We investigate both, experimentally and theoretically, commensurability oscillations in the low-field magnetoresistance of lateral superlattices with broken inversion symmetry. We find that ...pronounced minima develop in the resistivity when the flat band conditions of several relevant harmonics of the periodic potential nearly coincide.
ß-Mannan and mannanase in poultry nutrition SHASTAK, Y.; ADER, P.; FEUERSTEIN, D. ...
World's Poultry Science Journal,
03/2015, Letnik:
71, Številka:
1
Book Review, Journal Article
Recenzirano
Dietary plant ß-mannans are one of the major anti-nutritional components in monogastric nutrition. The presence of ß-mannans in poultry diets has been associated with many negative features ranging ...from high intestinal viscosity and low nutrient digestibility to adverse effects on innate immune response and microbial proliferation in the gut. ß-Mannanase supplementation to the feed of domestic fowl is one of the strategies for optimisation of nutritional value of ß-mannan containing diets. Research has shown positive effects of ß-mannanase supplementation on performance and nutrient digestibility in poultry fed corn-soybean meal-based diets as well as diets containing guar meal, copra meal, and palm kernel meal. Such performance and nutrient digestibility improvements are the result of single or combined modes of action due to ß-mannanase addition. Particularly over the last decade, it has become increasingly clear that these modes of action might be very complex and versatile. The identification and understanding of the mechanisms by which ß-mannanase supplementation affects nutrient digestion, metabolism, overall performance and health of birds, is important for the optimisation and broadening of the application of this enzyme in avian nutrition. This paper reviews various modes of action by ß-mannanase supplementation in poultry. Additionally, significance of single modes of action under different conditions is also discussed.
Functional foods need to be assessed for beneficial effects to support claims, but also for toxic effects. This report describes two examples of how complex food samples are initially characterized ...in human cells in vitro. Water extracts of green tea (GT) and black carrots (BC) were analyzed for key ingredients (catechins and anthocyanidins, respectively). Extracts, reconstituted mixtures of the major ingredients or individual compounds (−)-epigallocatechin gallate or cyanidin, respectively were evaluated in parallel using human colon cells (HT29 clone 19A). End points of cytotoxicity included determination of membrane integrity, proliferation inhibition, and genetic damage. Cells were pretreated with plant compounds at sub-toxic concentrations, and their resistance to toxicity of H
2O
2 was evaluated as a parameter of protection. The extracts reduced cell viability (BC) and cell growth (BC, GT) and caused DNA damage (BC, GT). They were more toxic than their key ingredients. Neither GT-samples nor BC protected against H
2O
2-induced DNA damage, whereas cyanidin did. In vitro analysis of extracts from functional foods firstly aims at defining the sub-toxic concentrations at which protective activities are then further characterized. It also allows comparing responses of complex samples and individual compounds, which is important since effects from protective food ingredients can be masked by accompanying toxic components.
Summary Background Adjuvant endocrine therapy compromises bone health in patients with breast cancer, causing osteopenia, osteoporosis, and fractures. Antiresorptive treatments such as ...bisphosphonates prevent and counteract these side-effects. In this trial, we aimed to investigate the effects of the anti-RANK ligand antibody denosumab in postmenopausal, aromatase inhibitor-treated patients with early-stage hormone receptor-positive breast cancer. Methods In this prospective, double-blind, placebo-controlled, phase 3 trial, postmenopausal patients with early hormone receptor-positive breast cancer receiving treatment with aromatase inhibitors were randomly assigned in a 1:1 ratio to receive either denosumab 60 mg or placebo administered subcutaneously every 6 months in 58 trial centres in Austria and Sweden. Patients were assigned by an interactive voice response system. The randomisation schedule used a randomly permuted block design with block sizes 2 and 4, stratified by type of hospital regarding Hologic device for DXA scans, previous aromatase inhibitor use, and baseline bone mineral density. Patients, treating physicians, investigators, data managers, and all study personnel were masked to treatment allocation. The primary endpoint was time from randomisation to first clinical fracture, analysed by intention to treat. As an additional sensitivity analysis, we also analysed the primary endpoint on the per-protocol population. Patients were treated until the prespecified number of 247 first clinical fractures was reached. This trial is ongoing (patients are in follow-up) and is registered with the European Clinical Trials Database, number 2005-005275-15, and with ClinicalTrials.gov , number NCT00556374. Findings Between Dec 18, 2006, and July 22, 2013, 3425 