A phytoremediation approach for the restoration of coal fly ash polluted sites: A review.

Coal fly ash (CFA) is a predominant waste by-product of coal combustion which is disposed of in open ash dams that utilize large pieces of land. This waste material is classified as a hazardous substance in South Africa as well as in other countries due to its fine particles that are easily blown to the atmosphere and the unacceptable levels of heavy metals and persistent organic pollutants. Contaminants in CFA can pollute surface and ground water, agricultural sites, soil and therefore pose risks to the health of humans and the environment.

The Potential of (Thunb.) Less. for the Restoration of Sites Polluted with Coal Fly Ash.

The disposal of coal fly ash (CFA) generated from coal-fired power stations has serious impact on the ecosystem, by converting large pieces of land to barren ash dams with the potential to contaminate groundwater, surface water, air and soil. The aim of this study was to clarify the potential of phytoremediation using (Thunb.) Less.

Application of coal fly ash for trace metal adsorption from wastewater: A review.

Environmental pollution has become a global issue due to continuing anthropogenic activities that result in the production of enormous amounts of waste and the subsequent release of hazardous trace metals. The increasing levels of trace metals in the environment must be monitored regularly and reduced to prevent contamination of food chain. Numerous conventional technologies that are widely used for the removal of trace metals from environmental matrices have many drawbacks.

Two Additional Connections between the Transcriptional Programs Controlling Invasion and Intracellular Replication of Salmonella: HilD-SprB Positively Regulates and .

Salmonella virulence relies on the ability of this bacterium to invade the intestinal epithelium and to replicate inside macrophages, which are functions mainly encoded in Salmonella pathogenicity islands 1 and 2 (SPI-1 and SPI-2), respectively. Complex regulatory programs control the expression of SPI-1 and SPI-2 and functionally related genes, involving the integration of ancestral regulators and regulators that Salmonella has acquired during its evolution. Interestingly, some previous studies have revealed cross talk between the regulatory programs for SPI-1 and SPI-2.

HilD induces expression of a novel Salmonella Typhimurium invasion factor, YobH, through a regulatory cascade involving SprB.

HilD is an AraC-like transcriptional regulator encoded in the Salmonella pathogenicity island 1 (SPI-1), which actives transcription of many genes within and outside SPI-1 that are mainly required for invasion of Salmonella into host cells. HilD controls expression of target genes directly or by acting through distinct regulators; three different regulatory cascades headed by HilD have been described to date. Here, by analyzing the effect of HilD on the yobH gene in Salmonella enterica serovar Typhimurium (S.

Information-Theoretic Inference of an Optimal Dictionary of Protein Supersecondary Structures.

We recently developed an unsupervised Bayesian inference methodology to automatically infer a dictionary of protein supersecondary structures (Subramanian et al., IEEE data compression conference proceedings (DCC), 340-349, 2017). Specifically, this methodology uses the information-theoretic framework of minimum message length (MML) criterion for hypothesis selection (Wallace, Statistical and inductive inference by minimum message length, Springer Science & Business Media, New York, 2005).

SlyA and HilD Counteract H-NS-Mediated Repression on the Virulence Operon of Serovar Typhimurium and Thus Promote Its Activation by OmpR.

H-NS-mediated repression of acquired genes and the subsequent adaptation of regulatory mechanisms that counteract this repression have played a central role in the pathogenicity evolution. The pathogenicity island 2 (SPI-2) is an acquired chromosomal region containing genes necessary for to colonize and replicate in different niches of hosts. The operon, located in SPI-2, encodes the two-component system SsrA-SsrB, which positively controls the expression of the SPI-2 genes but also other many genes located outside SPI-2.

Regulatory Evolution Drives Evasion of Host Inflammasomes by Salmonella Typhimurium.

Bacterial two-component regulatory systems (TCS) couple the detection of niche-specific cues with adaptive gene expression to optimize fitness. In Salmonella Typhimurium (STM), the SsrA-SsrB TCS regulates virulence genes needed for survival within host cells, yet the impact of this TCS on regulatory evolution in this pathogen remains incompletely understood. Here, we show that SsrB alters a transcriptional network controlling bacterial motility to limit inflammasome activation during host cell infection.

Publisher Correction: HilD and PhoP independently regulate the expression of grhD1, a novel gene required for Salmonella Typhimurium invasion of host cells.

