Effects of different ammonia energy ratio on soot formation and oxidation in an ammonia diesel dual-fuel engine.

Due to environmental pollution and energy crises, zero­carbon fuel ammonia (NH3) has attracted extensive attention as an alternative fuel for engines. In this paper, the effects of ammonia energy ratio (AER) and injection strategy on particulate emission characteristics of an ammonia diesel dual-fuel engine were examined by merging experimental and simulation results; additionally, soot formation and oxidation mechanism were investigated. Results showed that the reduction in particulate emission was substantially higher than the increase in AER. When AER increased to 60 %, the reduction in particulate mass concentration reached 97.5 %. The initial soot formation area gradually moved to the bottom of the piston bowl with increasing AER. When the piston reached the top dead center, the high-soot-concentration area was shifted to the center of the piston bowl as AER increased. The contents of acetylene (C2H2) and methyl (CH3) reduced considerably, which restricted the formation of soot precursors. With AER increasing, the contents of nitric oxides (NOx) and other nitrogen-containing species increased and reacted with CH3 and other carbon-containing species, which effectively reduced the number of C in soot formation pathway, thereby lowering particulate emissions. As AER increased, hydroxyl (OH) involved in soot formation gradually decreased, and only 14 % of OH was involved in the oxidation of n-heptane at 60 % AER, which was favorable for reducing the soot formation rate. Furthermore, OH is a substantial species in soot oxidation. The introduction of ammonia caused an increase in OH, which facilitated the removal of soot. The decrease in hydrogenium (H) hindered the hydrogen-abstraction-acetylene-addition (HACA) reaction, further limiting the soot surface growth. By optimizing the injection timing and AER, particulate emission was lowered to 4.31 × 10-5 µg/cm3, and particle size was reduced by 64.2 % when AER was 60 %, injection timing was -20° CA ATDC, and injection pressure was 60 MPa.

Effect of air and exhaust gas dilutions on ultra-fine particulate emissions in different combustion modes.

The effect of air and exhaust dilution ratios on the characteristics of ultra-fine particulate matter (PM) and combustion process in different combustion modes at low loads were investigated based on experimental and numerical simulation in this study. The combustion modes included partially premixed compression ignition (PPCI), diffusion combustion (DC), and modulated kinetics combustion (MKC). The air and exhaust gas dilution ratio varied from 0 % to 40 % and 0 % to 55 % respectively. Additionally, the effect of dilutions and combustion modes on PM characteristics is precisely analyzed by computational fluid dynamics. The NOx and Soot emission are reduced in PPCI and DC mode of combustion with the increase of air and exhaust gas dilution rate. However, NOx emission is decreases while Soot is increases in MKC mode. The concentration of particulate number increases in case of both PPCI and DC mode and achieved highest value as 3.3 × 107 and 1.4 × 107 N/cc respectively. Although, concentration of particulate number (PN) in MKC mode first starts climbing and after attaining the highest level of 1.3 × 107 N/cc it falls down. PN concentration in PPCI, MKC, and DC modes decreases as the exhaust gas dilution rate increases. The study of nuclear and accumulate mode of PM was performed separately where the diameter of particles is <1000 nm. Under variable air and exhaust gas dilution ratios, the value of PN is always lies between 40 and 90 % in the nuclear mode PM domain for PPCI and DC modes while for MKC mode, the proportion of PN fall under 13-57 % at exhaust gas ratio above 30 %. The proportion of nuclear mode particulate mass in PPCI mode is >10 % while its values is <1 % for DC and MKC modes.

Interleukin17A Promotes Postoperative Cognitive Dysfunction by Triggering ß-Amyloid Accumulation via the Transforming Growth Factor-ß (TGFß)/Smad Signaling Pathway.

Although postoperative cognitive dysfunction (POCD) is relatively common in elderly patients who have undergone major surgery, the mechanisms underlying this postoperative complication are unclear. Previously, we have investigated the role of cytokine-mediated hippocampal inflammation in the development of POCD in a rat model. Here, we sought to determine in mice the role of cytokine interleukin17A (IL17A) in POCD and to characterize the associated signaling pathways. Old mice underwent hepatectomy surgery in the presence or absence of IL17A monoclonal antibody, and cognitive function, hippocampal neuroinflammation, and pathologic markers of Alzheimer's disease (AD) were assessed. We found that the level of IL17A in the hippocampus was increased in hepatectomy mice and that cognitive impairment after surgery was associated with the appearance of certain pathological hallmarks of AD: activation of astrocytes, ß-amyloid1-42 (Aß1-42) production, upregulation of transforming growth factor-ß (TGFß), and increased phosphorylation of signaling mother against decapentaplegic peptide 3 (Smad3) protein in the hippocampus. Surgery-induced changes in cognitive dysfunction and changes in Aß1-42 and TGFß/Smad signaling were prevented by the administration of IL17A monoclonal antibody. In addition, IL17A-stimulated TGFß/Smad activation and Aß1-42 expression were reversed by IL17A receptor small interfering RNA and a TGFß receptor inhibitor in cultured astrocytes. Our findings suggest that surgery can provoke IL17A-related hippocampal damage, as characterized by activation of astrocytes and TGFß/Smad pathway dependent Aß1-42 accumulation in old subjects. These changes likely contribute to the cognitive decline seen in POCD.

