Deletion of both methionine sulfoxide reductase A and methionine sulfoxide reductase C genes renders Salmonella Typhimurium highly susceptible to hypochlorite stress and poultry macrophages

Molecular Biology Reports - Salmonella Typhimurium survives and replicates inside the oxidative environment of phagocytic cells. Proteins, because of their composition and location, are the...     

Prioritizing areas in the native range of hygrophila for surveys to collect biological control agents

Native to Southeast Asia, Hygrophila polysperma is an invasive aquatic weed of lotic habitats in the southern United States and Mexico. An increase in the number of water bodies invaded by hygrophila since 1990 suggests that current methods employed to control this weed are inadequate. Classical biological control may be a viable option for long term regulation of hygrophila in the invaded range. In this study, we used the Maximum Entropy Species Distribution Model (MaxEnt) to prioritize climatically suitable native habitats in India and Bangladesh for conducting exploratory surveys to collect biological control agents. In total, 164 point occurrences from the United States and Mexico and 20 predictor variables, including 19 bioclimatic variables and altitude, were used to predict the native distribution of hygrophila. Performance of the model was statistically verified using threshold dependent binomial tests and area under the curve (AUC) score of the receiver operating characteristic (ROC) curve plot. The results showed that the model performed significantly better than random in both binomial tests and AUC analyses. High suitability of occurrence of hygrophila was predicted in the northeastern region of India and northern and eastern parts of Bangladesh. Based on percent omission of known native occurrences, a color-coded final distribution map was prepared to prioritize areas for conducting future surveys. Our study proposes a technique that can be useful for prioritizing areas in native ranges for exploratory surveys to collect biological control agents.     

Small RNA profiling of Dengue virus-mosquito interactions implicates the PIWI RNA pathway in anti-viral defense

Background  

Small RNA (sRNA) regulatory pathways (SRRPs) are important to anti-viral defence in mosquitoes. To identify critical features of the virus infection process in Dengue serotype 2 (DENV2)-infected Ae. aegypti, we deep-sequenced small non-coding RNAs. Triplicate biological replicates were used so that rigorous statistical metrics could be applied.     

The effect of interactions on the cellular uptake of nanoparticles

We present a simple two-state model to understand the size-dependent endocytosis of nanoparticles. Using this model, we elucidate the relevant energy terms required to understand the size-dependent uptake mechanism and verify it by correctly predicting the behavior at large and small particle sizes. In the absence of interactions between the nanoparticles, we observe an asymmetric distribution of sizes with maximum uptake at intermediate sizes and a minimum size cut-off below which there can be no endocytosis. Including the effect of interactions in our model has remarkable effects on the uptake characteristics. Attractive interactions shift the minimum size cut-off and increase the optimal uptake while repulsive interactions make the distribution more symmetric lowering the optimal uptake.     

Mercuric Ion Stabilizes Levansucrase Secreted by <Emphasis Type="Italic">Acetobacter nitrogenifigens</Emphasis> Strain RG1<Superscript>T</Superscript>

The purification and characterization of an extracellular levansucrase enzyme produced by novel nitrogen-fixer Acetobacter nitrogenifigens strain RG1^T is described. Culture conditions were optimized for maximum levansucrase production. Levansucrase purified to homogeneity by tenfold purification has a molecular weight of 65 kDa, contained four cysteine residues, polymerized raffinose and was stable for 21 days at pH 6.0 when stored at 4 °C or −20 °C but was vulnerable to DTT and β-mercaptoethanol. Interestingly, this enzyme showed enhanced hydrolytic and polymerization activity in the presence of mercuric ion which, to our knowledge, is the first report for any levansucrase enzyme characterized so far. Evidences obtained from Native PAGE, tryptophan fluorescence study and activity measurements at different temperatures and in the presence of thiol modifying agents, show that mercuric ion stabilizes the enzyme. Levan, synthesized by the enzyme, has a molecular weight of 7,080 kDa and was shown to be a homopolymer of fructose.     

Validation of Arsenic Resistance in <Emphasis Type="Italic">Bacillus cereus</Emphasis> Strain AG27 by Comparative Protein Modeling of <Emphasis Type="Italic">ars</Emphasis>C Gene Product

