Adaptive time-step unscented kalman filtering (ATS-UKF) based observer design for urea selective catalytic reduction (SCR) performance of diesel engines.

To reduce the number of sensors in the SCR catalyst, state feedback and fault diagnosis information are provided. Firstly, a model based on the coupling of flow, heat transfer, and gas-solid phase catalytic reaction in the SCR system is investigated in this paper. The parabolic partial differential equations are simplified by the variable substitution method and the method of lines approach (MOL). The simplified system of equations is solved by backward differentiation formulas (BDF) with adaptive adjustment time step strategy. Meanwhile, the chemical reaction parameters are accurately calibrated per second using the Levenberg-Marquardt method. Secondly, the ATS-UKF is designed in this paper, and to ensure the synchronisation between the ATS-UKF and the SCR model calculations, the time step of solving the BDF by the SCR model is taken as the time step of propagating the sigma points. Two observation scenarios are assumed: (1) no downstream NH3 concentration sensor, ammonia coverage and downstream NH3 concentration are observed by ATS-UKF; (2) no downstream NOx sensor, ammonia coverage and downstream NOx concentration are observed by ATS-UKF. Finally, the paper carries out bench tests. In the first case, the ammonia coverage obtained by the ATS-UKF reached 0.99 with respect to the model-calculated value R². The mean absolute error (MAE) between the observed and experimental values of the ATS-UKF for the downstream NH3 concentration was 2.76 ppm. In the second case, the ammonia coverage obtained by the ATS-UKF reached 0.99 with respect to the model-calculated value R², and the MAE between the observed and experimental values of the ATS-UKF for the downstream NOx concentration was 1.53 ppm. ENVIRONMENTAL IMPLICATION: The Adaptive Time-Step Unscented Kalman Filtering (ATS-UKF) enhances urea Selective Catalytic Reduction (SCR) in diesel engines, improving environmental outcomes. This method minimizes sensor dependence, enabling more precise SCR system management and effective emission reduction. By advancing emission control technologies, ATS-UKF contributes to global air pollution mitigation efforts, supporting cleaner air and environmental sustainability. Its innovative approach in monitoring and predicting SCR performance marks a significant step towards eco-friendly diesel engine operation.

The Effect of Hippocampal Cognitive Impairment and XIAP on Glucose and Lipids Metabolism in Rats.

BACKGROUND/AIMS: To investigate the effect of cognitive impairment and X-linked inhibitor of apoptosis protein (XIAP) on glucolipid metabolism. MATERIALS AND METHODS: ß-amyloid (Aß 1-42) was injected into the hippocampus of rats to establish a cognitive impairment model. Trans-activator of transcription (TAT)-XIAP fusion protein (the TAT-XIAP group), PBS (the model group), or XIAP antisense oligonucleotides (the ASODN group) was injected into the lateral ventricles of the rats to increase and decrease the activity of XIAP in the hippocampus. To determine the level of blood glucose and lipids, adenosine monophosphate-activated protein kinase (AMPK) expression of liver and hipppocamual neuronal apoptosis. RESULTS: The levels of FPG, TG, TC and LDL were significantly higher in the TAT-XIAP group, the model group and the ASODN group than in the blank group (P < 0.05); however, the HDL level showed no significant change in all groups of rats. The apoptosis indexes of the rat hippocampal CA1 neuron were 68.44 ± 4.31%, 13.21 ± 2.30%, 56.68 ± 4.771%, and 87.51 ± 6.63% in the model group, the blank group, the TAT-XIAP group and the ASODN group, respectively. Gastrointestinal motility was less frequent (per time unit) in the model group, the ASODN group and the TAT-XIAP group than in the blank group. Compared with the model group, gastrointestinal motility was significantly less frequent in the ASODN group and was significantly more frequent in the TAT-XIAP group. Compared with the blank group, the model group had a significantly lower gastric emptying rate and intestinal propulsive rate. Compared with the model group, the gastric emptying rate and intestinal propulsive rate were significantly lower in the ASODN group and were significantly higher in the TAT-XIAP group. Compared with the blank group, the expressions of AMPK mRNA, and AMPK protein were significantly reduced in the model group, the TAT-XIAP group, and the ASODN group. AMPK expression was significantly increased in the TAT-XIAP group and was significantly decreased in the ASODN group than in the model group. CONCLUSION: Cognitive impairment and hippocampal neuron apoptosis can cause glucose and lipids metabolic abnormalities, possibly by regulating gastrointestinal motility and AMPK expression in the liver. The changes in the function of XIAP, which is an anti-apoptotic protein in the hippocampus, may affect the metabolism of glucose and lipids.

