考虑坝料振动硬化特性的高面板堆石坝地震反应研究

阿尔塔什面板坝最大坝高164.8 m,覆盖层深度94 m,大坝抗震按9度设防。坝基覆盖层与坝体总高度达258 m,按变形控制而言,为强震区300 m级超高面板堆石坝。根据坝料室内试验资料,考虑坝料振动过程中的硬化特性,对大坝和坝基组成的系统进行了整体三维有限元计算,通过分析坝体以及坝基防渗墙的地震加速度反应、动应力反应,分析了大坝震后永久变形以及面板与防渗墙连接部位的变形。结果表明:堆石体、面板及防渗墙最大加速度反应为9.8 m/s2,放大倍数在2.7～3.6倍之间,堆石体动剪应力不大于400 kPa,地震反应在容许范围内;大坝震后表现为体积震缩特性,最大震陷110 cm,占坝体与坝基可压缩层总高度的0.4%;大坝地震反应分布规律合理,坝体抗震安全性满足规范要求。研究成果可作为大坝抗震设计优化的依据。

前列地尔对冠脉粥样硬化患者血流动力学及其血浆内源性sRAGE、esRAGE和cRAGE水平的影响研究

目的探究前列地尔对冠脉粥样硬化患者血流动力学及其血浆内源性sRAGE、esRAGE和cRAGE水平的影响。方法将2009年7月～2011年7月于笔者医院就诊并选择内科保守治疗的76例冠脉粥样硬化患者平均随机分入前列地尔治疗组和对照组。对照组采用冠脉粥样硬化常规内科保守治疗,前列地尔治疗组患者在常规内科保守治疗基础上每天采用20μg前列地尔静脉滴注治疗2周。比较两组患者的临床疗效,血流动力学指标,血脂指标和血浆内源性sRAGE、esRAGE和cRAGE水平。结果前列地尔治疗组临床疗效显著优于对照组(P<0.05),血小板3min聚集率和血小板最大聚集率显著优于对照组(P<0.05),血浆内源性sRAGE、esRAGE和cRAGE水平显著低于对照组(P<0.05)。前列地尔治疗组患者其余指标与对照组患者无统计学差异(P>0.05)。结论前列地尔能够显著改善冠脉粥样硬化患者的血流动力学指标和血浆内源性sRAGE、esRAGE和cRAGE水平。

A GENERAL PROCEDURE TO CAPTURE THE "DYNAMIC STIFFNESS

A general procedure to capture the 'dynanmic Stiffness' is presented in this paper. The governing equations of motion are formulated for an arbitrary flexible body in large overall motion based on Kane's equations . The linearization is performed peroperly by means of geometrically nonlinear straindisplacement relations and the nonlinear expression of angular velocity so that the 'dynamical stiffness' terms can be captured naturally in a general tcase. The concept and formulations of partial velocity and angular velocity arrays of Huston's method are extended to the flexible body and form the basis of the analysis. The validity and generality of the procedure presented in the paper are verified by numerical results of its application in both the beam and plate models.

Relationship between angiotensin-(1-7) and angiotensin Ⅱ correlates with hemodynamic changes in human liver cirrhosis

