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This research examined the use of a single facultative pond for treatment of an intermittent discharge from a UK campsite. The system was monitored over an 11-month period to determine the optimum time for discharge in terms of quality standards. The results showed that based on organic strength, discharge was possible in winter between November and March but February was the optimum to meet nutrient and suspended solids requirements. The pond showed rapid acclimatisation to the influent wastewater, with biochemical oxygen demand removal rates during the filling period of around 60 kg ha-1 day-1 and removal efficiencies of ∼95% after maturation. The system proved simple to operate. A major design factor is the requirement for storage of net incoming precipitation, which may provide dilution of residual pollutants but requires additional system capacity. [ABSTRACT FROM AUTHOR]

The research investigated some factors influencing the rate of stabilisation of wastewater in the spring period in continental climate waste stabilisation ponds, and in particular the potential for bringing forward the discharge date by optimising storage capacity and dilution. Experiments using pilot and model- scale ponds were set up in Almaty, Kazakhstan. These simulated operating regimes for a facultative and storage/maturation pond system subject to ice cover from late November until late March. Two pilot-scale facultative ponds were operated at hydraulic retention times (HRT) of 20 and 30 days, with surface loading rates of 100 and 67 kg BOD ha-1 day-1. Effluent from the 20-day HRT facultative pond was then fed to two pilot-scale storage/maturation ponds which had been partially emptied and allowed to refill over the winter period with no removal of effluent. The paper discusses the results of the experiments with respect to selection of an operating regime to make treated wastewater available early in the spring. Preliminary results indicate that there may be potential for alternative operating protocols designed to maximise their performance and economic potential. [ABSTRACT FROM AUTHOR]

The first excited electronic state of molecular oxygen, O2(a1Δg), is formed in the upper atmosphere by the photolysis of O3. Its lifetime is over 70 min above 75 km, so that during the day its concentration is about 30 times greater than that of O3. In order to explore its potential reactivity with atmospheric constituents produced by meteoric ablation, the reactions of Mg, Fe, and Ca with O2(a) were studied in a fast flow tube, where the metal atoms were produced either by thermal evaporation (Ca and Mg) or by pulsed laser ablation of a metal target (Fe), and detected by laser induced fluorescence spectroscopy. O2(a) was produced by bubbling a flow of Cl2 through chilled alkaline H2O2, and its absolute concentration determined from its optical emission at 1270 nm (O2(a1Δg - X3Σg-). The following results were obtained at 296 K: k(Mg + O2(a) + N2 → MgO2 + N2) = (1.8 ± 0.2) × 10-30 cm6 molecule-2 s-1; k(Fe + O2(a) → FeO + O) = (1.1 ± 0.1) × 10-13 cm3 molecule-1 s-1; k(Ca + O2(a) + N2 → CaO2 + N2) = (2.9 ± 0.2) × 10-28 cm6 molecule-2 s-1; and k(Ca + O2(a) → CaO + O) = (2.7 ± 1.0) × 10-12 cm3 molecule-1 s-1. The total uncertainty in these rate coefficients, which mostly arises from the systematic uncertainty in the O2(a) concentration, is estimated to be ±40%. Mg + O2(a) occurs exclusively by association on the singlet surface, producing MgO2(1A1), with a pressure dependent rate coefficient. Fe + O2(a), on the other hand, shows pressure independent kinetics. FeO + O is produced with a probability of only ∼0.1%. There is no evidence for an association complex, suggesting that this reaction proceeds mostly by near-resonant electronic energy transfer to Fe(a5F) + O2(X). The reaction of Ca + O2(a) occurs in an intermediate regime with two competing pressure dependent channels: (1) a recombination to produce CaO2(1A1), and (2) a singlet/triplet non-adiabatic hopping channel leading to CaO + O(3P). In order to interpret the Ca + O2(a) results, we utilized density functional theory along with multireference and explicitly correlated CCSD(T)-F12 electronic structure calculations to examine the lowest lying singlet and triplet surfaces. In addition to mapping stationary points, we used a genetic algorithm to locate minimum energy crossing points between the two surfaces. Simulations of the Ca + O2(a) kinetics were then carried out using a combination of both standard and non-adiabatic Rice-Ramsperger-Kassel-Marcus (RRKM) theory implemented within a weak collision, multiwell master equation model. In terms of atmospheric significance, only in the case of Ca does reaction with O2(a) compete with O3 during the daytime between 85 and 110 km. [ABSTRACT FROM AUTHOR]

