Karakterizacija i antioksidativna svojstva hidrolizata proteina konoplje dobivenih pomoću enzima Neutrase®

Hemp protein hydrolysates with various yields of trichloroacetic acid (TCA)-soluble peptides (Ysp) and surface hydrophobicity (Ho) were obtained by Neutrase® hydrolysis from hemp protein isolate (HPI). The peptide profiles, amino acid composition and antioxidant activities (DPPH radical scavenging ability, reducing power and Fe2+ chelating ability) of the hydrolysates, obtained at 60–240 min, were evaluated. Higher DPPH radical scavenging (IC50, 2.3–2.4 mg/mL) and Fe2+ chelating (IC50, 1.7–1.8 mg/mL) abilities were observed for the hydrolysates with Ysp in the range of 28–30 and 18–28 %, respectively, while the high reducing power was only observed for the hydrolysate with Ysp of 18 %. The DPPH radical scavenging and Fe2+ chelating abilities were closely correlated with the peptide profiles and Ho of the hydrolysates. The peptide profiles of the hydrolysates with higher hydrophobic amino acids exhibited higher DPPH radical scavenging and Fe2+ chelating abilities.Hidrolizom izolata proteina pomoću enzima Neutrase® dobiveni su hidrolizati proteina konoplje s različitim prinosom peptida topljivih u trikloroctenoj kiselini (Ysp) i hidrofobnošću površine (Ho). Ispitan je peptidni profil, sastav aminokiselina i antioksidativna aktivnost (sposobnost uklanjanja DPPH radikala, reducirajuća snaga i sposobnost stvaranja helata Fe2+) hidrolizata dobivenih nakon 60-240 min. Uočena je veća sposobnost hidrolizata s Ysp=28-30 % da uklone DPPH radikale (IC50; 2,3-2,4 mg/mL), te veća mogućnost stvaranja helata Fe2+ s hidrolizatima vrijednosti Ysp=18-28 % (IC50; 1,7-1,8 mg/mL). Velika je reducirajuća snaga samo u hidrolizata s Ysp=18 %. Sposobnost uklanjanja DPPH radikala i stvaranja helata Fe2+ povezana je s peptidnim profilom i hidrofobnošću površine hidrolizata (Ho). Hidrolizati s većim udjelom hidrofobnih aminokiselina pokazali su bolju sposobnost uklanjanja DPPH radikala i stvaranja helata Fe2

Generation of quasi-monoenergetic protons from thin multi-ion foils by a combination of laser radiation pressure acceleration and shielded Coulomb repulsion

We study theoretically and numerically the acceleration of protons by a combination of laser radiation pressure acceleration and Coulomb repulsion of carbon ions in a multi-ion thin foil made of carbon and hydrogen. The carbon layer helps to delay the proton layer from disruption due to the Rayleigh–Taylor instability, to maintain the quasi-monoenergetic proton layer and to accelerate it by the electron-shielded Coulomb repulsion for much longer duration than the acceleration time using single-ion hydrogen foils. Particle-in-cell simulations with a normalized peak laser amplitude of a_0 = 5 show a resulting quasi-monoenergetic proton energy of about 70 MeV with the foil made of 90% carbon and 10% hydrogen, in contrast to 10 MeV using a single-ion hydrogen foil. An analytical model is presented to explain quantitatively the proton energy evolution; this model is in agreement with the simulation results. The energy dependence of the quasi-monoenergetic proton beam on the concentration of carbon and hydrogen is also studied

Poly[[[diaqua­cobalt(II)]-bis­[μ2-1,1′-(butane-1,4-di­yl)diimidazole-κ2 N 3:N 3′]] dinitrate]

In the title compound, {[Co(C10H14N4)2(H2O)2](NO3)2}n, the CoII ion lies on an inversion center and is six-coordinated in an octa­hedral environment by four N atoms from four different 1,1′-butane-1,4-diyldiimidazole ligands and two O atoms from the two water mol­ecules. The CoII atoms are bridged by ligands, generating a two-dimensional (4,4)-network. Adjacent fishnet planes are linked to the nitrate anions via O—H⋯O hydrogen bonds, forming a three-dimensional supra­molecular structure

Understanding variation in transcription factor binding by modeling transcription factor genome-epigenome interactions

