3,924 research outputs found

    Antioxidative Activities of Natural Hydroxy-Bearing Cinnamaldehydes and Cinnamic Acids: A Comparative Study

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    Purpose: To determine the potent antioxidants among six hydroxy-bearing cinnamaldehyde compounds and their corresponding acids.Methods: The antioxidative activities were evaluated by scavenging 2, 2’-diphenyl-1-picrylhydrazyl (DPPH) free radicals and anti-hemolysis of human red blood cells (RBCs). Fourier transform infrared spectrometry(FT-IR, nuclear magnetic resonance (NMR)and mass spectrometer(MS) evaluations were used to determine the synthesized compounds.Results: The scavenging ability of the compounds on DPPH radicals was in the following rank order: caffeic aldehyde (F) ≈ caffeic acid (C) > vitamin C (Vc) > o-coumaraldehyde (D) > p-coumaric acid (B) > p-coumaraldehyde (E) ≈o-coumaric acid. Inhibitory ability against 2′-Azobis(2-methylpropionamidine) dihydrochloride (AAPH)-induced erythrocyte hemolysis was ranked as follows: o-coumaraldehyde (D) > p-coumaraldehyde (E) ≈ caffeic aldehyde (F) > caffeic acid (C) ≈o-coumaric acid (A) > p-coumaric acid (B) > Vitamin C. The corresponding inhibition time (tinh ) of D and Vc was 63.6, and 23.7 min, respectively.Conclusion: Cinnamaldehydes demonstrated superior antioxidative activities to their corresponding acids. DPPH scavenging ability correlated directly with the number of hydroxyl groups on the catechol ring while the degree of lipophilicity of the compounds may be proportional to their anti-hemolytic activity.Keywords: DPPH scavenging, Cinnamaldehyde, Cinnamic acid, Antioxidative, Hemolysis

    Modelling the natural history of Huntington's disease progression.

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    BACKGROUND: The lack of reliable biomarkers to track disease progression is a major problem in clinical research of chronic neurological disorders. Using Huntington's disease (HD) as an example, we describe a novel approach to model HD and show that the progression of a neurological disorder can be predicted for individual patients. METHODS: Starting with an initial cohort of 343 patients with HD that we have followed since 1995, we used data from 68 patients that satisfied our filtering criteria to model disease progression, based on the Unified Huntington's Disease Rating Scale (UHDRS), a measure that is routinely used in HD clinics worldwide. RESULTS: Our model was validated by: (A) extrapolating our equation to model the age of disease onset, (B) testing it on a second patient data set by loosening our filtering criteria, (C) cross-validating with a repeated random subsampling approach and (D) holdout validating with the latest clinical assessment data from the same cohort of patients. With UHDRS scores from the past four clinical visits (over a minimum span of 2 years), our model predicts disease progression of individual patients over the next 2 years with an accuracy of 89-91%. We have also provided evidence that patients with similar baseline clinical profiles can exhibit very different trajectories of disease progression. CONCLUSIONS: This new model therefore has important implications for HD research, most obviously in the development of potential disease-modifying therapies. We believe that a similar approach can also be adapted to model disease progression in other chronic neurological disorders.This study was supported by the Cotswold Trust, the Rosetrees Trust, donations to the Huntington’s disease clinic in the John van Geest Centre for Brain Repair, and NIHR award of the Biomedical Research Centre - Cambridge University NHS Foundation Trust. This project was also supported by EPSRC through projects EP/I03210X/1 and EP/G066477/1.This article has been accepted for publication in Journal of Neurology, Neurosurgery, and Psychiatry, following peer review. The definitive copyedited, typeset version J Neurol Neurosurg Psychiatry doi:10.1136/jnnp-2014-308153 is available online at: http://jnnp.bmj.com/content/early/2014/12/16/jnnp-2014-308153.long

    Mapping Dynamic Histone Acetylation Patterns to Gene Expression in Nanog-depleted Murine Embryonic Stem Cells

