MECHANISM FOR DEAD CENTRE CHANGE AND PRESET STROKE INDICATION WHILE ADJUSTING STROKE OF ECCENTRIC PRESS RAM

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• 3. MECHANISM FOR DEAD CENTRE CHANGE AND PRESET STROKE INDICATION WHILE ADJUSTING STROKE OF ECCENTRIC PRESS RAM [P] . PL223586A1 . 1981-03-13

  机译： 调整偏心冲床行程时死点改变和预设行程指示的机制

• 4. Method for readjusting the camshaft gear when changing the stroke length on a mechanically driven eccentric press with ram stroke adjustment and a design for carrying out the working method [P] . 德国专利： DE3345464A1 . 1985-06-20

  机译： 在带有柱塞行程调节的机械驱动偏心压力机上改变行程长度时重新调节凸轮轴齿轮的方法和工作方法的设计

• 5. Stroke adjusting mechanism for stamping press - includes eccentric bush in joint in toggle mechanism, rotated to adjust stroke [P] . 德国专利： DE3703413A1 . 1988-08-18

  机译： 冲压机的行程调节机构-肘杆机构的关节处包括偏心衬套，可旋转以调节行程

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• 1. A Comparison between Volume Responsiveness Predicted by Changes in Pulse Pressure and by Changes in Stroke Volume Induced by Passive Leg Raising [J] . Lei Huang ,Wei-xing Zhang ,Wen-xun Cai . 麻醉与监护论坛 . 2011,第002期
• 2. 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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