Despite explosive growth in genomic datasets, the methods for studying epigenomic mechanisms of gene regulation remain primitive. Here we present a model-based approach to systematically analyze the epigenomic functions in modulating transcription factor-DNA binding. Based on the first principles of statistical mechanics, this model considers the interactions between epigenomic modifications and a cis-regulatory module, which contains multiple binding sites arranged in any configurations. We compiled a comprehensive epigenomic dataset in mouse embryonic stem (mES) cells, including DNA methylation (MeDIP-seq and MRE-seq), DNA hydroxymethylation (5-hmC-seq), and histone modifications (ChIP-seq). We discovered correlations of transcription factors (TFs) for specific combinations of epigenomic modifications, which we term epigenomic motifs. Epigenomic motifs explained why some TFs appeared to have different DNA binding motifs derived from in vivo (ChIP-seq) and in vitro experiments. Theoretical analyses suggested that the epigenome can modulate transcriptional noise and boost the cooperativity of weak TF binding sites. ChIP-seq data suggested that epigenomic boost of binding affinities in weak TF binding sites can function in mES cells. We showed in theory that the epigenome should suppress the TF binding differences on SNP-containing binding sites in two people. Using personal data, we identified strong associations between H3K4me2/H3K9ac and the degree of personal differences in NFκB binding in SNP-containing binding sites, which may explain why some SNPs introduce much smaller personal variations on TF binding than other SNPs. In summary, this model presents a powerful approach to analyze the functions of epigenomic modifications. This model was implemented into an open source program APEG (Affinity Prediction by Epigenome and Genome, http://systemsbio.ucsd.edu/apeg)

Understanding Variation in Transcription Factor Binding by Modeling Transcription Factor Genome-Epigenome Interactions

Despite explosive growth in genomic datasets, the methods for studying epigenomic mechanisms of gene regulation remain primitive. Here we present a model-based approach to systematically analyze the epigenomic functions in modulating transcription factor-DNA binding. Based on the first principles of statistical mechanics, this model considers the interactions between epigenomic modifications and a cis-regulatory module, which contains multiple binding sites arranged in any configurations. We compiled a comprehensive epigenomic dataset in mouse embryonic stem (mES) cells, including DNA methylation (MeDIP-seq and MRE-seq), DNA hydroxymethylation (5-hmC-seq), and histone modifications (ChIP-seq). We discovered correlations of transcription factors (TFs) for specific combinations of epigenomic modifications, which we term epigenomic motifs. Epigenomic motifs explained why some TFs appeared to have different DNA binding motifs derived from in vivo (ChIP-seq) and in vitro experiments. Theoretical analyses suggested that the epigenome can modulate transcriptional noise and boost the cooperativity of weak TF binding sites. ChIP-seq data suggested that epigenomic boost of binding affinities in weak TF binding sites can function in mES cells. We showed in theory that the epigenome should suppress the TF binding differences on SNP-containing binding sites in two people. Using personal data, we identified strong associations between H3K4me2/H3K9ac and the degree of personal differences in NFκB binding in SNP-containing binding sites, which may explain why some SNPs introduce much smaller personal variations on TF binding than other SNPs. In summary, this model presents a powerful approach to analyze the functions of epigenomic modifications. This model was implemented into an open source program APEG (Affinity Prediction by Epigenome and Genome, http://systemsbio.ucsd.edu/apeg).</p

Karakterizacija i antioksidativna svojstva hidrolizata proteina konoplje dobivenih pomoću enzima Neutrase®

Hemp protein hydrolysates with various yields of trichloroacetic acid (TCA)-soluble peptides (Ysp) and surface hydrophobicity (Ho) were obtained by Neutrase® hydrolysis from hemp protein isolate (HPI). The peptide profiles, amino acid composition and antioxidant activities (DPPH radical scavenging ability, reducing power and Fe2+ chelating ability) of the hydrolysates, obtained at 60–240 min, were evaluated. Higher DPPH radical scavenging (IC50, 2.3–2.4 mg/mL) and Fe2+ chelating (IC50, 1.7–1.8 mg/mL) abilities were observed for the hydrolysates with Ysp in the range of 28–30 and 18–28 %, respectively, while the high reducing power was only observed for the hydrolysate with Ysp of 18 %. The DPPH radical scavenging and Fe2+ chelating abilities were closely correlated with the peptide profiles and Ho of the hydrolysates. The peptide profiles of the hydrolysates with higher hydrophobic amino acids exhibited higher DPPH radical scavenging and Fe2+ chelating abilities.Hidrolizom izolata proteina pomoću enzima Neutrase® dobiveni su hidrolizati proteina konoplje s različitim prinosom peptida topljivih u trikloroctenoj kiselini (Ysp) i hidrofobnošću površine (Ho). Ispitan je peptidni profil, sastav aminokiselina i antioksidativna aktivnost (sposobnost uklanjanja DPPH radikala, reducirajuća snaga i sposobnost stvaranja helata Fe2+) hidrolizata dobivenih nakon 60-240 min. Uočena je veća sposobnost hidrolizata s Ysp=28-30 % da uklone DPPH radikale (IC50; 2,3-2,4 mg/mL), te veća mogućnost stvaranja helata Fe2+ s hidrolizatima vrijednosti Ysp=18-28 % (IC50; 1,7-1,8 mg/mL). Velika je reducirajuća snaga samo u hidrolizata s Ysp=18 %. Sposobnost uklanjanja DPPH radikala i stvaranja helata Fe2+ povezana je s peptidnim profilom i hidrofobnošću površine hidrolizata (Ho). Hidrolizati s većim udjelom hidrofobnih aminokiselina pokazali su bolju sposobnost uklanjanja DPPH radikala i stvaranja helata Fe2

