Integrating properties and conditions to predict spray performance of alternative aviation fuel by ANN model.

Alternative aviation fuel has been confirmed benefits for GHGs reduction and energy saving. Alternative fuel use should meet drop-in fuel requirement, and one of the important factors to ensure combustion completeness is to achieve spray requirement in the whole envelop of flight. Alternative fuels are characterized different fuel properties at low temperature comparison with traditional jet fuel. For understanding fuel properties and spray-related processes under different conditions, alternative aviation fuel, including Fischer Tropsch (FT), cellulose hydrotreating jet fuel (CHJ) and traditional jet fuel (RP-3), were investigated spray performance. According to empirical equation deduced from experiment data (283 K-343 K), deviations to RP-3 enhanced significantly on surface tension and viscosity at low temperature aera (243 K-273 K). As the complex and discontinuous interaction between nozzle structure and fuel properties with temperature, and thus it is difficult to obtain appropriate empirical equation or simulation results at low temperature. Moreover, non-drop-in fuel like pure FT fuel cannot comply with the same spray mechanism as drop-in fuel. The artificial neural network (ANN) approaches have been involved to solve the complex relationship of properties with spray performance. ANN-spray model coupling with ANN-mass flow can predict not only cone angle and liquid length but also SMD and velocity in liquid zone and droplet zone with above 0.99 total correlation coefficient. Coupling simulation results of mass flow and spray performance, FT and CHJ as well as blend fuels present more obvious difference to RP-3 in droplet size distribution and velocity distribution at low temperature.

Tg(Δ113p53:cmyc) Transgene Upregulates glut1 Expression to Promote Zebrafish Heart Regeneration.

The heart switches its main metabolic substrate from glucose to fatty acids shortly after birth, which is one of reasons for the loss of heart regeneration capability in adult mammals. On the contrary, metabolic shifts from oxidative phosphorylation to glucose metabolism promote cardiomyocyte (CM) proliferation after heart injury. However, how glucose transportation in CMs is regulated during heart regeneration is still not fully understood. In this report, we found that the expression of Glut1 (slc2a1) was upregulated around the injury site of zebrafish heart, accompanied by an increase in glucose uptake at the injury area. Knockout of slc2a1a impaired zebrafish heart regeneration. Our previous study has demonstrated that the expression of Δ113p53 is activated after heart injury and Δ113p53+ CMs undergo proliferation to contribute to zebrafish heart regeneration. Next, we used the Δ113p53 promoter to generate the Tg(Δ113p53:cmyc) zebrafish transgenic line. Conditional overexpression of cmyc not only significantly promoted zebrafish CM proliferation and heart regeneration but also significantly enhanced glut1 expression at the injury site. Inhibiting Glut1 diminished the increase in CM proliferation in Tg(Δ113p53:cmyc) injured hearts of zebrafish. Therefore, our results suggest that the activation of cmyc promotes heart regeneration through upregulating the expression of glut1 to speed up glucose transportation.

Loss-of-function of p53 isoform Δ113p53 accelerates brain aging in zebrafish.

Reactive oxygen species (ROS) stress has been demonstrated as potentially critical for induction and maintenance of cellular senescence, and been considered as a contributing factor in aging and in various neurological disorders including Alzheimer's disease (AD) and amyotrophic lateral sclerosis (ALS). In response to low-level ROS stress, the expression of Δ133p53, a human p53 isoform, is upregulated to promote cell survival and protect cells from senescence by enhancing the expression of antioxidant genes. In normal conditions, the basal expression of Δ133p53 prevents human fibroblasts, T lymphocytes, and astrocytes from replicative senescence. It has been also found that brain tissues from AD and ALS patients showed decreased Δ133p53 expression. However, it is uncharacterized if Δ133p53 plays a role in brain aging. Here, we report that zebrafish Δ113p53, an ortholog of human Δ133p53, mainly expressed in some of the radial glial cells along the telencephalon ventricular zone in a full-length p53-dependent manner. EDU-labeling and cell lineage tracing showed that Δ113p53-positive cells underwent cell proliferation to contribute to the neuron renewal process. Importantly, Δ113p53M/M mutant telencephalon possessed less proliferation cells and more senescent cells compared to wild-type (WT) zebrafish telencephalon since 9-months old, which was associated with decreased antioxidant genes expression and increased level of ROS in the mutant telencephalon. More interestingly, unlike the mutant fish at 5-months old with cognition ability, Δ113p53M/M zebrafish, but not WT zebrafish, lost their learning and memory ability at 19-months old. The results demonstrate that Δ113p53 protects the brain from aging by its antioxidant function. Our finding provides evidence at the organism level to show that depletion of Δ113p53/Δ133p53 may result in long-term ROS stress, and finally lead to age-related diseases, such as AD and ALS in humans.

p53 isoform Δ113p53 promotes zebrafish heart regeneration by maintaining redox homeostasis.

Neonatal mice and adult zebrafish can fully regenerate their hearts through proliferation of pre-existing cardiomyocytes. Previous studies have revealed that p53 signalling is activated during cardiac regeneration in neonatal mice and that hydrogen peroxide (H2O2) generated near the wound site acts as a novel signal to promote zebrafish heart regeneration. We recently demonstrated that the expression of the p53 isoform Δ133p53 is highly induced upon stimulation by low-level reactive oxygen species (ROS) and that Δ133p53 coordinates with full-length p53 to promote cell survival by enhancing the expression of antioxidant genes. However, the function of p53 signalling in heart regeneration remains uncharacterised. Here, we found that the expression of Δ113p53 is activated in cardiomyocytes at the resection site in the zebrafish heart in a full-length p53- and ROS signalling-dependent manner. Cell lineage tracing showed that Δ113p53-positive cardiomyocytes undergo cell proliferation and contribute to myocardial regeneration. More importantly, heart regeneration is impaired in Δ113p53M/M mutant zebrafish. Depletion of Δ113p53 significantly decreases the proliferation frequency of cardiomyocytes but has little effect on the activation of gata4-positive cells, their migration to the edge of the wound site, or apoptotic activity. Live imaging of intact hearts showed that induction of H2O2 at the resection site is significantly higher in Δ113p53M/M mutants than in wild-type zebrafish, which may be the result of reduced induction of antioxidant genes in Δ113p53M/M mutants. Our findings demonstrate that induction of Δ113p53 in cardiomyocytes at the resection site functions to promote heart regeneration by increasing the expression of antioxidant genes to maintain redox homeostasis.

Molecular identification, tissue distribution and functional analysis of somatostatin receptors (SSTRs) in red-spotted grouper (Epinephelus akaara).

In the present study, four full-length cDNAs of somatostatin receptor (sstr) were cloned from the forebrain and pituitary of red-spotted grouper. The four full-length cDNAs were designated 2292, 1522, 1873 and 1789 bp and identified as sstr1, sstr2, sstr3, and sstr5 by BLAST analysis; the corresponding sizes of the open reading frames (ORFs) were 1155, 1113, 1467 and 1503 bp, which encoding 384, 370, 488 and 500 aa, respectively. The four receptors have seven transmembrane structures and contain the YANSCANPI/VLY sequence, which is the conserved amino acid sequence of the SSTR family. A tissue distribution study showed that the four sstrs had different expression patterns, suggesting that they may play different roles in regulating different physiological processes. The four receptors mediate ERK1/2 phosphorylation by SS-14 in HEK293 cells, and SS-14 promotes ATK and ERK1/2 phosphorylation in primary hepatocytes of red-spotted grouper. These results facilitate the study of SSTRs-mediated intracellular signaling pathways.