The fluoride reactivation process was evaluated for measuring the level of sarin or soman nerve agents reactivated from substrates in plasma and tissue from in vivo exposed guinea pigs (Cava porcellus), in blood from in vivo exposed rhesus monkeys (Macaca mulatta), and in spiked human plasma and purified human albumin. Guinea pig exposures ranged from 0.05 to 44 LD50, and reactivated nerve agent levels ranged from 1.0 ng/mL in plasma obtained from 0.05 LD50 sarin‐exposed guinea pigs to an average of 147 ng/g in kidney tissue obtained from two 2.0 LD50 soman‐exposed guinea pigs. Positive dose–response relationships were observed in all low‐level, 0.05 to 0.4 LD50, exposure studies. An average value of 2.4 ng/mL for reactivated soman was determined in plasma obtained from two rhesus monkeys three days after a 2 LD50 exposure. Of the five types of guinea pig tissue studied, plasma, heart, liver, kidney and lung, the lung and kidney tissue yielded the highest amounts of reactivated agent. In similar tissue and with similar exposure procedures, reactivated soman levels were greater than reactivated sarin levels. Levels of reactivated agents decreased rapidly with time while the guinea pig was alive, but decreased much more slowly after death. This latter chemical stability should facilitate forensic retrospective identification. The high level of reactivated agents in guinea pig samples led to the hypothesis that the principal source of reactivated agent came from the agent‐carboxylesterase adduct. However, there could be contributions from adducts of the cholinesterases, albumin and fibrous tissue, as well. Quantitative analysis was performed with a GC‐MS system using selected ion monitoring of the 99 and 125 ions for sarin and the 99 and 126 ions for soman. Detection levels were as low as 0.5 ng/mL. The assay was precise and easy to perform, and has potential for exposure analysis from organophosphate nerve agents and pesticides in other animal species. [ABSTRACT FROM AUTHOR]

Background More than 70% of patients diagnosed with colorectal cancer with liver metastasis have unresectable disease, so the available treatment is systemic chemotherapy that has limited efficacy and causes harmful side-effects. Thus novel and more effective drugs are needed to improve patients' survival and quality of life. Recent studies have identified several genomic alterations in CRLM that can theoretically be targeted by novel cancer-specific drugs. Among those is the gain-of-function mutations in PIK3CA – the gene encoding the p110a catalytic subunit of PI3K – that are present in 18% of metastatic colorectal tumours. Following the recent FDA-approval of Alpelisib (a PI3Ka-specific inhibitor) HR-positive breast cancer, there is increasing interest to test this drug efficacy to treat CRLM patients with PIK3CA mutations. Although widely used to test cancer cell response, immortalized cell lines fail to represent tumour genomic alterations and heterogeneity. Our goal is to develop patient-derived primary cell models that can be used to reliably test patients' drug response. Methods Fresh colorectal cancer liver metastasis surgical specimens were dissociated and digested into single cells and seeded in matrigel with appropriate culture media. Originated organoid cultures were then submitted to a minimum of 5 passages followed by a freeze-thaw cycle before deemed established culture. To validate organoid tumour origin, we then performed whole-genome sequencing of paired organoid and respective fresh tumour. Results The established patient-derived organoids from colorectal liver metastasis add an overall mutation match of > 80% when compared to with the original tumour. We have found so far two CRLM organoid lines with mutations in the helical domain of PIK3CA (E545A and E542K). Conclusions We have demonstrated patient-derived organoids recapitulate the genome of their tumour of origin. Libraries of these primary cell models should in the near future be used to more accurately determine drug effectiveness prior to clinical trials. Ongoing testing of Alpelisib alone or in combination with other PI3K pathway target genes will determine whether these patients could benefit from these drugs. Legal entity responsible for the study Barros-Silva, J.D. Funding Cancer Research UK. Disclosure All authors have declared no conflicts of interest. [ABSTRACT FROM AUTHOR]