Rejection of organic micro-pollutants from water by a tubular, hydrophilic pervaporative membrane designed for irrigation applications

The links between chemical properties, including those relating to molecular size, solubility, hydrophobicity and vapour pressure, and rejection of model aromatic micro-pollutants by a tubular, hydrophilic polymer pervaporation membrane designed for irrigation applications were investigated. Open air experiments were conducted at room temperature for individual solutions of fluorene, naphthalene, phenol, 1,2-dichlorobenzene, 1,2-diethylbenzene and 2-phenoxyethanol. Percentage rejection generally increased with increased molecular size for the model micro-pollutants (47–86%). Molecular weight and log Kow had the strongest positive relationships with rejection, as demonstrated by respective correlation coefficients of r = 0.898 and 0.824. Rejection was also strongly negatively correlated with aqueous solubility and H-bond δ. However, properties which relate to vapour phase concentrations of the micro-pollutants were not well correlated with rejection. Thus, physicochemical separation processes, rather than vapour pressure, drive removal of aromatic contaminants by the investigated pervaporation tube. This expanded knowledge could be utilized in considering practical applications of pervaporative irrigation systems for treating organic-contaminated waters such as oilfield-produced waters

The formation of disinfection by-products from the chlorination and chloramination of amides

This study examined the potential of six aliphatic and aromatic amides, commonly found in natural waters or used as chemical aids in water treatment, to act as organic precursors for nine haloacetamides (HAcAms), five haloacetonitriles (HANs), regulated trihalomethanes (THMs) and haloacetic acids (HAAs) upon chlorination and chloramination. The impact of key experimental conditions, representative of drinking water, including pH (7 & 8), retention time (4 & 24 h) and bromide levels (0 & 100 μg/L), on the generation of the target DBPs was investigated. The highest aggregate DBP yields upon chlor(am)ination were reported for the aromatic and hydrophobic hydroxybenzamide; 2.7% ± 0.1% M/M (chlorination) and 1.7% M/M (chloramination). Increased reactivity was observed in aliphatic and hydrophilic compounds, acrylamide (2.5 ± 0.2% M/M) and acetamide (1.3 ± 0.2% M/M), in chlorination and chloramination, respectively. The addition of bromide increased average DBP yields by 50–70%. Relative to chlorination, the application of chloramines reduced DBP formation by 66.5% (without Br−) and by 46.4% (with Br−). However, bromine incorporation in HAAs and HAcAms was enhanced following chloramination, of concern due to the higher toxicological potency of brominated compounds

Structural basis of dimerization and nucleic acid binding of human DBHS proteins NONO and PSPC1.

The Drosophila behaviour/human splicing (DBHS) proteins are a family of RNA/DNA binding cofactors liable for a range of cellular processes. DBHS proteins include the non-POU domain-containing octamer-binding protein (NONO) and paraspeckle protein component 1 (PSPC1), proteins capable of forming combinatorial dimers. Here, we describe the crystal structures of the human NONO and PSPC1 homodimers, representing uncharacterized DBHS dimerization states. The structures reveal a set of conserved contacts and structural plasticity within the dimerization interface that provide a rationale for dimer selectivity between DBHS paralogues. In addition, solution X-ray scattering and accompanying biochemical experiments describe a mechanism of cooperative RNA recognition by the NONO homodimer. Nucleic acid binding is reliant on RRM1, and appears to be affected by the orientation of RRM1, influenced by a newly identified 'β-clasp' structure. Our structures shed light on the molecular determinants for DBHS homo- and heterodimerization and provide a basis for understanding how DBHS proteins cooperatively recognize a broad spectrum of RNA targets

Mutations in pericentrin cause Seckel syndrome with defective ATR-dependent DNA damage signaling

Large brain size is one of the defining characteristics of modern humans. Seckel syndrome (MIM 210600), a disorder of markedly reduced brain and body size, is associated with defective ATR-dependent DNA damage signaling. Only a single hypomorphic mutation of ATR has been identified in this genetically heterogeneous condition. We now report that mutations in the gene encoding pericentrin (PCNT)--resulting in the loss of pericentrin from the centrosome, where it has key functions anchoring both structural and regulatory proteins--also cause Seckel syndrome. Furthermore, we find that cells of individuals with Seckel syndrome due to mutations in PCNT (PCNT-Seckel) have defects in ATR-dependent checkpoint signaling, providing the first evidence linking a structural centrosomal protein with DNA damage signaling. These findings also suggest that other known microcephaly genes implicated in either DNA repair responses or centrosomal function may act in common developmental pathways determining human brain and body size

A Small Conductance Calcium-Activated K⁺ Channel in C. elegans, KCNL-2, Plays a Role in the Regulation of the Rate of Egg-Laying

In the nervous system of mice, small conductance calcium-activated potassium (SK) channels function to regulate neuronal excitability through the generation of a component of the medium afterhyperpolarization that follows action potentials. In humans, irregular action potential firing frequency underlies diseases such as ataxia, epilepsy, schizophrenia and Parkinson's disease. Due to the complexity of studying protein function in the mammalian nervous system, we sought to characterize an SK channel homologue, KCNL-2, in C. elegans, a genetically tractable system in which the lineage of individual neurons was mapped from their early developmental stages. Sequence analysis of the KCNL-2 protein reveals that the six transmembrane domains, the potassium-selective pore and the calmodulin binding domain are highly conserved with the mammalian homologues. We used widefield and confocal fluorescent imaging to show that a fusion construct of KCNL-2 with GFP in transgenic lines is expressed in the nervous system of C. elegans. We also show that a KCNL-2 null strain, kcnl-2(tm1885), demonstrates a mild egg-laying defective phenotype, a phenotype that is rescued in a KCNL-2-dependent manner. Conversely, we show that transgenic lines that overexpress KCNL-2 demonstrate a hyperactive egg-laying phenotype. In this study, we show that the vulva of transgenic hermaphrodites is highly innervated by neuronal processes and by the VC4 and VC5 neurons that express GFP-tagged KCNL-2. We propose that KCNL-2 functions in the nervous system of C. elegans to regulate the rate of egg-laying. © 2013 Chotoo et al