AIM： To measure circulating angiotensins at different stages of human cirrhosis and to further evaluate a possible relationship between renin angiotensin system （RAS） components and hemodynamic changes. METHODS： Patients were allocated into 4 groups： mild-to-moderate liver disease （MLD）, advanced liver disease （ALD）, patients undergoing liver transplantation, and healthy controls. Blood was collected to determine plasma renin activity （PRA）, angiotensin （Ang） Ⅰ, Ang Ⅱ, and Ang-（1-7） levels using radioimmunoassays. During liver transplantation, hemodynamic parameters were determined and blood was simultaneously obtained from the portal vein and radial artery in order to measure RAS components. RESULTS： PRA and angiotensins were elevated in ALD when compared to MLD and controls （P 〈 0.05）. In contrast, Ang Ⅱ was significantly reduced in MLD. Ang-（1-7）/Ang Ⅱ ratios were increased in MLD when compared to controls and ALD. During transplantation, Ang Ⅱ levels were lower and Ang-（1-7）/Ang Ⅱ ratios were higher in the splanchnic circulation than in the peripheral circulation （0.52 ± 0.08 vs 0.38 ±0.04, P 〈 0.02）, whereas the peripheral circulating Ang Ⅱ/Ang Ⅰ ratio was elevated in comparison to splanchnic levels （0.18 ±0.02 vs 0.13 ±0.02, P 〈 0.04）. Ang-（1-7）/ Ang Ⅱ ratios positively correlated with cardiac output （r = 0.66） and negatively correlated with systemic vascular resistance （r = -0.70）. CONCLUSION： Our findings suggest that the relationship between Ang-（1-7） and Ang Ⅱ may play a role in the hemodynamic changes of human cirrhosis.

Hemodynamic analysis of esophageal varices in patients with liver cirrhosis using color Doppler ultrasound

AIM： To study the portal hemodynamics and their relationship with the size of esophageal varices seen at endoscopy and to evaluate whether these Doppler ultrasound parameters might predict variceal bleeding in patients with liver cirrhosis and portal hypertension. METHODS： One hundred and twenty cirrhotic patients with esophageal varices but without any previous bleeding were enrolled in the prospective study. During a 2-year observation period, 52 patients who had at least one episode of acute esophageal variceal hemorrhage constituted the bleeding group, and the remaining 68 patients without any previous hemorrhage constituted the non-bleeding group. All patients underwent endoscopy before or after color Doppler-ultrasonic examination, and images were interpreted independently by two endoscopists. The control group consisted of 30 healthy subjects, matched to the patient group in age and gender. Measurements of diameter, flow direction and flow velocity in the left gastric vein （LGV） and the portal vein （PV） were done in all patients and controls using color Doppler unit. After baseline measurements, 30 min after oral administration of 75 g glucose in 225 mL, changes of the diameter, flow velocity and direction in the PV and LGV were examined in 60 patients with esophageal varices and 15 healthy controls. RESULTS： The PV and LGV were detected successfully in 115 （96%） and 105 （88%） of 120 cirrhotic patients, respectively, and in 27 （90%） and 21 （70%） of 30 healthy controls, respectively. Among the 120 cirrhotic patients, 37 had F1, 59 had F2, and 24 had F3 grade varices. Compared with the healthy controls, cirrhotic group had a significantly lower velocity in the PV, a significantly greater diameter of the PV and LGV, and a higher velocity in the LGV. In the cirrhotic group, no difference in portal flow velocity and diameter were observed between patients with or without esophageal variceal bleeding （EVB）. However, the diameter and blood flow velocity of the LGV were significantly higher for EVB （＋） group compared with EVB （-） group （P〈0.01）. Diameter of the LGV increased with enlarged size of varices. There were differences between F1 and F2, F1 and F3 varices, but no differences between F2 and F3 varices （P = 0.125）. However, variceal bleeding was more frequent in patients with a diameter of LGV 〉6 mm. The flow velocity in the LGV of healthy controls was 8.70＋1.91 cm/s （n = 21）. In patients with liver cirrhosis, it was 10.3＋2.1 cm/s （n = 12） when the flow was hepatopetal and 13.5＋2.3 cm/s （n = 87） when it was hepatofugal. As the size of varices enlarged, hepatofugal flow velocity increased （P〈0.01） and was significantly different between patients with F1 and F2 varices and between patients with F2 and F3 varices. Variceal bleeding was more frequent in patients with a hepatofugal flow velocity 〉15 cm/s （32 of 52 patients, 61.5%）. Within the bleeding group, the mean LGV blood flow velocity was 16.6＋2.62 cm/s. No correlation was observed between the portal blood flow velocity and EVB. In all healthy controls, the flow direction in the LGV was hepatopetal, toward the PV. In patients with F1 varices, flow direction was hepatopetal in 10 patients, to-and-fro state in 3 patients, and hepatofugal in the remaining 18. The flow was hepatofugal in 91% patients with F2 and all F3 varices. Changes in diameter of the PV and LGV were not significant before and after ingestion of glucose （PV： 1.41＋1.5 cm before and 1.46＋1.6 cm after; LGV： 0.57＋1.7 cm before and 0.60＋1.5 cm after）. Flow direction in the LGV was hepatopetal and to-and-fro in 16 patients and hepatofugal in 44 patients before ingestion of glucose. Flow direction changed to hepatofugal in 9 of 16 patients with hepatopetal and to-and-fro blood flow after ingestion of glucose. In 44 patients with hepatofugal blood flow in the LGV, a significant increase in hepatofugal flow velocity was observed in 38 of 44 patients （86%） with esophageal varices. There was a relationship between the percentage changes in flow velocity and the size of varices. Patients who responded excessively to food ingestion might have a high risk for bleeding. The changes of blood flow velocity in the LGV were greater than those in the PV （LGV： 28.3＋26.1%, PV： 7.2＋13.2%, P〈0.01）, whereas no significant changes in the LGV occurred before and after ingestion of glucose in the control subjects. CONCLUSION： Hemodynamics of the PV is unrelated to the degree of endoscopic abnormalities in patients with liver cirrhosis. The most important combinations are endoscopic findings followed by the LGV hemodynamics. Duplex-Doppler ultrasonography has no value in the identification of patients with cirrhosis at risk of variceal bleeding. Hemodynamics of the LGV appears to be superior to those of the PV in predicting bleeding.

