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METHOD AND SYSTEM FOR FEEDBACK CONTROLLING/CONTROLLING A TOTAL AIR FUEL RATIO OF A REFORMER

机译：反馈控制/控制变形器总空气比的方法和系统

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摘要

The invention relates to a method for closed/open loop control of a total lambda value of a reformer (10) comprising at least a combustion zone (12) and an evaporation zone (14) connected to the combustion zone (12). In accordance with the invention for closed/open loop control of the total lambda value, closed loop control of the lambda value of the combustion zone (12) and open loop control of the fuel performance supplied to the evaporation zone (14) is provided.;The invention relates furthermore to a system with a reformer (10) comprising at least a combustion zone (12) and an evaporation zone (14) connected to the combustion zone (12) and with a a controller (26) for closed/open loop control of a total lambda value. In accordance with the invention the controller (26) is suitable for closed/open loop control of the total lambda value by closed loop control of the lambda value of the combustion zone (12) and open loop control of the fuel performance supplied to the combustion zone (12) and the evaporation zone (14) each.

机译：用于控制/控制至少包括燃烧区（ 12 ）和蒸发区的重整器（ 10 ）的总λ值的方法（ 14 ）连接到燃烧区（ 12 ）。根据本发明，用于总λ值的闭环/开环控制，燃烧区（ 12 ）的λ值的闭环控制和提供给蒸发的燃料性能的开环控制。本发明还涉及一种具有重整器（ 10 ）的系统，该重整器至少包括燃烧区（ 12 ）。）和连接到燃烧区（ 12 ）并带有用于闭环/开环控制的控制器（ 26 ）的蒸发区（ 14 ）总lambda值。根据本发明，控制器（ 26 ）适用于通过燃烧区（ 12 ）的λ值的闭环控制来对总λ值进行闭环/开环控制。 >）并分别控制供给燃烧区（ 12 ）和蒸发区（ 14 ）的燃油性能。 展开▼

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公开/公告号US2009263685A1

专利类型

公开/公告日2009-10-22

原文格式PDF

申请/专利权人 JEREMY LAWRENCE;STEFAN KADING;SU ZHOU;NORBERT GUNTHER;
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申请/专利号US20070440229

发明设计人 JEREMY LAWRENCE;STEFAN KADING;SU ZHOU;NORBERT GUNTHER;
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申请日2007-08-03

分类号H01M8/06;

国家 US

入库时间 2022-08-21 19:35:52

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3. METHOD AND SYSTEM FOR FEEDBACK CONTROLLING/CONTROLLING A TOTAL AIR FUEL RATIO OF A REFORMER [P] . IN2009CN01384A . 2016-08-31

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5. Method and system for adjusting / controlling the total air ratio of a reformer [P] . 日本专利： JP2010503598A . 2010-02-04

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4. BACKGROUND： Vibrio vulnifi cus inside the body could activate the NF-!B signaling pathwayand initiate the inflammatory cascade. The lung is one of the earliest organs affected by sepsisassociated with acute lung injury. High mobility group protein B1 （HMGB1） is an important late-actingpro-infl ammatory cytokine involving in the pathophysiology of sepsis. It is also involved in the injuryprocess in the lung, liver and intestine. There has been no report on the involvement of HMGB1 inVibrio vulnifi cus sepsis-induced lung injury.METHODS： Sixty rats were randomly divided into a normal control group （group A, n=10） anda Vibrio vulnificus sepsis group （group B, n=50）. Sepsis was induced in the rats by subcutaneousinjection of Vibrio vulnificus （concentration 6×108 cfu/mL, volume 0.1 mL/100g）） into the left lowerlimbs. The rats in group B were sacrifi ced separately 1, 6, 12, 24, and 48 hours after the infection.Their lungs were stored as specimens, lung water content was measured, and lung pathology wasobserved under a light microscope. The expressions of the HMGB1 gene and protein in the lungswere detected by RT-PCR and Western blot. Data were analyzed with one-way analysis of variance（ANOVA） and the LSD method for pair-wise comparison between the two groups. P〈0.05 wasconsidered statistically signifi cant.RESULTS： Compared to group A （0.652±0.177）, HMGB1 mRNA expression in the lungs ofgroup B was signifi cantly higher at 0 hour （1.161±0.358, P=0.013）, 24 hours （1.679±0.235, P=0.000）,and 48 hours （1.258±0.274, P=0.004）（P〈0.05）, and peaked at 24 hours. Compared to group A（0.594±0.190）, HMGB1 protein expression at 6 hours （1.408±0.567, P=0.026） after infection wassignificantly increased （P〈0. 05）, and peaked at 24 hours （2.415±1.064, P=0.000） after infection.Compared to group A （0.699±0.054）, lung water content was significantly increased at 6 hours（0.759±0.030, P=0.001）,12 hours （0.767±0.023, P=0.000）, 24 hours （0.771±0.043, P=0.000） and 48hours （0.789±0.137, P=0.000） after infection （P〈0.05）. Compared to group A, pathological changesat 12 hours in group B indicate marked pulmonary vascular congestion, interstitial edema andinfl ammatory infi ltration. Alveolar cavity collapse and boundaries of the alveolar septum could not beclearly identifi ed.CONCLUSION： Vibrio vulnifi cus sepsis can lead to injury in rat lungs, and increased HMGB1expression in lung tissue may be one of the mechanisms for injury from Vibrio vulnifi cus sepsis. [J] . Qiao-meng Qiu ,Zhong-wang Li ,Lu-ming Tang . 世界急诊医学杂志(英文) . 2011,第4期

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