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2021 ◽  
Author(s):  
Yan Zihui ◽  
Cong Liang

With the development of DNA synthesis and sequencing technologies, DNA becomes a promising medium forlong-term data storage. Three types of errors may occur in the DNA strand, insertions, deletions and substitutions,which we collectively call edit errors. It is still challenging to design a code that can correct multiple edit errors onnon-binary alphabets. In this paper, we propose a new coding schema for correcting multiple edit errors on DNAstrands by splitting the whole strand into consecutive blocks with appropriate length and correcting a single editerror in each block. Our method, called theDNA-LMcode, could be considered a generalization of the Levenshteincode combined with the marker code. We provide a linear encoding and decoding algorithm for ourDNA-LMcode.Compared to other encoding methods for DNA strands of several hundred base-pairs, ourDNA-LMcode achievedsimilar code rates and a much lower average nucleotide error rate in decoding.


2021 ◽  
Author(s):  
Yan Zihui ◽  
Cong Liang

With the development of DNA synthesis and sequencing technologies, DNA becomes a promising medium forlong-term data storage. Three types of errors may occur in the DNA strand, insertions, deletions and substitutions,which we collectively call edit errors. It is still challenging to design a code that can correct multiple edit errors onnon-binary alphabets. In this paper, we propose a new coding schema for correcting multiple edit errors on DNAstrands by splitting the whole strand into consecutive blocks with appropriate length and correcting a single editerror in each block. Our method, called theDNA-LMcode, could be considered a generalization of the Levenshteincode combined with the marker code. We provide a linear encoding and decoding algorithm for ourDNA-LMcode.Compared to other encoding methods for DNA strands of several hundred base-pairs, ourDNA-LMcode achievedsimilar code rates and a much lower average nucleotide error rate in decoding.


Biomolecules ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 1313
Author(s):  
Selina F. Darling-Reed ◽  
Yasmeen Nkrumah-Elie ◽  
Dominique T. Ferguson ◽  
Hernan Flores-Rozas ◽  
Patricia Mendonca ◽  
...  

Garlic has long been used medicinally for many diseases, including cancer. One of the active garlic components is diallyl sulfide (DAS), which prevents carcinogenesis and reduces the incidence rate of several cancers. In this study, non-cancerous MCF-10A cells were used as a model to investigate the effect of DAS on Benzo (a)pyrene (BaP)-induced cellular carcinogenesis. The cells were evaluated based on changes in proliferation, cell cycle arrest, the formation of peroxides, 8-hydroxy-2-deoxyguanosine (8-OHdG) levels, the generation of DNA strand breaks, and DNA Polymerase β (Pol β) expression. The results obtained indicate that when co-treated with BaP, DAS inhibited BaP-induced cell proliferation (p < 0.05) to levels similar to the negative control. BaP treatment results in a two-fold increase in the accumulation of cells in the G2/M-phase of the cell cycle, which is restored to baseline levels, similar to untreated cells and vehicle-treated cells, when pretreated with 6 μM and 60 μM DAS, respectively. Co-treatment with DAS (60 μM and 600 μM) inhibited BaP-induced reactive oxygen species (ROS) formation by 132% and 133%, respectively, as determined by the accumulation of H2O2 in the extracellular medium and an increase in 8-OHdG levels of treated cells. All DAS concentrations inhibited BaP-induced DNA strand breaks through co-treatment and pre-treatment methods at all time points evaluated. Co-Treatment with 60 μM DAS increased DNA Pol β expression in response to BaP-induced lipid peroxidation and oxidative DNA damage. These results indicate that DAS effectively inhibited BaP-induced cell proliferation, cell cycle transitions, ROS, and DNA damage in an MCF-10A cell line. These results provide more experimental evidence for garlic’s antitumor abilities and corroborate many epidemiological studies regarding the association between the increased intake of garlic and the reduced risk of several types of cancer.


2021 ◽  
pp. 130645
Author(s):  
Yinping Deng ◽  
Jun Du ◽  
Donghua Chen ◽  
Guo-Jiang Mao ◽  
Bin Yang ◽  
...  

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Emilio Di Ianni ◽  
Johanna Samulin Erdem ◽  
Peter Møller ◽  
Nicklas Mønster Sahlgren ◽  
Sarah Søs Poulsen ◽  
...  