eligible patients were enrolled into the trial, of whom 3420 were randomly assigned to receive denosumab 60 mg (n=1711) or placebo (n=1709) subcutaneously every 6 months. Compared with the placebo group, patients in the denosumab group had a significantly delayed time to first clinical fracture (hazard ratio HR 0·50 95% CI 0·39–0·65, p<0·0001). The overall lower number of fractures in the denosumab group (92) than in the placebo group (176) was similar in all patient subgroups, including in patients with a bone mineral density T-score of −1 or higher at baseline (n=1872, HR 0·44 95% CI 0·31–0·64, p<0·0001) and in those with a bone mineral density T-score of less than −1 already at baseline (n=1548, HR 0·57 95% CI 0·40–0·82, p=0·002). The patient incidence of adverse events in the safety analysis set (all patients who received at least one dose of study drug) did not differ between the denosumab group (1366 events, 80%) and the placebo group (1334 events, 79%), nor did the numbers of serious adverse events (521 vs 511 30% in each group). The main adverse events were arthralgia and other aromatase-inhibitor related symptoms; no additional toxicity from the study drug was reported. Despite proactive adjudication of every potential osteonecrosis of the jaw by an international expert panel, no cases of osteonecrosis of the jaw were reported. 93 patients (3% of the full analysis set) died during the study, of which one death (in the denosumab group) was thought to be related to the study drug. Interpretation Adjuvant denosumab 60 mg twice per year reduces the risk of clinical fractures in postmenopausal women with breast cancer receiving aromatase inhibitors, and can be administered without added toxicity. Since a main side-effect of adjuvant breast cancer treatment can be substantially reduced by the addition of denosumab, this treatment should be considered for clinical practice. Funding Amgen.
A gene of Thermoanaerobacterium thermosulfurigenes EM1 encoding a protein with similarity to the maltose-binding protein of Escherichia coli was cloned and sequenced. It was located in the amy gene ...region of the chromosome downstream of the pullulanase-encoding amyB gene and upstream of amyDC, encoding membrane components of an ABC transport system, and the alpha-amylase gene amyA. The gene was designated amyE. Analysis of mRNA by Northern (RNA) blotting revealed that expression of the amy gene region is repressed during growth on glucose. Maximum levels of mRNA were detected with maltose as a substrate. An operon which was transcribed in the order amyBEDC was identified. However, an additional transcription start point was found in front of amyE. The amyA gene represented a monocistronic operon. Putative -35 and -10 promoter sites were deduced from the-thin transcription start sites of the amy gene region, and possible regulatory regions mediating induction by maltose and catabolite repression by glucose were identified by sequence analysis and comparison. The biochemical characterization of maltose uptake in T. thermosulfurigenes EM1 revealed two transport systems with Km values of 7 micromolar (high affinity) and 400 micromolar (low affinity). We conclude that the high-affinity system, which is specific for maltose and maltotriose, is a binding-protein-dependent transporter encoded by amyEDC. The gene for the putative ATP-binding protein has not yet been identified, and in contrast to similar systems in other bacteria, it is not located in the immediate vicinity of the chromosome
Mutagenized dockerin domains of endoglucanase CelD (type I) and of the cellulosome-integrating protein CipA (type II) were constructed by swapping residues 10 and 11 of the first or the second ...duplicated segment between the two polypeptides. These residues have been proposed to determine the specificity of cohesin−dockerin interactions. The dockerin domain of CelD still bound to the seventh cohesin domain of CipA (CohCip7), provided that mutagenesis occurred in one segment only. Binding was no longer detected by nondenaturing gel electrophoresis when both segments were mutagenized. The dockerin domain of CipA bound to the cohesin domain of SdbA as long as the second segment was intact. None of the mutated dockerins displayed detectable binding to the noncognate cohesin domain. Isothermal titration calorimetry showed that binding of the CelD dockerin to CohCip7 occurred with a high affinity K a = (2.6 ± 0.5) × 109 M-1 and a 1:1 stoichiometry. The reaction was weakly exothermic (ΔH° = −2.22 ± 0.2 kcal mol-1) and largely entropy driven (TΔS° = 10.70 ± 0.5 kcal mol-1). The heat capacity change on complexation was negative (ΔCp = −305 ± 15 cal mol-1 K-1). These values show that cohesin−dockerin binding is mainly hydrophobic. Mutations in the first or the second dockerin segment reduced or enhanced, respectively, the hydrophobic character of the interaction. Due to partial enthalpy−entropy compensation, these mutations induced only small changes in binding affinity. However, the binding affinity was strongly decreased when both segments were mutated, indicating strong negative cooperativity between the two mutated sites.
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