Hemodynamic and morphologic changes of peripheral hepatic vasculature in cirrhotic liver disease: A preliminary study using contrast-enhanced coded phase inversion harmonic ultrasonography

AIM: To provide the useful information for the diagnosis of liver cirrhosis by observing the morphology of peripheral hepatic vessels and the hemodynamics of microbubble arrival time in these vessels.METHODS: Twenty-one subjects including 5 normal volunteers and 16 patients (liver cirrhosis, n=10;chronic hepatitis, n=6) were studied by contrast-enhanced coded phase inversion harmonic sonography (GE LOGIQ9 series) using a 6-8 MHz convex-arrayed wide-band transducer. The images of peripheral hepatic artery,portal and hepatic vein were observed in real-time for about 2 min after intravenous injection of Levovist. The time when microbubbles appeared in the peripheral vessels (microbubble arrival time) was also recorded. The morphologic changes of peripheral hepatic vasculature were classified as marked, slight, and no changes based on the regularity in caliber, course, ramification, and the delineation of vessels compared to normal subjects.RESULTS: The microbubble arrival time at peripheral artery, portal, and hepatic vein was shorter in cirrhotic patients than in chronic hepatitis patients and normal subjects. The marked, slight and no morphologic changes of peripheral hepatic vasculature found in 5 (5/6,83.3%), 1 (1/6, 16.7% ), and 0 (0/6, 0%) liver cirrhosis patients, respectively, and in 1 (1/10, 10%), 6 (6/10,60%), and 3 (3/10, 30%) chronic hepatitis patients,respectively. There was a significant difference between the two groups (P＜0.001).CONCLUSION: Evaluation of the hemodynamics and morphology of peripheral hepatic vasculature by contrast-enhanced coded pulse inversion harmonic sonography can provide useful information for the diagnosis of liver cirrhosis.

