1,216 research outputs found

    Study on the insecticidal activity compounds of the essential oil from Syzygium aromaticum against stored grain insect pests

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    Insect pests are a major cause of damage in stored grain around the world. To control the stored grain insects, synthetic insecticides have been used extensively for many years, resulting in insect populations that are resistant to insecticides. Consequently there is an interest to find alternatives to chemical pesticides. The essential oil from Syzygium aromaticum (clove oil) has a number of bioactive compounds. The chemical constituents of the clove oil were analyzed by GC-MS, and 9 of 18 compounds were identified. The main compound (83%) was 2-methoxy-4-(2-propenyl)-phenol the second most common compound (12%) was trans-caryophyllene. These two pure compounds and clove oil were tested for toxicity and repellency against Rhyzopertha dominica, Sitophilus oryzae and Tribolium castaneum. The pure compounds were tested at the dosages found in clove oil. The mortality from 2-methoxy-4-(2-propenyl)-phenol was not significantly different from clove oil, suggesting that the activity of clove oil was solely due to this major compound. The repellency results were more complex. 2-methoxy-4-(2-propenyl)-phenol was more repellant than clove oil. Trans-caryophyllene was less toxic and less repellant than both clove oil and 2-methoxy-4-(2-propenyl)- phenol. The potential for these compounds to be used to control stored product insects is discussed. Keywords: Essential oils, Syzygium aromaticum, Clove oil, Insecticidal activity compounds, Stored grain insect

    Comparison of chemical profiles and effectiveness between Erxian decoction and mixtures of decoctions of its individual herbs : a novel approach for identification of the standard chemicals

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    Acknowledgements This study was partially supported by grants from the Seed Funding Programme for Basic Research (Project Number 201211159146 and 201411159213), the University of Hong Kong. We thank Mr Keith Wong and Ms Cindy Lee for their technical assistances.Peer reviewedPublisher PD

    Repurposing the aldose reductase inhibitor and diabetic neuropathy drug epalrestat for the congenital disorder of glycosylation PMM2-CDG

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    Phosphomannomutase 2 deficiency, or PMM2-CDG, is the most common congenital disorder of glycosylation and affects over 1000 patients globally. There are no approved drugs that treat the symptoms or root cause of PMM2-CDG. To identify clinically actionable compounds that boost human PMM2 enzyme function, we performed a multispecies drug repurposing screen using a novel worm model of PMM2-CDG, followed by PMM2 enzyme functional studies in PMM2-CDG patient fibroblasts. Drug repurposing candidates from this study, and drug repurposing candidates from a previously published study using yeast models of PMM2-CDG, were tested for their effect on human PMM2 enzyme activity in PMM2-CDG fibroblasts. Of the 20 repurposing candidates discovered in the worm-based phenotypic screen, 12 were plant-based polyphenols. Insights from structure-activity relationships revealed epalrestat, the only antidiabetic aldose reductase inhibitor approved for use in humans, as a first-in-class PMM2 enzyme activator. Epalrestat increased PMM2 enzymatic activity in four PMM2-CDG patient fibroblast lines with genotypes R141H/F119L, R141H/E139K, R141H/N216I and R141H/F183S. PMM2 enzyme activity gains ranged from 30% to 400% over baseline, depending on genotype. Pharmacological inhibition of aldose reductase by epalrestat may shunt glucose from the polyol pathway to glucose-1,6-bisphosphate, which is an endogenous stabilizer and coactivator of PMM2 homodimerization. Epalrestat is a safe, oral and brain penetrant drug that was approved 27 years ago in Japan to treat diabetic neuropathy in geriatric populations. We demonstrate that epalrestat is the first small molecule activator ofPMM2 enzyme activity with the potential to treat peripheral neuropathy and correct the underlying enzyme deficiency in a majority of pediatric and adult PMM2-CDG patients

    Sparse classification with MRI based markers for neuromuscular disease categorization

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    International audienceIn this paper, we present a novel method for disease classification between two patient populations based on features extracted from Magnetic Resonance Imaging (MRI) data. Anatomically meaningful features are extracted from structural data (T1- and T2-weighted MR images) and Diffusion Tensor Imaging (DTI) data, and used to train a new machine learning algorithm, the k-support SVM (ksup-SVM). The k-support regularized SVM has an inherent feature selection property, and thus it eliminates the requirement for a separate feature selection step. Our dataset consists of patients that suffer from facioscapulohumeral muscular dystrophy (FSH) and Myotonic muscular dystrophy type 1 (DM1) and our proposed method achieves a high performance. More specifically, it achieves a mean Area Under the Curve (AUC) of 0.7141 and mean accuracy 77% ± 0.013. Moreover, we provide a sparsity visualization of the features in order to indentify their discriminative value. The results suggest the potential of the combined use of MR markers to diagnose myopathies, and the general utility of the ksup-SVM. Source code is also available at https://gitorious.org/ksup-svm

    DRAM-3 modulates autophagy and promotes cell survival in the absence of glucose

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    Macroautophagy is a membrane-trafficking process that delivers cytoplasmic constituents to lysosomes for degradation. The process operates under basal conditions as a mechanism to turnover damaged or misfolded proteins and organelles. As a result, it has a major role in preserving cellular integrity and viability. In addition to this basal function, macroautophagy can also be modulated in response to various forms of cellular stress, and the rate and cargoes of macroautophagy can be tailored to facilitate appropriate cellular responses in particular situations. The macroautophagy machinery is regulated by a group of evolutionarily conserved autophagy-related (ATG) proteins and by several other autophagy regulators, which either have tissue-restricted expression or operate in specific contexts. We report here the characterization of a novel autophagy regulator that we have termed DRAM-3 due to its significant homology to damage-regulated autophagy modulator (DRAM-1). DRAM-3 is expressed in a broad spectrum of normal tissues and tumor cells, but different from DRAM-1, DRAM-3 is not induced by p53 or DNA-damaging agents. Immunofluorescence studies revealed that DRAM-3 localizes to lysosomes/autolysosomes, endosomes and the plasma membrane, but not the endoplasmic reticulum, phagophores, autophagosomes or Golgi, indicating significant overlap with DRAM-1 localization and with organelles associated with macroautophagy. In this regard, we further proceed to show that DRAM-3 expression causes accumulation of autophagosomes under basal conditions and enhances autophagic flux. Reciprocally, CRISPR/Cas9-mediated disruption of DRAM-3 impairs autophagic flux confirming that DRAM-3 is a modulator of macroautophagy. As macroautophagy can be cytoprotective under starvation conditions, we also tested whether DRAM-3 could promote survival on nutrient deprivation. This revealed that DRAM-3 can repress cell death and promote long-term clonogenic survival of cells grown in the absence of glucose. Interestingly, however, this effect is macroautophagy-independent. In summary, these findings constitute the primary characterization of DRAM-3 as a modulator of both macroautophagy and cell survival under starvation conditions
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