Thermal Cracking of Endothermic Hydrocarbon Fuel in Regenerative Cooling Channels with Different Geometric Structures

The chemical heat sink of endothermic hydrocarbon fuels (EHFs) is generally dependent on its thermal cracking in the cooling channel, which is accompanied and limited by the formation of carbon deposit. In this work, HF-1 (a kerosene-based EHF) was electrically heated in the rectangular, square, and circular channels with the same cross-sectional area under 3.5 MPa to study the effect of cooling channel geometric structures on the thermal cracking and carbon deposition behaviors. It was found that under similar conditions (inlet flow rate of fuel, pressure, outlet temperature), conversions of HF-1 in both rectangular and square channels were slightly higher than that in the circular one with high selectivity to methane but lower selectivities to the primary cracking products (such as 1-hexene and 1-heptene, etc.). In addition, more carbon deposits were formed in the rectangular and square channels, especially around the corners of channels. Based on the CFD simulation, the possible reasons should be ascribed to the difference in the gradient uniformity near the wall of different channels. The higher temperature and lower velocity in the boundary layer of the quadratic channels might cause the thermal cracking to be slightly severer and the rapid secondary reactions to form carbon deposit

Additional file 3: of Inhibition of glutamate oxaloacetate transaminase 1 in cancer cell lines results in altered metabolism with increased dependency of glucose

Figure S3. Partial prevention of ischemic-like-cell-death morphological changes by NAD+. Bars indicate 25 Οm. (TIF 1353 kb

Additional file 2: of Inhibition of glutamate oxaloacetate transaminase 1 in cancer cell lines results in altered metabolism with increased dependency of glucose

Figure S2. Rescue of GOT1 down-regulated and GOT1-null cells by oxaloacetate. Relative cell viabilities after 8 h (a) and 24 h (b) in wild type 143B cells and 8 h (c) and 24 h (d) in wild type A549 cells. Relative cell viabilities after 8 h (e) and 24 h (f) in GOT1 siRNA knock-down A549 cells. Rescue of GOT1-null 143B cells with OAA at different concentrations upon glucose deprivation (g). Mean ± s.d. from 3 independent experiments. One-way ANOVA test was performed. *** p < 0.001; ** p < 0.01;* p < 0.05. NS: not significant. (TIF 230 kb

General Characteristics of Patients with Active Ocular Toxoplasmosis.

<p><b>†</b>Central subfield is defined as the subfield in the center of an ETDRS (early treatment diabetic retinopathy study) grid.</p><p>OT = ocular toxoplasmosis; OD = right eye; OS = left eye; VA = visual acuity; d = days; m = months; NA = not available; ONH = optic nerve head, CME = cystoid macular edema; CNV = choroidal neovascularization; SRF = subretinal fluid.</p><p>General Characteristics of Patients with Active Ocular Toxoplasmosis.</p

Subretinal fluid (SRF) in typical active ocular toxoplasmosis as seen by optical coherence tomography (OCT) (Patient 9, Table 1).

<p><b>Parts A-D</b>: fundus photos (FP) and OCT images on the initial visit. <b>Part A</b>: a fresh whitish inflammatory lesion superior to the macula in the extramacular area, with intraretinal hemorrhage and SRF surrounding the necrosis. <b>Parts B-D</b>: OCT B-scans corresponding to the lines B-D shown in Part A. Vitreous cells were present with normal retinal structure through the fovea (Part B). In areas surrounding the active lesion, SRF was visable (Part C-D). Full-thickness retina destruction (retinal necrosis) accompanied by largely increased choroidal thickness (744 μm) was present (Part D). <b>Parts E-H:</b> FP and OCT images 6 weeks after the initial visit. <b>Part E</b>: previous whitish inflammatory lesion was smaller without visible SRF. <b>Parts F-H</b>: OCT B-scans corresponding to the lines F-H shown in Part E. Absence of SRF and dramatically lessened vitreous cells in the macula and area around the active lesion were observed (Part F-H). Retina got thinner, but still with full-thickness necrosis at the previous active site (Part H). The choroid thickness decreased to 345 μm (Part H). <b>Parts C1-C2</b> showed the segmentation of retinal layers in OCT B-scan corresponding to Figure C. <b>Part C3-C5</b>: quantitative measurement results from manual segmentation. <b>Part C3:</b> the color bar showing the correlation of thickness and color range. <b>Parts C4-C5:</b> mean retinal thickness and mean SRF height shown in early treatment diabetic retinopathy study (ETDRS) grid using foveola as the center of the grid. The correlation of numbers and subfields are as follows: 1 = superior outer macula; 2 = temporal outer macula; 3 = inferior outer macula; 4 = nasal outer macula; 5 = superior inner macula; 6 = temporal inner macula; 7 = inferior inner macula; 8 = nasal inner macula; 9 = central subfield). ILM = internal limiting membrane; PR = photoreceptor layer; RPE = retinal pigment epithelium.</p

Subretinal fluid (SRF) in eyes with typical active ocular toxoplasmosis associated with retinal necrosis in the macula as seen on optical coherence tomography (OCT) (Patients 1–8, Table 1).