A correction to this article has been published and is linked from the HTML and PDF versions of this paper. The error has been fixed in the paper.

HilD and PhoP independently regulate the expression of grhD1, a novel gene required for Salmonella Typhimurium invasion of host cells.

When Salmonella is grown in the nutrient-rich lysogeny broth (LB), the AraC-like transcriptional regulator HilD positively controls the expression of genes required for Salmonella invasion of host cells, such as the Salmonella pathogenicity island 1 (SPI-1) genes. However, in minimal media, the two-component system PhoP/Q activates the expression of genes necessary for Salmonella replication inside host cells, such as the SPI-2 genes. Recently, we found that the SL1344_1872 hypothetical gene, located in a S.

The transcriptional regulator SsrB is involved in a molecular switch controlling virulence lifestyles of Salmonella.

The evolution of bacterial pathogenicity, heavily influenced by horizontal gene transfer, provides new virulence factors and regulatory connections that alter bacterial phenotypes. Salmonella pathogenicity islands 1 and 2 (SPI-1 and SPI-2) are chromosomal regions that were acquired at different evolutionary times and are essential for Salmonella virulence. In the intestine of mammalian hosts, Salmonella expresses the SPI-1 genes that mediate its invasion to the gut epithelium.

What do Constraint Programming Users Want to See? Exploring the Role of Visualisation in Profiling of Models and Search.

Constraint programming allows difficult combinatorial problems to be modelled declaratively and solved automatically. Advances in solver technologies over recent years have allowed the successful use of constraint programming in many application areas. However, when a particular solver's search for a solution takes too long, the complexity of the constraint program execution hinders the programmer's ability to profile that search and understand how it relates to their model.

On Representing Protein Folding Patterns Using Non-Linear Parametric Curves.

Proteins fold into complex three-dimensional shapes. Simplified representations of their shapes are central to rationalise, compare, classify, and interpret protein structures. Traditional methods to abstract protein folding patterns rely on representing their standard secondary structural elements (helices and strands of sheet) using line segments.

HilD induces expression of Salmonella pathogenicity island 2 genes by displacing the global negative regulator H-NS from ssrAB.

Salmonella pathogenicity islands 1 and 2 (SPI-1 and SPI-2) have essential roles in the pathogenesis of Salmonella enterica. Previously, we reported transcriptional cross talk between SPI-1 and SPI-2 when the SPI-1 regulator HilD induces expression of the SsrA/B two-component system, the central positive regulator of SPI-2, during the growth of Salmonella to late stationary phase in LB rich medium. Here, we further define the mechanism of the HilD-mediated expression of ssrAB.

Cooperative effects in the substrate specificity of the complement protease C1s.

Complement is a key component of the immune system, but can contribute to inflammatory diseases. The substrate specificity of C1s protease has been successfully investigated using a combinatorial approach, while a positional scanning method failed. The lack of success of the latter approach is possibly due to cooperativity in the active site, which could confound such analyses.

RCPdb: An evolutionary classification and codon usage database for repeat-containing proteins.

Over 3% of human proteins contain single amino acid repeats (repeat-containing proteins, RCPs). Many repeats (homopeptides) localize to important proteins involved in transcription, and the expansion of certain repeats, in particular poly-Q and poly-A tracts, can also lead to the development of neurological diseases. Previous studies have suggested that the homopeptide makeup is a result of the presence of G+C-rich tracts in the encoding genes and that expansion occurs via replication slippage.

Elucidation of the substrate specificity of the C1s protease of the classical complement pathway.

The complement system is a central component of host defense but can also contribute to the inflammation seen in pathological conditions. The C1s protease of the first complement component, the C1 complex, initiates the pathway. In this study we have elucidated the full specificity of the enzyme for the first time using a randomized phage display library.

Functional insights from the distribution and role of homopeptide repeat-containing proteins.

Expansion of "low complex" repeats of amino acids such as glutamine (Poly-Q) is associated with protein misfolding and the development of degenerative diseases such as Huntington's disease. The mechanism by which such regions promote misfolding remains controversial, the function of many repeat-containing proteins (RCPs) remains obscure, and the role (if any) of repeat regions remains to be determined. Here, a Web-accessible database of RCPs is presented.