Role of echo Doppler ultrasonography in the evaluation of postprandial hyperemia in cirrhotic patients

AIM: To assess the role of echo-Doppler ultrasonography in postprandial hyperemia in cirrhotic patients by comparing the results with the hepatic vein catheterization technique.METHODS: Patients with cirrhosis, admitted to the portal hemodynamic laboratory were included into the study. After an overnight fast, echo-Doppler ultrasonography (basal and 30 min after a standard meal) and hemodynamic studies by hepatic vein catheterization (basal, 15 min and 30 min after a standard meal) were performed. Ensure Plus (Abbot Laboratories, North Chicago, IL) was used as the standard liquid meal. Correlation analysis of the echo-Doppler and hepatic vein catheterization measurements were done for the basal and postprandial periods.RESULTS: Eleven patients with cirrhosis (5 Child A, 4 Child B, 2 Child C) were enrolled into the study. After the standard meal, 8 of the 11 patients showed postprandial hyperemia with increase in portal blood flow, portal blood velocity and hepatic venous pressure gradient. Hepatic venous pressure gradient in the postprandial period correlated positively with postprandial portal blood velocity (r = 0.8, P < 0.05) and correlated inversely with postprandial superior mesenteric artery pulsatility index (r = -1, P < 0.01).CONCLUSION: Postprandial hyperemia can be efficiently measured by echo-Doppler ultrasonography and the results are comparable to those obtained with the hemodynamic studies.

Systemic inflammatory response following acute myocardial infarction

Acute cardiomyocyte necrosis in the infarcted heart generates damage-associated molecular patterns, activating complement and toll-like receptor/interleukin-1 signaling, and triggering an intense inflammatory response. Iuflammasomes also recognize danger signals and mediate sterile inflammatory response following acute myocardial infarction （AMI）, Inflammatory response serves to repair the heart, but excessive inflammation leads to adverse left ventricular remodeling and heart failure. In addition to local inflammation, profound systemic inflammation response has been documented in patients with AMI, which includes elevation of circulating inflammatory cytokines, chemokines and cell adhesion molecules, and activation of peripheral leukocytes and platelets. The excessive inflammatory response could be caused by a deregulated immune system. AMI is also associated with bone marrow activation and spleen monocytopoiesis, which sustains a continuous supply of monocytes at the site of inflammation. Accumulating evidence has shown that systemic inflammation aggravates atherosclerosis and markers for systemic inflammation are predictors of adverse clinical outcomes （such as death, recurrent myocardial in- farction, and heart failure） in patients with AMI.

Diagnostic value of fine motor deficits in patients with low-grade hepatic encephalopathy

AIM: The role of motor dysfunction in early diagnosis of low-grade hepatic encephalopathy remains uncertain. We performed a pilot study to comparatively investigate the kinematic characteristics of small and large rapid alternating movements in patients with liver cirrhosis and low-grade hepatic encephalopathy.METHODS: A kinematic analysis of alternating handwriting (7.5 mm) and large drawing movements (DM, 175 mm) was performed in 30 patients with liver cirrhosis (no hepatic encephalopathy: n = 10; minimal hepatic encephalopathy: n = 9; grade I hepatic encephalopathy: n = 11; healthy controls: n = 12). The correlation between kinematic parameters, clinical neuro-psychiatric symptoms of cerebral dysfunction and the grade of encephalopathy was investigated.RESULTS: Both movement types, handwriting and drawing, were significantly slower in cirrhotic patients. In contrast to large DM, the deterioration of handwriting movements significantly correlated with the increase of symptoms of motor dysfunction and differentiated significantly within the group of cirrhosis patients corresponding to the degree of hepatic encephalopathy. CONCLUSION: The deterioration of fine motor control is an important symptom of low-grade hepatic encephalopathy. The kinematic analysis of handwriting allows the quantitative analysis of alterations of motor function and is a possible tool for diagnostics and monitoring of motor dysfunction in patients with low-grade hepatic encephalopathy.

Factors Influencing the Disturbed Flow Patterns Downstream of Curved Atherosclerotic Arteries

Pulsatile blood flows in curved atherosclerotic arteries are studied by computer simulations. Computations are carried out with various values of physiological parameters to examine the effects of flow parameters on the disturbed flow patterns downstream of a curved artery with a stenosis at the inner wall. The numerical results indicate a strong dependence of flow pattern on the blood viscosity and inlet flow rate, while the influence of the inlet flow profile to the flow pattern in downstream is negligible.