Vitamin D improves cognitive function and modulates Th17/T reg cell balance after hepatectomy in mice.

It is known that surgery-induced tissue damage activates the peripheral immune system resulting in the release of inflammatory mediators and cognitive impairment in aged mice. Vitamin D has been shown to have immunomodulatory function, but the molecular basis for it has not been well understood. In this study, we mainly investigated the efficacy and mechanism of vitamin D against postoperative cognitive dysfunction (POCD). The treatment of C57BL mice with vitamin D significantly preserves postoperative cognitive function, markedly inhibits surgery-induced interleukin (IL)-17, IL-6, transforming growth factor beta (TGF-ß), and retinoic acid-related orphan receptor (RORγt) production, and obviously induces IL-10 and forkhead box p3 (Foxp3) expression. These findings indicate that vitamin D amelioration of POCD is, to a large extent, due to inhibit inflammatory CD4_T cell lineage, T helper 17 (Th17) cells, accompanied with expansion in regulatory T cells (Treg cells), a subset of CD4_T cells that are important in inhibiting inflammation. Our results suggest that Th17 and Treg cell imbalance may play a role in the development of POCD. Vitamin D is useful in the control of inflammatory diseases.

Protective effects of lithium treatment for spatial memory deficits induced by tau hyperphosphorylation in splenectomized rats.

1. Postoperative cognitive dysfunction has become more prevalent in recent years. We used a splenectomized rat model with postoperative spatial learning and memory deficits to investigate the role of tau hyperphosphorylation and glycogen synthase kinase-3ß (GSK-3ß) within the hippocampus. 2. Cognitive function was assessed in a Y-maze 1 day before and 1, 3 and 7 days after surgery. We measured site-specific phosphorylation of hippocampal tau (Thr-205 and Ser-396), GSK-3ß activity and expression of interleukin-1ß (IL-1ß), tumour necrosis factor-α (TNF-α) mRNA and protein as markers of inflammation. We also tested the effects of treatment with lithium chloride (LiCl), a GSK-3ß inhibitor. 3. Splenectomy was associated with learning and memory impairment 3 days later, as well as a rapid and massive hyperphosphorylation of hippocampal tau at Thr-205 and Ser-396, activated GSK-3ß, and increased IL-1ß and TNF-α expression. LiCl completely restored tau hyperphosphorylation to control levels. 4. These data from the splenectomized rat model suggest that inflammatory factors affect tau pathology through the GSK-3ß signalling pathway and that LiCl is a promising treatment for postoperative cognitive deficits.

Tau hyperphosphorylation is associated with memory impairment after exposure to 1.5% isoflurane without temperature maintenance in rats.

BACKGROUND AND OBJECTIVE: There is increasing interest in studying the role of tau hyperphosphorylation associated with memory impairment. We examined the involvement of tau hyperphosphorylation in memory impairment after hypothermia following isoflurane anaesthesia in rats. METHODS: Adult rats were randomly divided into three groups: the control group received no treatment and others were subjected to 1.5% isoflurane anaesthesia with or without temperature control for 2 h. On the day before anaesthesia and on postanaesthetic days 1, 3 and 7, cognitive functions were assessed in a Y-maze test paradigm. To find the relationship between memory results and tau, we measured the site-specific phosphorylation of tau at Thr-205 and Ser-396 and the activity of protein phosphatase 2A within the hippocampus. RESULTS: The spatial learning and memory of animals with hypothermia were impaired at day 1 after anaesthesia, compared with nonanaesthetized rats. Anaesthesia and hypothermia led to tau hyperphosphorylation at the Thr-205 and Ser-396 epitopes in the hippocampus. There was no significant difference in the protein phosphatase 2A activity between the control and the postanaesthetic rat hippocampal samples, whereas nearly 45% protein phosphatase 2A inhibition was detected in the anaesthetized without temperature maintenance rat samples. CONCLUSION: Our results indicate that tau phosphorylation is not a direct result of anaesthesia per se, but it is due to anaesthesia-induced hypothermia and this leads to the inhibition of phosphatase activity as well as tau hyperphosphorylation. Tau hyperphosphorylation is associated with the observed deficits in spatial learning and memory following anaesthesia in hypothermic rats.

[Effects of glutamine on changes of nuclear factor-kappa B in acute lipopolysaccharide lung injury: experiment with rats].