Abstract Background Multi-walled carbon nanotubes (MWCNT) have received attention due to extraordinary properties, resulting in concerns for occupational health and safety. Costs and ethical concerns of animal testing drive a need for in vitro models with predictive power in respiratory toxicity. The aim of this study was to assess pro-inflammatory response (Interleukin-8 expression, IL-8) and genotoxicity (DNA strand breaks) caused by MWCNT with different physicochemical properties in different pulmonary cell models and correlate these to previously published in vivo data. Seven MWCNT were selected; two long/thick (NRCWE-006/Mitsui-7 and NM-401), two short/thin (NM-400 and NM-403), a pristine (NRCWE-040) and two surface modified; hydroxylated (NRCWE-041) and carboxylated (NRCWE-042). Carbon black Printex90 (CB) was included as benchmark material. Human alveolar epithelial cells (A549) and monocyte-derived macrophages (THP-1a) were exposed to nanomaterials (NM) in submerged conditions, and two materials (NM-400 and NM-401) in co-cultures of A549/THP-1a and lung fibroblasts (WI-38) in an air-liquid interface (ALI) system. Effective doses were quantified by thermo-gravimetric-mass spectrometry analysis (TGA-MS). To compare genotoxicity in vitro and in vivo, we developed a scoring system based on a categorization of effects into standard deviation (SD) units (< 1, 1, 2, 3 or 4 standard deviation increases) for the increasing genotoxicity. Results Effective doses were shown to be 25 to 53%, and 21 to 57% of the doses administered to A549 and THP-1a, respectively. In submerged conditions (A549 and THP-1a cells), all NM induced dose-dependent IL-8 expression. NM-401 and NRCWE-006 caused the strongest pro-inflammatory response. In the ALI-exposed co-culture, only NM-401 caused increased IL-8 expression, and no DNA strand breaks were observed. Strong correlations were found between in vitro and in vivo inflammation when doses were normalized by surface area (also proxy for diameter and length). Significantly increased DNA damage was found for all MWCNT in THP-1a cells, and for short MWCNT in A549 cells. A concordance in genotoxicity of 83% was obtained between THP-1a cells and broncho-alveolar lavaged (BAL) cells. Conclusion This study shows correlations of pro-inflammatory potential in A549 and THP-1a cells with neutrophil influx in mice, and concordance in genotoxic response between THP-1a cells and BAL cells, for seven MWCNT.


2021 ◽  
Author(s):  
Simon Boulton ◽  
Roopesh Anand ◽  
Erika Buechelmaier ◽  
Ondrej Belan ◽  
Matt Newton ◽  
...  

Abstract DNA double strand breaks (DSBs) are deleterious lesions, and their incorrect repair can drive cancer development1. HELQ is a superfamily 2 helicase with 3’ to 5’ polarity, whose disruption in mice confers germ cells loss, infertility and increased predisposition to ovarian and pituitary tumours2-4. At the cellular level, defects in HELQ result in hypersensitivity to cisplatin and mitomycin C and, persistence of RAD51 foci upon DNA damage3,5. Notably, HELQ binds to RPA and the RAD51 paralog BCDX2 complex but the relevance of these interactions and how HELQ functions in DSB repair remains unclear3,5,6. Here, we report that HELQ helicase activity and a previously unappreciated DNA strand annealing function are differentially regulated by RPA and RAD51. Using biochemistry and single-molecule imaging (SMI), we establish that RAD51 forms a co-complex with and strongly stimulates HELQ as it translocates during DNA unwinding. Conversely, RPA inhibits DNA unwinding by HELQ but strongly stimulates DNA strand annealing. Mechanistically, we show that HELQ possesses an intrinsic ability to capture RPA-bound DNA strands and then displace RPA to facilitate annealing of complementary strands. Finally, we show that HELQ deficiency in cells compromises single-strand annealing (SSA) and microhomology-mediated end joining (MMEJ) pathways and increases long-tract gene conversion tracts (LTGC) during homologous recombination. Thus, our results implicate HELQ in multiple arms of DSB repair by virtue of co-factor dependent modulation of intrinsic translocase and DNA strand annealing activities.


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