The regulation effect of AMPK in immune related diseases

AMP-activated protein kinase (AMPK) is a sensor of cellular energy status that plays a key role in energetic metabolism regulation.Metabolic changes in immune cells, such as dendritic cell (DC), macrophages, neutrophils and lymphocytes that participate in the signal directed programs that promote or inhibit immune mediated diseases, including cancer, atherosclerosis and inflammatory diseases. Multiple pathogenic mechanisms are involved in the initiation and progression of disease, and many pathways have been uncovered. The mechanistic overlap in the metabolic changes and inflammation could indicate that some of the targets they have are in common, whereas AMPK could be useful in treatment of both disorders. The insight into identification of AMPK responsible for specific immune regulation, anti-inflammatory actions and understanding of the underlying molecular mechanism will promote the generation of novel AMPK activators, and provide novel therapy strategy.

Enhanced External Counterpulsation Inducing Arterial Hemodynamic Variations and Its Chronic Effect on Endothelial Function

To make clear the precise hemodynamic mechanism underlying the anti-atherogenesis benefit of enhanced external couterpulsation(EECP) treatment, and to investigate the proper role of some important hemodynamic factors during the atherosclerotic progress, a comprehensive study combining long-term animal experiment and numerical solving was conducted in this paper. An experimentally induced hypercholesterolemic porcine model was developed and the chronic EECP intervention was subjected. Basic hemodynamic measurement was performed in vivo, as well as the arterial endothelial samples were extracted for physiological examination. Meanwhile, a numerical model was introduced to solve the complex hemodynamic factors such as WSS and OSI. The results show that EECP treatment resulted in significant increase of the instant levels of arterial WSS, blood pressure, and OSI. During EECP treatment, the instant OSI level of the common carotid arteries over cardiac cycles raised to a mean value of 8.58 ×10-2±2.13 ×10-2. Meanwhile, the chronic intervention of EECP treatment significantly reduced the atherosclerotic lesions in abdominal aortas and the endothelial cellular adherence. The present study suggests that the unique blood flow pattern induced by EECP treatment and the augmentation of WSS level in cardiac cycles may be the most important hemodynamic mechanism that contribute to its anti-atherogenesis effect. And as one of the indices that cause great concern in current hemodynamic study, OSI may not play a key role during the initiation of atherosclerosis.

Enhanced External Counterpulsation Treatment Inhibitting Advanced Atherosclerotic Plaque Progression by Augmenting the Plaque Wall Stress： An in vivo FSI Study Based on Animal Experiment

Enhance extemal counterpulsation （ECP） procedure has exhbited itself to be an effective therapy for the m anagem entof ischem ic card iovascu lar diseases, However, considering that EECP significantly increases the acute diastolic pressure, whether it will intervene in the chronic progression of advanced plaque causing great concern in clilical applkation, but yet rein ains elusive presently. In the current paper, a flu id-structure interface （FSI） num erical model of artery with p iaque corn ponent w as developed based on in vivo hem odynam ic m easurem entperfotm ed h a porcine model, to caku late the m echanical stresses of the plaque before and during EECP, and h lum to assess the potential effects of long-term EECP treatm ent on plaque progression. The resu Its show that E E C P augm ented the wall shear stress （WSS） and plaque w all stress （PWS） over the card lac cycles, aswell as the spacial oscillatory of W SS （WSSG ）. Durhg EECP treatm ent, the PW S level respectively raised 6.82% and 6.07% in two simulation cases. The currentpilot study suggests that E E C P treatm entre ay p lay a positive effect on inh biting the conthued plaque progression by hcreashg the PW S level over the card iac cycles. Meanwhile, the plaque morphology should be taken into consideration while m aking patient- specific plan for Ion g- term E E C P treatment in clinic.