Nanostructured Aluminum Nitride (AlN) has been prepared by carbothermal reduction followed by nitridation (CTRN) of alumina gel over a temperature range 1200°C–1350°C and time period of 30 min to ...3 h. Before heat treatment the gel is repeatedly evacuated and purged with ammonia. The nanopores of the gel are filled with ammonia which acts as a source of in situ nitrogen at heat‐treatment temperature. Dextrose also decomposes at the reduction temperature and generates ultrafine carbon. The stability diagram of the carbon saturated Al–N–O system is constructed and it shows that extremely low partial pressure of oxygen is required for the stability of AlN. The ultrafine carbon as well as hydrogen from the cracking of ammonia is not sufficient to create the extremely low partial pressure of oxygen required for the stabilization of AlN. So the sample is heat treated in charcoal boat in nitrogen atmosphere to achieve an extremely low partial pressure of oxygen required for the formation of AlN. The material has been characterized through XRD, FESEM, and HRTEM analyses. The spherical particle size of AlN is obtained ∼21 nm.
At the triple point of a repulsive screened Coulomb system, a fcc crystal, a bcc crystal, and a fluid phase coexist. At their intersection, these three phases form a liquid groove, the triple ...junction. Using confocal microscopy, we resolve the triple junction on a single-particle level in a model system of charged PMMA colloids in a nonpolar solvent. The groove is found to be extremely deep and the incommensurate solid-solid interface to be very broad. Thermal fluctuations hence appear to dominate the solid-solid interface. This indicates a very low interfacial energy. The fcc-bcc interfacial energy is quantitatively determined based on Young's equation and, indeed, it is only about 1.3 times higher than the fcc-fluid interfacial energy close to the triple point.
Abstract
The Metropolitan Water District of Southern California (Metropolitan) and the Sanitation Districts of Los Angeles County (Sanitation Districts) are exploring the potential of a Regional ...Recycled Water Program (RRWP) to beneficially reuse water currently discharged to the Pacific Ocean. The program would consist of a new advanced water treatment (AWT) facility at the Sanitation Districts' Joint Water Pollution Control Plant (JWPCP) in Carson, California, USA, capable of producing an ultimate flow of 581 MLD (150 MGD). The full-scale facility would treat effluent from the JWPCP using an AWT train comprising a membrane bioreactor (MBR), followed by reverse osmosis (RO) and ultraviolet light advanced oxidation (UV/AOP). After MBR-RO-UV/AOP treatment, the treated water would be distributed to groundwater basins in Los Angeles and Orange counties to recharge their aquifers. This program would diversify the region's water resources and significantly contribute to long-term water supply targets outlined in Metropolitan's Integrated Water Resources Plan. A feasibility study for the RRWP was completed in 2016, confirming its technical viability. Currently, Metropolitan and the Sanitation Districts recently completed conceptual planning studies to investigate implementation options for a full-scale program, and constructed a 1.9 MLD (0.5 MGD) AWT demonstration facility. Although large facilities employing membrane filtration (MF)-RO-UV/AOP are currently permitted and operating in California, there are no facilities using an MBR-RO-UV/AOP train. The AWT demonstration facility – the Regional Recycled Water Advanced Purification Center – will build on recent research in Australia and the USA to develop a regulatory strategy to incorporate MBR into a potable reuse advanced treatment train.
The study examined the effect of operating conditions of the Fenton process on biodegradability improvement and mineralization of amoxicillin, ampicillin and cloxacillin antibiotics in aqueous ...solution. In addition, degradation of amoxicillin, ampicillin and cloxacillin under optimum operating conditions were evaluated. The optimum operating conditions for an aqueous solution containing 104, 105 and 103
mg/L amoxicillin, ampicillin, and cloxacillin, respectively were observed to be COD/H
2O
2/Fe
2+ molar ratio 1:3:0.30 and pH 3. Under optimum operating conditions, complete degradation of amoxicillin, ampicillin and cloxacillin occurred in 2
min. In addition, biodegradability improved from ∼0 to 0.37 in 10
min, and COD and DOC degradation were 81.4% and 54.3%, respectively in 60
min. Maximum biodegradability (BOD
5/COD ratio) improvement was achieved in 10, 20 and 40
min at antibiotics concentration 100, 250 and 500
mg/L, respectively for each antibiotic in aqueous solution. Increase in nitrate and ammonia concentration were observed due to mineralization of organic nitrogen, concentration of nitrate increased from 0.3 to 10
mg/L and concentration of ammonia increased from 8 to 13
mg/L in 60
min. The study indicated that Fenton process can be used for pretreatment of amoxicillin, ampicillin and cloxacillin wastewater for biological treatment.
Accumulation of unfolded or misfolded proteins in the endoplasmic reticulum (ER) lumen triggers an unfolded protein response (UPR) for stress adaptation, the failure of which induces cell apoptosis ...and tissue/organ damage. The molecular switches underlying how the UPR selects for stress adaptation over apoptosis remain unknown. Here, we discovered that accumulation of unfolded/misfolded proteins selectively induces N6-adenosine-methyltransferase-14 (METTL14) expression. METTL14 promotes C/EBP-homologous protein (CHOP) mRNA decay through its 3′ UTR N6-methyladenosine (m6A) to inhibit its downstream pro-apoptotic target gene expression. UPR induces METTL14 expression by competing against the HRD1-ER-associated degradation (ERAD) machinery to block METTL14 ubiquitination and degradation. Therefore, mice with liver-specific METTL14 deletion are highly susceptible to both acute pharmacological and alpha-1 antitrypsin (AAT) deficiency-induced ER proteotoxic stress and liver injury. Further hepatic CHOP deletion protects METTL14 knockout mice from ER-stress-induced liver damage. Our study reveals a crosstalk between ER stress and mRNA m6A modification pathways, termed the ERm6A pathway, for ER stress adaptation to proteotoxicity.
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•UPR selectively induces m6A writer METTL14 protein expression•METTL14 suppresses CHOP-induced apoptosis for ER stress adaptation•HRD1 is a METTL14 ubiquitin ligase and UPR suppresses HRD1-mediated METTL14 degradation•CHOP suppression rescues METTL14 null mice from proteotoxic liver damage
ERAD is critical for ER-stress adaptation, and its failure triggers cell apoptosis. Wei et al. discovered that ER stress induces N6-adenosine-methyltransferase METTL14 expression by suppressing HRD1-mediated ubiquitination to promote CHOP mRNA decay for inhibiting CHOP-induced apoptosis. This study defines an ERm6A pathway, underlying how ERAD selects stress adaptation over apoptosis.
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