A Two-Antibody Pan-Ebolavirus Cocktail Confers Broad Therapeutic Protection in Ferrets and Nonhuman Primates

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A Persistence Detector for Metabolic Network Rewiring in an Animal

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Plant–soil feedback during biological invasions: effect of litter decomposition from an invasive plant (Sphagneticola trilobata) on its native congener (S. calendulacea)

生物入侵过程中的植物-土壤反馈：一种入侵植物的凋落物分解对其本地近缘植物的影响 植物入侵可通过正或负的植物-土壤反馈效应改变土壤的生物和非生物性质,从而影响入侵栖息地的土壤理化性质。许多入侵物种的凋落物分解可增加土壤养分,降低本地植物多样性,并导致进一步的植物入侵。关于入侵植物凋落物在不同土壤类型及深度分解及反馈效应的研究依然很少。本研究旨在明确入侵植物南美蟛蜞菊(Sphagneticola trilobata)凋落物在不同土壤类型和不同土壤深度条件下的分解情 况及其对本地近缘植物蟛蜞菊(S. calendulacea)生理生长的影响。将装有南美蟛蜞菊凋落物的尼龙袋加入到不同深度(即0、2、4 和6 cm)的砂土、营养土和粘土中,经6个月的分解后,回收凋落物袋并计算分解速率,随后在凋落物分解处理后的土壤中种植本地蟛蜞菊,并在生长期结束时测量其生理生态指标。研究结果表明,所有处理土壤类型中,凋落物在土壤深度为2和4 cm处分解后显著增加了土壤养分,而对本 地蟛蜞菊的叶片叶绿素、叶氮含量等生长指标表现为负效应。因此,入侵植物南美蟛蜞菊凋落物分解对土壤养分表现为正的反馈效应,而对本地植物蟛蜞菊的生长表现为负效应。我们的研究结果还表明,入侵植物的凋落物分解对土壤和本地物种的影响还因凋落物分解所在的土壤深度而显著不同。未来的研究应侧重于入侵栖息地中更多本地和入侵物种的植物-土壤反馈效应,以及更多土壤类型和土壤深度的入侵植物凋落物效应。     

A flavone from the ethyl acetate extract of Leea rubra leaves with DNA damage protection and antineoplastic activity

Among the major constituents of Leea rubra (Family Vitaceae) leaves, phenolic and flavonoind compounds are most important for therapeutic purposes and the plant parts have been used in traditional medicine to treat several diseases for long. Thus, in order to scientifically confirm the traditional uses of the L. rubra leaves, the present study was designed to investigate the efficacy of the isolated flavones against AAPH induced oxidative damage to pUC19 DNA by gel electrophoresis and antineoplastic activity was evaluated on Ehrlich ascites carcinoma (EAC) bearing Swiss albino mice by evaluating percentage inhibition of cell growth, morphological changes of EAC cells and hematological parameters of the mice. The isolation was carried out by column chromatography and structure was revealed by ¹H-NMR and ¹³C NMR. The result shows that, the isolated compound was identified as myricetin 4'-methoxy-3-O-α-l-rhamnopyranoside based on previously reported data. The isolated flavone effectively inhibited AAPH-induced oxidative damage to DNA; because it could inhibit the formation of circular and linear forms of the DNA. In anti-proliferative assay, 76% growth inhibition of EAC cells was observed as compare to the control mice (p<0.05) at a dose 100 mg/kg body weight. Thus the isolated flavone showed great importance as a possible therapeutic agent in preventing oxidative damage to DNA and the chronic diseases caused by such DNA damage, and can also become important in cancer chemotherapy.     

Novel mutation assay with high sensitivity based on direct measurement of genomic DNA alterations: comparable results to the Ames test

Almost all of the methodologies developed to date to assay the potential mutagenicity of chemical substances are based on detection of altered phenotypic traits. The alternative approach of directly screening the whole genome for mutations is not feasible because of the logistics of carrying out mass sequencing of genes. Here we describe a novel and highly sensitive mutation assay, which we term the 'genome profiling-based mutation assay' (GPMA) that directly detects mutations generated in genomic DNA. We used GPMA to detect mutations caused by known mutagens such as AF2 and ethidium bromide even at concentrations of 30 ppb. The number of mutations detected was dependent on the number of generations in culture and the concentrations of the mutagens. Almost complete agreement was observed between GPMA and the Ames test in the discrimination of mutagens (63 out of 64). Owing to the high sensitivity of GPMA, the effects of long-term and low-dose exposures and the influence of chemicals of low solubility can also be screened. Thus, genotype-based GPMA can complement the Ames test, which is the standard technology in this field and is based on phenotypic traits.     