<p><b>Parts A1-H1</b>: fundus photos (FP) or infrared (IR) images of the macula overlying with early treatment diabetic retinopathy study (ETDRS) grid, for eyes with active OT. Red arrows in each eye indicated areas with active retinitis. <b>Parts A2-H2:</b> mean retinal thickness maps shown in the ETDRS grid corresponding to the overlapped grid in Figure A1-H1. <b>Parts A3-H3:</b> maps of mean SRF height shown in ETDRS grid corresponding to the overlapped grid in Figure A1-H1. 1 = superior outer macula; 2 = temporal outer macula; 3 = inferior outer macula; 4 = nasal outer macula; 5 = superior inner macula; 6 = temporal inner macula; 7 = inferior inner macula; 8 = nasal inner macula; 9 = central subfield.</p

Table1_Ginsenoside Rd protects transgenic Caenorhabditis elegans from β-amyloid toxicity by activating oxidative resistant.XLS

Alzheimer’s disease (AD) is a serious public health issue but few drugs are currently available for the disease, and these only target the symptoms. It is well established that oxidative stress plays a crucial role in AD, and there is compelling evidence linking oxidative stress to β-amyloid (Aβ). An exciting source of potential new AD therapeutic medication possibilities is medicinal plants. Ginsenoside Rd (GS-Rd) is one of the main bioactive substances in ginseng extracts. In our study, we used a network pharmacology analysis to identify overlapping GS-Rd (therapeutic) and AD (disease)-relevant protein targets, gene ontology (GO) and bio-process annotation, and the KEGG pathway analysis data predicted that GS-Rd impacts multiple targets and pathways, such as the MAPK signal pathway and the JAT-STAT3 signaling pathway. We then assessed the role of GS-Rd in C. elegans and found that GS-Rd prolongs lifespan, improves resistance to heat stress, delays physical paralysis and increases oxidative stress responses. Overall, these results suggest that GS-Rd protects against the toxicity of Aβ. The RNA-seq analysis revealed that GS-Rd achieves its effects by regulating gene expressions like daf-16 and skn-1, as well as by participating in many AD-related pathways like the MAPK signaling pathway. In addition, in CL4176 worms, GS-Rd decreased reactive oxygen species (ROS) levels and increased SOD activity. Additional research with transgenic worms showed that GS-Rd aided in the movement of DAF-16 from the cytoplasm to the nucleus. Taken together, the results indicate that GS-Rd significantly reduces Aβ aggregation by targeting the MAPK signal pathway, induces nuclear translocation of DAF-16 to activate downstream signaling pathways and increases resistance to oxidative stress in C. elegans to protect against Aβ-induced toxicity.</p

DataSheet1_Ginsenoside Rd protects transgenic Caenorhabditis elegans from β-amyloid toxicity by activating oxidative resistant.PDF

Alzheimer’s disease (AD) is a serious public health issue but few drugs are currently available for the disease, and these only target the symptoms. It is well established that oxidative stress plays a crucial role in AD, and there is compelling evidence linking oxidative stress to β-amyloid (Aβ). An exciting source of potential new AD therapeutic medication possibilities is medicinal plants. Ginsenoside Rd (GS-Rd) is one of the main bioactive substances in ginseng extracts. In our study, we used a network pharmacology analysis to identify overlapping GS-Rd (therapeutic) and AD (disease)-relevant protein targets, gene ontology (GO) and bio-process annotation, and the KEGG pathway analysis data predicted that GS-Rd impacts multiple targets and pathways, such as the MAPK signal pathway and the JAT-STAT3 signaling pathway. We then assessed the role of GS-Rd in C. elegans and found that GS-Rd prolongs lifespan, improves resistance to heat stress, delays physical paralysis and increases oxidative stress responses. Overall, these results suggest that GS-Rd protects against the toxicity of Aβ. The RNA-seq analysis revealed that GS-Rd achieves its effects by regulating gene expressions like daf-16 and skn-1, as well as by participating in many AD-related pathways like the MAPK signaling pathway. In addition, in CL4176 worms, GS-Rd decreased reactive oxygen species (ROS) levels and increased SOD activity. Additional research with transgenic worms showed that GS-Rd aided in the movement of DAF-16 from the cytoplasm to the nucleus. Taken together, the results indicate that GS-Rd significantly reduces Aβ aggregation by targeting the MAPK signal pathway, induces nuclear translocation of DAF-16 to activate downstream signaling pathways and increases resistance to oxidative stress in C. elegans to protect against Aβ-induced toxicity.</p

Subretinal fluid (SRF) associated with cystoid macular edema (CME) in one eye with previous diagnosis of ocular toxoplasmosis as seen on optical coherence tomography (OCT) (Patients 16, Table 1).

<p><b>Parts A1, B1, C1, D1</b> showed characteristics of SRF and CME seen on OCT B-scans through the fovea. <b>Parts A2, B2, C2, D2</b> demonstrated mean retinal thickness maps shown in early treatment diabetic retinopathy study (ETDRS) grid. <b>Parts A3, B3, C3, D3</b> were maps of mean SRF height shown in ETDRS grid. SRF and CME kept relatively unchanged for the first 3 visits, and started to respond to treatment on the 4th visit. <b>Parts E-K</b> revealed absence of SRF in the following visits, after 3 intraocular injection of 1.25 mg bevacizumab. However, CME remained persistent, although minimization at one time point (H) was temporally seen.</p

The same panel of sections as in Fig 12 were stained for collagen.

<p>The same panel of sections as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0125961#pone.0125961.g012" target="_blank">Fig 12</a> were stained for collagen.</p