The ars gene system provides arsenic resistance to a variety of microorganisms and can be chromosomal or plasmid-borne. The arsC gene, which codes for an arsenate reductase is essential for arsenate resistance and transforms arsenate into arsenite, which is extruded from the cell. Therefore, arsC gene from Bacillus cereus strain AG27 isolated from soil was amplified, cloned and sequenced. The strain exhibited a minimum inhibitory concentration of 40 and 35 mM to sodium arsenate and sodium arsenite, respectively. Homology of the sequence, when compared with available database using BLASTn search showed that 300 bp amplicons obtained possess partial arsC gene sequence which codes for arsenate reductase, an enzyme involved in the reduction of arsenate to arsenite which is then effluxed out of the cell, thereby indicating the presence of efflux mechanism of resistance in strain. The efflux mechanism was further confirmed by atomic absorption spectroscopy and scanning electron microscopy studies. Moreover, three dimensional structure of modeled arsC from Bacillus cereus strain shares significant structural similarity with arsenate reductase protein of B.subtilis, consisting of, highly similar overall fold with single α/β domain containing a central four stranded, parallel, open-twisted β-sheet flanked by α-helices on both sides. The structure harbors the arsenic binding motif AB loop or P-loop that is highly conserved in arsenate reductase family.     

Infant and child mortality in India in the last two decades: a geospatial analysis

BACKGROUND: Studies examining the intricate interplay between poverty, female literacy, child malnutrition, and child mortality are rare in demographic literature. Given the recent focus on Millennium Development Goals 4 (child survival) and 5 (maternal health), we explored whether the geographic regions that were underprivileged in terms of wealth, female literacy, child nutrition, or safe delivery were also grappling with the elevated risk of child mortality; whether there were any spatial outliers; whether these relationships have undergone any significant change over historical time periods. METHODOLOGY: The present paper attempted to investigate these critical questions using data from household surveys like NFHS 1992-1993, NFHS 1998-1999 and DLHS 2002-2004. For the first time, we employed geo-spatial techniques like Moran's-I, univariate LISA, bivariate LISA, spatial error regression, and spatiotemporal regression to address the research problem. For carrying out the geospatial analysis, we classified India into 76 natural regions based on the agro-climatic scheme proposed by Bhat and Zavier (1999) following the Census of India Study and all estimates were generated for each of the geographic regions. RESULT/CONCLUSIONS: This study brings out the stark intra-state and inter-regional disparities in infant and under-five mortality in India over the past two decades. It further reveals, for the first time, that geographic regions that were underprivileged in child nutrition or wealth or female literacy were also likely to be disadvantaged in terms of infant and child survival irrespective of the state to which they belong. While the role of economic status in explaining child malnutrition and child survival has weakened, the effect of mother's education has actually become stronger over time.     

Diet-induced obesity impairs endothelium-derived hyperpolarization via altered potassium channel signaling mechanisms

Background

The vascular endothelium plays a critical role in the control of blood flow. Altered endothelium-mediated vasodilator and vasoconstrictor mechanisms underlie key aspects of cardiovascular disease, including those in obesity. Whilst the mechanism of nitric oxide (NO)-mediated vasodilation has been extensively studied in obesity, little is known about the impact of obesity on vasodilation to the endothelium-derived hyperpolarization (EDH) mechanism; which predominates in smaller resistance vessels and is characterized in this study.

Methodology/Principal Findings

Membrane potential, vessel diameter and luminal pressure were recorded in 4^th order mesenteric arteries with pressure-induced myogenic tone, in control and diet-induced obese rats. Obesity, reflecting that of human dietary etiology, was induced with a cafeteria-style diet (∼30 kJ, fat) over 16–20 weeks. Age and sexed matched controls received standard chow (∼12 kJ, fat). Channel protein distribution, expression and vessel morphology were determined using immunohistochemistry, Western blotting and ultrastructural techniques. In control and obese rat vessels, acetylcholine-mediated EDH was abolished by small and intermediate conductance calcium-activated potassium channel (SK_Ca/IK_Ca) inhibition; with such activity being impaired in obesity. SK_Ca-IK_Ca activation with cyclohexyl-[2-(3,5-dimethyl-pyrazol-1-yl)-6-methyl-pyrimidin-4-yl]-amine (CyPPA) and 1-ethyl-2-benzimidazolinone (1-EBIO), respectively, hyperpolarized and relaxed vessels from control and obese rats. IK_Ca-mediated EDH contribution was increased in obesity, and associated with altered IK_Ca distribution and elevated expression. In contrast, the SK_Ca-dependent-EDH component was reduced in obesity. Inward-rectifying potassium channel (K_ir) and Na⁺/K⁺-ATPase inhibition by barium/ouabain, respectively, attenuated and abolished EDH in arteries from control and obese rats, respectively; reflecting differential K_ir expression and distribution. Although changes in medial properties occurred, obesity had no effect on myoendothelial gap junction density.

Conclusion/Significance

In obese rats, vasodilation to EDH is impaired due to changes in the underlying potassium channel signaling mechanisms. Whilst myoendothelial gap junction density is unchanged in arteries of obese compared to control, increased IK_Ca and Na⁺/K⁺-ATPase, and decreased K_ir underlie changes in the EDH mechanism.