C1-C2 alkyl aminiums in urban aerosols: Insights from ambient and fuel combustion emission measurements in the Yangtze River Delta region of China

We measured low molar-mass alkyl aminiums (methylaminium, dimethylaminium, ethylaminium and diethylaminium) in urban aerosols in the Yangtze River Delta region of eastern China in August 2014 and from November 2015 to May 2016. After examining artifact formation on sample filters, methylaminium, dimethylaminium and ethylaminium concentrations were quantified. The three C1-C2 aminiums exhibited a unimodal size distribution that maximized between 0.56 and 1.0 μm. Their concentrations in PM2.5 were 5.7 ± 3.2 ng m−3, 7.9 ± 5.4 ng m−3 and 20.3 ± 16.6 ng m−3, respectively, with higher concentrations during the daytime and in warm seasons. On new particle growth days, amine uptake to particles larger than 56 nm was barely enhanced. The molar ratios of individual aminium/NH4+ in PM2.5 were on the order of 10−4 and 10−3. Aminiums were thus far less to out-compete ammonium (NH4+) in neutralizing acidic species in particle sizes down to 56 nm. Abundant nitrate (NO3−/SO42− molar ratio = ∼3) and its correlation to methylaminium and ethylaminium implied that nitrate might be more important aminium salt than sulfate in urban aerosols of this area. Direct measurement of particle-phase amine emission from coal and biomass burning showed that coal burning is an important atmospheric amine source, considering coal burning is top-ranked particulate matter source in China

Characterization and phylogenetic analysis of the complete mitochondrial genome of Rhinogobius sp. (Perciformes, Gobiidae)

The genus Rhinogobius was widely distributed in East Asia. In the present study, the complete mitochondrial genome of Rhinogobius sp., possible a new species of freshwater goby from Anhui province of China, was sequenced for the first time. Sequence analysis showed that it is 16,511 bp in length with A + T content of 52.3%, consisting of 13 protein-coding genes, 22 transfer RNAs, two ribosomal RNAs, and a control region (CR). Phylogenetic analyses placed Rhinogobius sp. in a well-supported monophyletic cluster with other Rhinogobius fish and the phylogenetic position of Rhinogobius sp. was closer to Rhinogobius cliffordpopei

Substantial Decrease in Plasmalogen in the Heart Associated with Tafazzin Deficiency

Tafazzin is the mitochondrial enzyme that catalyzes transacylation between a phospholipid and a lysophospholipid in remodeling. Mutations in tafazzin cause Barth syndrome, a potentially life-threatening disease with the major symptom being cardiomyopathy. In the tafazzin-deficient heart, cardiolipin (CL) acyl chains become abnormally heterogeneous unlike those in the normal heart with a single dominant linoleoyl species, tetralinoleoyl CL. In addition, the amount of CL decreases and monolysocardiolipin (MLCL) accumulates. Here we determine using high-resolution ³¹P nuclear magnetic resonance with cryoprobe technology the fundamental phospholipid composition, including the major but oxidation-labile plasmalogens, in the tafazzin-knockdown (TAZ-KD) mouse heart as a model of Barth syndrome. In addition to confirming a lower level of CL (6.4 ± 0.1 → 2.0 ± 0.4 mol % of the total phospholipid) and accumulation of MLCL (not detected → 3.3 ± 0.5 mol %) in the TAZ-KD, we found a substantial reduction in the level of plasmenylcholine (30.8 ± 2.8 → 18.1 ± 3.1 mol %), the most abundant phospholipid in the control wild type. A quantitative Western blot revealed that while the level of peroxisomes, where early steps of plasmalogen synthesis take place, was normal in the TAZ-KD model, expression of Far1 as a rate-determining enzyme in plasmalogen synthesis was dramatically upregulated by 8.3 (±1.6)-fold to accelerate the synthesis in response to the reduced level of plasmalogen. We confirmed lyso-plasmenylcholine or plasmenylcholine is a substrate of purified tafazzin for transacylation with CL or MLCL, respectively. Our results suggest that plasmenylcholine, abundant in linoleoyl species, is important in remodeling CL in the heart. Tafazzin deficiency thus has a major impact on the cardiac plasmenylcholine level and thereby its functions

Distinct effects of tafazzin deletion in differentiated and undifferentiated mitochondria

Tafazzin is a conserved mitochondrial protein that is required to maintain normal content and composition of cardiolipin. We used electron tomography to investigate the effect of tafazzin deletion on mitochondrial structure and found that cellular differentiation plays a crucial role in the manifestation of abnormalities. This conclusion was reached by comparing differentiated cardiomyocytes with embryonic stem cells from mouse and by comparing different tissues from Drosophila melanogaster. The data suggest that tafazzin deficiency affects cardiolipin in all mitochondria, but significant alterations of the ultrastructure, such as remodeling and aggregation of inner membranes, will only occur after specific differentiatio

Distinct effects of tafazzin deletion in differentiated and undifferentiated mitochondria

Tafazzin is a conserved mitochondrial protein that is required to maintain normal content and composition of cardiolipin. We used electron tomography to investigate the effect of tafazzin deletion on mitochondrial structure and found that cellular differentiation plays a crucial role in the manifestation of abnormalities. This conclusion was reached by comparing differentiated cardiomyocytes with embryonic stem cells from mouse and by comparing different tissues from Drosophila melanogaster. The data suggest that tafazzin deficiency affects cardiolipin in all mitochondria, but significant alterations of the ultrastructure, such as remodeling and aggregation of inner membranes, will only occur after specific differentiatio