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    Embryonic stem cells (ESC) have the potential to self-renew indefinitely and to differentiate into any of the three germ layers. The molecular mechanisms for self-renewal, maintenance of pluripotency and lineage specification are poorly understood, but recent results point to a key role for epigenetic mechanisms. In this study, we focus on quantifying the impact of histone 3 acetylation (H3K9,14ac) on gene expression in murine embryonic stem cells. We analyze genome-wide histone acetylation patterns and gene expression profiles measured over the first five days of cell differentiation triggered by silencing Nanog, a key transcription factor in ESC regulation. We explore the temporal and spatial dynamics of histone acetylation data and its correlation with gene expression using supervised and unsupervised statistical models. On a genome-wide scale, changes in acetylation are significantly correlated to changes in mRNA expression and, surprisingly, this coherence increases over time. We quantify the predictive power of histone acetylation for gene expression changes in a balanced cross-validation procedure. In an in-depth study we focus on genes central to the regulatory network of Mouse ESC, including those identified in a recent genome-wide RNAi screen and in the PluriNet, a computationally derived stem cell signature. We find that compared to the rest of the genome, ESC-specific genes show significantly more acetylation signal and a much stronger decrease in acetylation over time, which is often not reflected in an concordant expression change. These results shed light on the complexity of the relationship between histone acetylation and gene expression and are a step forward to dissect the multilayer regulatory mechanisms that determine stem cell fate.Comment: accepted at PLoS Computational Biolog

    Quantum optical coherence can survive photon losses: a continuous-variable quantum erasure correcting code

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    A fundamental requirement for enabling fault-tolerant quantum information processing is an efficient quantum error-correcting code (QECC) that robustly protects the involved fragile quantum states from their environment. Just as classical error-correcting codes are indispensible in today's information technologies, it is believed that QECC will play a similarly crucial role in tomorrow's quantum information systems. Here, we report on the first experimental demonstration of a quantum erasure-correcting code that overcomes the devastating effect of photon losses. Whereas {\it errors} translate, in an information theoretic language, the noise affecting a transmission line, {\it erasures} correspond to the in-line probabilistic loss of photons. Our quantum code protects a four-mode entangled mesoscopic state of light against erasures, and its associated encoding and decoding operations only require linear optics and Gaussian resources. Since in-line attenuation is generally the strongest limitation to quantum communication, much more than noise, such an erasure-correcting code provides a new tool for establishing quantum optical coherence over longer distances. We investigate two approaches for circumventing in-line losses using this code, and demonstrate that both approaches exhibit transmission fidelities beyond what is possible by classical means.Comment: 5 pages, 4 figure

    A massive, quiescent galaxy at redshift of z=3.717

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    In the early Universe finding massive galaxies that have stopped forming stars present an observational challenge as their rest-frame ultraviolet emission is negligible and they can only be reliably identified by extremely deep near-infrared surveys. These have revealed the presence of massive, quiescent early-type galaxies appearing in the universe as early as z\sim2, an epoch 3 Gyr after the Big Bang. Their age and formation processes have now been explained by an improved generation of galaxy formation models where they form rapidly at z\sim3-4, consistent with the typical masses and ages derived from their observations. Deeper surveys have now reported evidence for populations of massive, quiescent galaxies at even higher redshifts and earlier times, however the evidence for their existence, and redshift, has relied entirely on coarsely sampled photometry. These early massive, quiescent galaxies are not predicted by the latest generation of theoretical models. Here, we report the spectroscopic confirmation of one of these galaxies at redshift z=3.717 with a stellar mass of 1.7×\times1011^{11} M_\odot whose absorption line spectrum shows no current star-formation and which has a derived age of nearly half the age of the Universe at this redshift. The observations demonstrates that the galaxy must have quickly formed the majority of its stars within the first billion years of cosmic history in an extreme and short starburst. This ancestral event is similar to those starting to be found by sub-mm wavelength surveys pointing to a possible connection between these two populations. Early formation of such massive systems is likely to require significant revisions to our picture of early galaxy assembly.Comment: 6 pages, 7 figures. This is the final preprint corresponding closely to the published version. Uploaded 6 months after publication in accordance with Nature polic
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