[Influence of the VEGF antibody targeted vascular therapy on the expression of collagen type I in hyperplastic].

OBJECTIVE: To investigate the influence of the vascular endothelial growth factor( VEGF) antibody targeted vascular therapy on the expression of human collagen type I in hyperplastic scar of nude mice. METHODS: The hyperplastic scar from one female burn patient with 1% TBSA deep-partial thickness burns were implanted into subcutaneous skin of scapular region of 48 nude mice. Three weeks later, the nude mice were divide into large dose (LA) , medium dose (MD) , small dose (SD) and control groups, with 12 mice in each group. The mice in LA,MD and SD groups were injected with 200 microl of 15,10, 5 microg/ml VEGF monoclonal antibody diluted in 0.01 mol/L PBS, respectively in the scar twice a week for 3 weeks, while those in C group were injected with equal amount of 0. 01 mol/L PBS. The area and volume of the scar in each group were calculated and histological changes were observed, and the expression of collagen type I mRNA and its protein in each group were determined 3 days after treatment. RESULTS: The volume of scar in LA, MD, SD and C groups were (55.3 +/-4.1, 67.9 +/-5.7, 78.9 +/-5.5, 85.0 +7.3) mm(3), respectively. Compared with that in C group, the volume of the scar were significantly decreased in AD and MD groups ( P <0.05). A few number of vessels and fibroblasts were observed in LD, MD groups, with decreased number of collagen fibers arranged in order. Compared with that in C group ,The expression of procollagen type I mRNA and its protein in C group was obviously higher than those in LD and MD groups ( P < 0. 05) , but it was similar to those in SD group. CONCLUSION: VEGF targeted vascular therapy is beneficial for the inhibition of the angiopoietins of hyperplastic scar, the expression of collagen , and the growth of scar.

[Synergetic cytotoxicity of cisplatin and etoposide to leukemia cell line K562 and its mechanism].

BACKGROUND & OBJECTIVE: Etoposide (VP-16) is one of the most common chemotherapy drugs, but its usage is limited by drug resistance. Some researches on solid tumors show that cisplatin (DDP) have synergetic effect with VP-16. This study was to evaluate synergetic cytotoxicity of VP-16 and DDP to leukemia cell line K562, and explore the mechanism. METHODS: K562 cells were treated with VP-16 (0 or 5 microg/ml) and DDP (0, 0.3, 3, 15, or 30 microg/ml) in different combination patterns. Inhibitory effect of VP-16 and DDP on survival of K562 cells was measured by MTT assay. Cell apoptosis was evaluated by AO/EB double fluorescent labeling. The expression of topoisomerase (TOPO) II alpha and II beta, and transcription factor Sp1 and Sp3 were measured by semi-quantitive reverse transcription-polymerase chain reaction (RT-PCR) and Western blot. RESULTS: MTT assay showed significant synergetic cytotoxicity of VP-16 and DDP. VP-16 in combination with DDP obviously enhanced cell apoptosis. RT-PCR showed that DDP significantly up-regulated the expression of TOPO II and Sp1 in concentration-dependent manners (TOPO II alpha, II beta, and Sp1 were up-regulated by 36%, 25%, and 75% of control, respectively, when treated with 30 microg/ml of DDP), and down-regulated Sp3 by 49% of control; VP-16 (5 microg/ml) down-regulated TOPO II alpha by 71.9%, and up-regulated Sp3 by 14%; VP-16 (5 microg/ml) in combination with DDP (30 microg/ml) up-regulated TOPO II alpha by 83%, II beta by 11%, and Sp1 by 58% when compared with using VP-16 alone (but the levels were lower than using DDP alone), and down-regulated Sp3 by 61.3% when compared with using DDP alone. Western blot showed similar results to RT-PCR. CONCLUSION: Through up-regulating TOPO II, DDP could enhance the chemotherapeutic effect of VP-16 on K562 cells by provide more target enzyme to act on.