An Eye-Shaped Ultra-Sensitive Localized Surface Plasmon Resonance–Based Biochemical Sensor

Plasmonics - This research illustrates a parametric study based on surface plasmon resonance of a slightly gold-coated photonic crystal fiber (PCF). In verifying sensing accuracy, the proposed...     

Biophysical and Computational Approaches to Unravel pH-Dependent Conformational Change of PspA Assist PspA-PspF Complex Formation in Yersinia enterocolitica

The Protein Journal - In enteropathogen, Yersinia enterocolitica, the genes encoding phage shock proteins are organized in an operon (pspA-E), which is activated at the various types of cellular...     

Genetic variation,demographic history and phylogeography of tire track eel,Mastacembelus favus (Synbranchiformes: Mastacembelidae) in Southeast Asia

The complex climatic and geological history of Southeast Asia has been hypothesised to determine the most important aspects of the current phylogeographical structure and distribution of living organisms throughout the region. To test existing hypotheses, the genetic structure of the tire track eel, Mastacembelus favus, was investigated using 823 bp of mitochondrial DNA cytochrome b from 469 individuals from 51 localities encompassing its native range. The results classified all haplotypes into two major lineages, Lineage 1, which was further divided into Lineages 1a (lower Mekong, eastern Gulf of Thailand and Malay—Thai Peninsula), 1b (Banpakong River), 1c (Chao Phraya, Gulf of Thailand and Malay—Thai Peninsula) and 1d (Khlang Yai River), and Lineage 2, the upper reaches of the lower Mekong and the middle Mekong. Strong genetic discontinuities dated approximately 5 MYA were discovered in the Mekong with limited geographical overlap, suggesting a historically dissected drainage between two sections and species colonisation via different routes. The widespread Lineage 1 showed a strong signature of population expansion during the Pleistocene climate oscillation. Haplotype characteristics in the Malay—Thai Peninsula are hypothesised to result from postglacial dispersal from the Mekong and Chao Phraya through an extended Pleistocene drainage network.

     

Autophagic dysfunction in Alzheimer’s disease: Cellular and molecular mechanistic approaches to halt Alzheimer’s pathogenesis

Autophagy is a preserved cytoplasmic self-degradation process and endorses recycling of intracellular constituents into bioenergetics for the controlling of cellular homeostasis. Functional autophagy process is essential in eliminating cytoplasmic waste components and helps in the recycling of some of its constituents. Studies have revealed that neurodegenerative disorders may be caused by mutations in autophagy-related genes and alterations of autophagic flux. Alzheimer’s disease (AD) is an irrevocable deleterious neurodegenerative disorder characterized by the formation of senile plaques and neurofibrillary tangles (NFTs) in the hippocampus and cortex. In the central nervous system of healthy people, there is no accretion of amyloid β (Aβ) peptides due to the balance between generation and degradation of Aβ. However, for AD patients, the generation of Aβ peptides is higher than lysis that causes accretion of Aβ. Likewise, the maturation of autophagolysosomes and inhibition of their retrograde transport creates favorable conditions for Aβ accumulation. Furthermore, increasing mammalian target of rapamycin (mTOR) signaling raises tau levels as well as phosphorylation. Alteration of mTOR activity occurs in the early stage of AD. In addition, copious evidence links autophagic/lysosomal dysfunction in AD. Compromised mitophagy is also accountable for dysfunctional mitochondria that raises Alzheimer’s pathology. Therefore, autophagic dysfunction might lead to the deposit of atypical proteins in the AD brain and manipulation of autophagy could be considered as an emerging therapeutic target. This review highlights the critical linkage of autophagy in the pathogenesis of AD, and avows a new insight to search for therapeutic target for blocking Alzheimer’s pathogenesis.