Seed germination ability and protein profiling of salt marsh plants at different concentration of sodium chloride

757-765Soil salinity is an increasing problem in agriculture throughout the world. The utilization of halophytic plants for pasture and fodder production in saline soils is the only economic solution presently available. The present study discusses the effects of different concentrations of sodium chloride on seed germination and its impact was determined by protein profiling on Sesuvium portulacastrum, Suaeda maritima and Salicornia brachiata. Seeds germination was substantially delayed and reduced with an increase in NaCl to above threshold level. Changes in the pattern of protein expression were found to be prominent between control and NaCl treated seeds.pproximately 42 kDa, 26 kDa and 20 kDa were found to be up-regulated as the concentration of salt increases in Sesuvium portulacastrum. Whereas, significant variation in the protein patterns were observed in Suaeda maritima such as ~20 to 30 kDa protein bands were not visible and protein band of 55 kDa was particularly increased after 300 mM NaCl treatment. Similarly in Salicornia brachiata expression of 45 kDa protein was up regulated and approximately 25 kDa protein expression was down regulated as the concentration of salt increased to about 1.5 M, 2 M and 2.5 M. However, the upper limit for the survival of the seedling was 200 mM, 300 mM and 1 M for Sesuvium portulacastrum, Suaeda maritima and Salicornia brachiata, respectively. On the basis of the present investigation, this study suggests that optimal application of NaCl can benefit plant growth on stress tolerance studies and also helps for further investigation of the salt tolerance networks

Quantitative Description of Glycan-Receptor Binding of Influenza A Virus H7 Hemagglutinin

In the context of recently emerged novel influenza strains through reassortment, avian influenza subtypes such as H5N1, H7N7, H7N2, H7N3 and H9N2 pose a constant threat in terms of their adaptation to the human host. Among these subtypes, it was recently demonstrated that mutations in H5 and H9 hemagglutinin (HA) in the context of lab-generated reassorted viruses conferred aerosol transmissibility in ferrets (a property shared by human adapted viruses). We previously demonstrated that the quantitative binding affinity of HA to α2→6 sialylated glycans (human receptors) is one of the important factors governing human adaptation of HA. Although the H7 subtype has infected humans causing varied clinical outcomes from mild conjunctivitis to severe respiratory illnesses, it is not clear where the HA of these subtypes stand in regard to human adaptation since its binding affinity to glycan receptors has not yet been quantified. In this study, we have quantitatively characterized the glycan receptor-binding specificity of HAs from representative strains of Eurasian (H7N7) and North American (H7N2) lineages that have caused human infection. Furthermore, we have demonstrated for the first time that two specific mutations; Gln226→Leu and Gly228→Ser in glycan receptor-binding site of H7 HA substantially increase its binding affinity to human receptor. Our findings contribute to a framework for monitoring the evolution of H7 HA to be able to adapt to human host.National Institutes of Health (U.S.) (GM R37 GM057073-13)Singapore-MIT Alliance for Research and Technolog

Mechanism of Neuronal versus Endothelial Cell Uptake of Alzheimer's Disease Amyloid β Protein

Alzheimer's disease (AD) is characterized by significant neurodegeneration in the cortex and hippocampus; intraneuronal tangles of hyperphosphorylated tau protein; and accumulation of β-amyloid (Aβ) proteins 40 and 42 in the brain parenchyma as well as in the cerebral vasculature. The current understanding that AD is initiated by the neuronal accumulation of Aβ proteins due to their inefficient clearance at the blood-brain-barrier (BBB), places the neurovascular unit at the epicenter of AD pathophysiology. The objective of this study is to investigate cellular mechanisms mediating the internalization of Aβ proteins in the principle constituents of the neurovascular unit, neurons and BBB endothelial cells. Laser confocal micrographs of wild type (WT) mouse brain slices treated with fluorescein labeled Aβ40 (F-Aβ40) demonstrated selective accumulation of the protein in a subpopulation of cortical and hippocampal neurons via nonsaturable, energy independent, and nonendocytotic pathways. This groundbreaking finding, which challenges the conventional belief that Aβ proteins are internalized by neurons via receptor mediated endocytosis, was verified in differentiated PC12 cells and rat primary hippocampal (RPH) neurons through laser confocal microscopy and flow cytometry studies. Microscopy studies have demonstrated that a significant proportion of F-Aβ40 or F-Aβ42 internalized by differentiated PC12 cells or RPH neurons is located outside of the endosomal or lysosomal compartments, which may accumulate without degradation. In contrast, BBME cells exhibit energy dependent uptake of F-Aβ40, and accumulate the protein in acidic cell organelle, indicative of endocytotic uptake. Such a phenomenal difference in the internalization of Aβ40 between neurons and BBB endothelial cells may provide essential clues to understanding how various cells can differentially regulate Aβ proteins and help explain the vulnerability of cortical and hippocampal neurons to Aβ toxicity

Acute Gastroenteritis Surveillance through the National Outbreak Reporting System, United States

Implemented in 2009, the National Outbreak Reporting System provides surveillance for acute gastroenteritis outbreaks in the United States resulting from any transmission mode. Data from the first 2 years of surveillance highlight the predominant role of norovirus. The pathogen-specific transmission pathways and exposure settings identified can help inform prevention efforts