticle/Pichia pastoris composites: a microorganism-mediated approach

Fundamental Research Funds for Central Universities [2010121051]; NSFC projects [21106117, 21036004]Synthesis of metal nanoparticles (NPs) is in the limelight in modern nanotechnology. In this present study, bimetallic Au/Pd NP/Pichia pastoris composites were successfully fabricated through a one-pot microbial reduction of aqueous HAuCl4 and PdCl2 in the presence of H-2 as an electron donor. Interestingly, flower-like alloy Au/Pd NP/Pichia pastoris composites were obtained under the following conditions, NaCl concentration 0.9% (w/v), molar ratio of Au/Pd (1 : 2) and the time for pre-adsorption of Au(III) and Pd(II) ions 15 min, through fresh yeast reduction. The mapping results from scanning transmission electron microscopy (STEM) with a high-angle annular dark field detector confirmed that the Au/Pd NPs on the surface of the yeast were indeed alloy. Furthermore, the energy dispersive X-ray (EDX) and X-ray photoelectron spectroscopy (XPS) measurements showed that the composition of the bimetallic NPs were consistent with the initial molar ratio of the precursors