[Performance Study of Bromochloracetonitrile Degradation in Drinking Water by Fe/Cu Catalytic Reduction].

The paper used the method of iron copper catalyst reduction to degrade low concentrations of bromochloracetonitrile (BCAN) to lighten the damage to human being, which is a kind of disinfection by-products (DBPs) produced during the chlorination process of drinking water. The removal efficiency of BCAN and its influencing factors were investigated. The mechanism of degradation and kinetics were also explored. The results indicated that iron copper had a greater degradation ability towards BCAN, and the degradation rate of iron copper (mass ratio of 10:1) was 1.5 times that of the zero-valent iron. The removal of BCAN increased obviously with the increase of Fe/Cu dosage. When the initial concentration was set at 20 microg x L(-1), after a reaction time of 150 min, removal of BCAN was improved from 51.1% to 89.5% with the increase of iron copper (mass ratio of 10:1) dosage from 5 g x L(-1) to 10 g x L(-1). The temperature also had great impact on BCAN removal and the removal increased with the increase of temperature. However, BCAN removal did not change a lot with the variation of the initial concentration of BCAN when it was at a low level. The BCAN degradation by iron copper catalytic-reduction followed the first-order kinetics model.

[Formation process of nitrogenous disinfection byproduct trichloronitromethane in drinking water and its influencing factors].

A novel method is described in this paper, which uses methyl tertiary butyl ether (MTBE) as extractant and 1,2-dibromopropane as internal standard for the determination of nitrogenous disinfection byproduct trichloronitromethane (TCNM) by gas chromatography mass spectrometry (GC-MS). The formation process of TCNM and its influencing factors were evaluated with methylamine as the precursor during chlorination. The results indicated that the TCNM amount produced under alkaline condition was higher than those produced under the neutral and acidic conditions, and the TCNM amount increased with the increase of pH value. It was found that the TCNM amount increased with the increase of chlorine addition when the chlorine dosage was in the range of 2-8 mmol x L(-1). However, the TCNM amount was reduced when the chlorine dosage was enhanced from 8 mmol x L(-1) to 12 mmol x L(-1), under which conditions the concentration of free chlorine was higher and methylamine was turned into nitriles and aldehydes through other reactions. It was also found that the TCNM amount increased with the increase of methylamine addition when the methylamine dosage was in the range of 0.5-4 mmol x L(-1). Temperature was another important factor that affected the TCNM formation from methylamine especially in the range of 10-30 degrees C and the higher the temperature, the more the TCNM amount produced. The formation process of TCNM from methylamine by chlorination was in accordance with the mechanism of an electrophilic reaction, in which HClO and ClO(-) could be used as the electrophilic reagents to attack methylamine and then to form TCNM.

Gain control of N-methyl-D-aspartate receptor activity by receptor-like protein tyrosine phosphatase alpha.

Src kinase regulation of N-methyl-D-aspartate (NMDA) subtype glutamate receptors in the central nervous system (CNS) has been found to play an important role in processes related to learning and memory, ethanol sensitivity and epilepsy. However, little is known regarding the mechanisms underlying the regulation of Src family kinase activity in the control of NMDA receptors. Here we report that the distal phosphatase domain (D2) of protein tyrosine phosphatase alpha (PTPalpha) binds to the PDZ2 domain of post-synaptic density 95 (PSD95). Thus, Src kinase, its activator (PTPalpha) and substrate (NMDA receptors) are linked by the same scaffold protein, PSD95. Removal of PTPalpha does not affect the association of Src with NMDA receptors, but turns off the constitutive regulation of NMDA receptors by the kinase. Further more, we found that application of the PTPalpha catalytic domains (D1 + D2) into neurones enhances NMDA receptor-mediated synaptic responses. Conversely, the blockade of endogenous PTPalpha inhibits NMDA receptor activity and the induction of long-term potentiation in hippocampal neurones. Thus, PTPalpha is a novel up-regulator of synaptic strength in the CNS.