Spatiotemporal clustering of the epigenome reveals rules of dynamic gene regulation

Spatial organization of different epigenomic marks was used to infer functions of the epigenome. It remains unclear what can be learned from the temporal changes of the epigenome. Here, we developed a probabilistic model to cluster genomic sequences based on the similarity of temporal changes of multiple epigenomic marks during a cellular differentiation process. We differentiated mouse embryonic stem (ES) cells into mesendoderm cells. At three time points during this differentiation process, we used high-throughput sequencing to measure seven histone modifications and variants—H3K4me1/2/3, H3K27ac, H3K27me3, H3K36me3, and H2A.Z; two DNA modifications—5-mC and 5-hmC; and transcribed mRNAs and noncoding RNAs (ncRNAs). Genomic sequences were clustered based on the spatiotemporal epigenomic information. These clusters not only clearly distinguished gene bodies, promoters, and enhancers, but also were predictive of bidirectional promoters, miRNA promoters, and piRNAs. This suggests specific epigenomic patterns exist on piRNA genes much earlier than germ cell development. Temporal changes of H3K4me2, unmethylated CpG, and H2A.Z were predictive of 5-hmC changes, suggesting unmethylated CpG and H3K4me2 as potential upstream signals guiding TETs to specific sequences. Several rules on combinatorial epigenomic changes and their effects on mRNA expression and ncRNA expression were derived, including a simple rule governing the relationship between 5-hmC and gene expression levels. A Sox17 enhancer containing a FOXA2 binding site and a Foxa2 enhancer containing a SOX17 binding site were identified, suggesting a positive feedback loop between the two mesendoderm transcription factors. These data illustrate the power of using epigenome dynamics to investigate regulatory functions

catena-Poly[[tetra­aqua­zinc(II)]-μ-1,3,4-thia­diazol-2,5-diyldithio­diacetato-κ2 O:O′]

In the title linear coordination polymer, [Zn(C6H4N2O4S3)(H2O)4]n, the ZnII atom is coordinated by four O atoms from four water mol­ecules and two O atoms from two [5-(carb­oxyl­atomethyl­sulfan­yl)-1,3,4-thia­diazol-2-ylsulfan­yl]acetate units in an octa­hedral coordination environment. The chains are linked into a three-dimensional supra­molecular network via O—H⋯O and O—H⋯N hydrogen bonds

A Quantitative Sequencing Method for 5-Formylcytosine in RNA

5-Formylcytosine (f5C) modification is present in human mitochondrial methionine tRNA (mt-tRNAMet) and cytosolic leucine tRNA (ct-tRNALeu), with their formation mediated by NSUN3 and ALKBH1. f5C has also been detected in yeast mRNA and human tRNA, but its transcriptome-wide distribution in mammals has not been studied. Here we report f5C-seq, a quantitative sequencing method to map f5C transcriptome-wide in HeLa and mouse embryonic stem cells (mESCs). We show that f5C in RNA can be reduced to dihydrouracil (DHU) by pic-borane, and DHU can be exclusively read as T during reverse transcription (RT) reaction, allowing the detection and quantification of f5C sites by a unique C-to-T mutation signature. We validated f5C-seq by identifying and quantifying the two known f5C sites in tRNA, in which the f5C modification fractions dropped significantly in ALKBH1-depleted cells. By applying f5C-seq to chromatin-associated RNA (caRNA), we identified several highly modified f5C sites in HeLa and mouse embryonic stem cells (mESC)