OBJECTIVE: To investigate the effects of glutamine on the changes of nuclear factor (NF)-kappaB and lung pathology in acute lung injury. METHODS: Forty SD rats underwent injection of lipopolysaccharide (LPS) 5 mg/kg into the femoral vein, and were randomly divided into 4 equal groups: Group B: undergoing injection of glutamine 0.75 g/kg into the femoral vein 1 h before LPS injection, Group C undergoing injection of glutamine and LPS simultaneously, and Group D undergoing injection of glutamine 1 h after LPS injection, and Group E without glutamine injection. Another 10 rats underwent injection of normal saline to be used as controls (Group A). Four hours after the LPS injection the rats were killed with their lungs taken out RT-PCR was used to detect the level of nuclear factor (NF)-kappaB mRNA expression. ELISA was used to detect the tumor necrosis factor (TNF) - in lung. The activity of superoxide dismutase (SOD) was examined by hydroxylamine method, and the malondialdehyde level was determined by thiobarbituric acid (TBA) method. RESULTS: The lung NF-kappaB mRNA expression levels and TNF- levels of Groups B, C, D, and E were all significantly higher than that of Group A (all P < 0.01). The lung NF-kappaB mRNA expression levels and TNF- levels of Groups C and D were all significantly lower than those of Group B (P < 0.01). However, there were no significant differences in lung NF-kappaB mRNA expression level and TNF- level between Group B and Group E (both P > 0.05). The SOD activity of Group B was significantly lower than that of Group A and the MDA content of Group B was significantly higher than that of Group A (both P < 0.05). The SOD activity levels of Groups C and D were significantly higher than that of Group B and the MDA content of Groups C and D were significantly lower than that of Group B (P < 0.01 or P < 0.05). However there were no significant differences in lung SDD activity and MDA content between Groups B and E (both P > 0.05). Obvious inflammatory changes were seen in the lungs of Groups B and E at the similar extent. Only slight infiltration could be seen in Groups C and D. The lung of Group A was normal. CONCLUSION: Early glutamine administration protects the lung against acute LPS injury. The mechanism may be inhibition of the overexpression of NF-kappaB mRNA.

[Myocardial protection by non-invasive limb preconditioning: the role of nuclear factor kappa-B].

AIM: To investigate a possible role for the transcription factor nuclear factor kappa-B (NF-kappaB) in preconditioning of the heart to ischemia by remote, early protection. METHODS: 48 Wistar rats were randomly divided into three experimental groups. In group I/R, the rats underwent 30 min occlusion of the left anterior descending coronary artery, and 120 min reperfusion. In group PL, the rats underwent four cycles of 5 min occlusion and reperfusion of both hind limbs using a tourniquet before the experiment was continued as in Group I/R. In Group P(L-D), we administered NF-kappaB specific inhibitor, ProDTC 125 mg/kg peritoneally, 15 min before IPG. Infarct size as a percentage of the area at risk was determined by triphenyltetrazolium chloride staining. And another 8 rats in each group were killed and myocardium were stored in liquid nitrogen for the measurement of NF-kappaB mRNA. RESULTS: The myocardial infarct size (IS) was decreased significantly in Group PL compared with group I/R, and the IS/AAR was 34.5% +/- 7.6% and 58.5% +/- 8.5%, respectively ( P < 0.05). The IS/AAR was 54.4% +/- 8.9% in group P(L-D), and there was no significant difference compared with group I/R (P > 0.05). The NF-kappaBmRNA was weaker in P(L) group than that in I/R Group,but is stronger than that in P(L-D) group (P < 0.05). There was almost no expression of NF-kappaB mRNA in P(L-D) group. CONCLUSION: Noninvasive limb IPC is effective in protecting the myocardium from ischemia reperfusion injury. NF-kappaB plays an important role in the mechanism of this acute remote preconditioning.

[Mechanism of the protective effects of noninvasive limbs preconditioning on myocardial ischemia-reperfusion injury].

BACKGROUND: This study aimed at assessing the effect of noninvasive limb preconditioning on myocardial infarct size, and determining whether nitric oxide and neurogenic pathway play an important role in the mechanism of acute remote ischemic preconditioning (IPC). METHODS: Forty Wistar rats were randomly divided into four experimental groups. In Group I, the rats underwent 30-minute occlusion of the left anterior descending coronary artery, and 120-minute reperfusion. In Group PL, the rats underwent four cycles of 5-minute occlusion and reperfusion of both hind limbs using a tourniquet before the experiment was continued as in Group I. In Group PL-N and Group PL-H, we administered L-nitro-arginine methyl ester (L-NAME) 10 mg/kg or hexamethonium chloride 20 mg/kg intravenously, 10 minutes before IPC. Infarct size as a percentage of the area at risk was determined by triphenyltetrazolium chloride staining. RESULTS: There were no statistically significant differences in mean arterial pressure and heart rate among these groups at any time point during the experiment (P>0.05). The myocardial infarct size (IS) was decreased significantly in Group PL and Group PL-H compared with Group I, and the IS/AAR was 34.5%+/-7.6%, 35.9%+/-8.6% and 58.5%+/-8.5%, respectively (P< 0.05). The IS/AAR was 49.1%+/- 6.5% in Group PL-N, and there was no significant difference compared with Group I (P>0.05). CONCLUSIONS: Noninvasive limb IPC is effective in protecting the myocardium from ischemia reperfusion injury. Nitric oxide plays an important role in the mechanism of acute remote IPC, in which the neurogenic pathway is not involved.