摩擦提升滑绳制动机理的研究

摩擦提升滑绳制动机理的研究中国矿业大学朱真才，葛世荣开滦矿务局付贵祥，郑瑞林摩擦提升防滑问题的研究、目前国内外大体上可分为３个方面：①防滑计算方法的研究；②钢丝绳与摩擦轮衬垫岸联系数的研究；③绞车制动器的研究。国内外对摩擦提升的防滑问题都非常重视．日...

齿轮马达的制动机理研究及性能最大化措施

为明晰齿轮马达密闭介质的制动机理及其制动性能的最大化措施,从齿轮副的啮合过程出发,由马达内介质作用的液压转矩等于马达外的负载转矩,推导出负载驱动转速的定量公式,并就制动性能最大化对齿形参数执行最优化设计。结果表明:啮合点的位置不同,负载驱动转速也不同,其中,最小困油位置处的最高,节点啮合处的最低;齿形参数对负载驱动转速的影响很大,案例优化前后的制动性能提高了31.2%~46.1%;负载转矩与马达内客观存在的泄漏途径为驱动转速产生的外因与内因,齿轮较小的宽径比和齿顶高系数能有效控制马达内泄漏等。研究成果为高质量齿轮马达的进一步研究与开发,提供一定的理论依据。

电动汽车新型再生机械耦合线控制动系统机理研究

本文中对一种新型电动汽车再生-机械耦合线控制动系统进行研究。首先,构建新型再生-机械耦合线控制动系统动力学模型,基于动力学模型进行系统制动性能分析,获得再生-机械耦合线控制动系统摩擦制动转矩和电磁制动转矩的匹配关系。接着,根据该再生制动系统特性和制动工况,提出电磁制动和耦合制动两种工作模式,低制动强度下采用电磁制动模式,高制动强度下采用耦合制动模式;在耦合制动模式下,提出通过电机电磁转矩和摩擦制动转矩集成控制,实现电磁控制、摩擦控制和耦合控制3种制动转矩控制方式。最后,分别进行了38和15km/h两种车速下电磁制动和耦合制动台架试验,对新型再生-机械耦合线控制动系统耦合制动机理进行了验证。

重型载重汽车制动热衰退的机理与鉴定方法探讨

随着现代化技术以及信息化手段的飞速发展,社会已经全面进入到了科技时代当中,这也为重型载重汽车的发展奠定了坚实基础,而重型载重汽车在高速制动或是连续制动的状态中,其内部制动器的温度会逐步提升,并且在制动器内部的具体摩擦系数也会逐步减小,大幅度降低相应的摩擦力矩,不仅会引发制动效能热衰退的问题出现,甚至还会使得制动系统直接失效,引发出各类安全事故出现。因此,文章首先对热衰退的主要机理加以明确;其次,对降低制动器热衰退的具体措施展开深入分析;在此基础上,提出热衰退导致重型载重汽车制动失效的鉴定措施。

液力制动器在下运带式输送机上的应用研究

参照下运带式输送机的制动特点 ,对液力制动器的制动机理和各种工况下的测试数据进行了分析 ,阐明了液力制动器实现安全可靠制动的可行性 ,同时介绍了液力制动系统的工作原理。

Correlation between TIMP-1 expression and liver fibrosis in two rat liver fibrosis models

AIM： To evaluate serum TIMP-1 level and the correlation between TIMP-1 expression and liver fibrosis in immuneinduced and CCL4-induced liver fibrosis models in rats. METHODS： Immune-induced and CCL4-induced liver fibrosis models were established by dexamethasone （0.01 mg） and CCL4 respectively. Serum TIMP-1 level was detected with ELISA, while histopathological grade of liver biopsy was evaluated. Spearman rankcorrelation test was used to analyse the difference of the correlation between the TIMP-1 expression and hepatic fibrosis in the two fibrosis models. Furthermore,in situ hybridization was used to determine the expression difference of TIMP-1 mRNA in the two models. RESULTS： Positive correlation existed between serum TIMP-1 level of immune induced group and the histopathological stages of fibrosis liver of corresponding rats （Spearman rank-correlation test, rs = 0.812, P 0.05）, and the positive in situ hybridization signal of TIMP-1 mRNA was strong. In CCL4-induced liver fibrosis model, the correlation between the serum TIMP-1 level and the severity of hepatic fibrosis was not statistically significant（Spearman rank-correlation test, rs = 0.229, P 〉 0.05）. And compared with immune-induced model, the positivein situ hybridization signal of TIMP-1 mRNA was weaker, while the expression variation was higher in hepatic fibrosis of the same severity. CONCLUSION： The correlations between TIMP-1 expression and liver fibrosis in two rat liver fibrosis models are different. In immune-induced model, serum TIMP-1 level could reflect the severity of liver fibrosis, while in CCL4-induced model, the correlation between the serum TIMP-1 level and the severity of hepatic fibrosis was not statistically significant.

GFAP promoter directs lacZ expression specifically in a rat hepatic stellate cell line

AIM： The GFAP was traditionally considered to be a biomarker for neural gila （mainly astrocytes and nonmyelinating Schwann cells）. Genetically, a 2.2-kb human GFAP promoter has been successfully used to target astrocytes in vitro and in vivo. More recently, GFAP was also established as one of the several makers for identifying hepatic stellate cells （HSC）. In this project, possible application of the same 2.2-kb human GFAP promoter for targeting HSC was investigated. METHODS： The GFAP-lacZ transgene was transfected into various cell lines （HSC, hepatocyte, and other nonHSC cell types）. The transgene expression specificity was determined by X-gal staining of the β-galactosidase activity. And the responsiveness of the transgene was tested with a typical pro-fibrotic cytokine TGF-β1. The expression of endogenous GFAP gene was assessed by real-time RT-PCR, providing a reference for the transgene expression. RESULTS： The results demonstrated for the first time that the 2.2 kb hGFAP promoter was not only capable of directing HSC-specific expression, but also responding to a known pro-fibrogenic cytokine TGF-β1 by upregulation in a doseand time-dependent manner, similar to the endogenous GFAP. CONCLUSION： In conclusion, these findings suggested novel utilities for using the GFAP promoter to specifically manipulate HSC for therapeutic purpose.

Prediction of Planing Craft Motion Based on Grey System Theory

In order to minimize the harm caused by the instability of a planing craft, a motion prediction model is essential. This paper analyzed the feasibility of using an MGM（1,N） model in grey system theory to predict planing craft motion and carried out the numerical simulation experiment. According to the characteristics of planing craft motion, a recurrence formula was proposed of the parameter matrix of an MGMfl,N） model. Using this formula, data can be updated in real-time without increasing computational complexity significantly. The results of numerical simulation show that using an MGM（1,N） model to predict planing motion is feasible and useful for prediction. So the method proposed in this study can reflect the planing craft motion mechanism successfully, and has rational and effective functions of forecasting and analyzing trends.

Anomalous origin of left pulmonary artery branch from the aorta with Fallot's tetralogy:one case report

We report the case of a ten-year-old boy who had often presented with respiratory distress since born. Chest X-ray showed an enlarged right ventricle. Echocardiography demonstrated characteristic features of Fallot＇s tetralogy and the left pulmonary artery could not be visualized. However, cardiac catheterization disclosed that the left pulmonary artery had an anomalous origin in the ascending aorta. The patient underwent total surgical correction of the defects. Nine days later, he was discharged. We present the results of a literature review of the incidence, physiopathological, clinical, diagnostic, and surgical characteristics of this rare disease.

Generation and characterization of a transgenic mouse model for pancreatic cancer

AIM： To generate a SV40Tag transgenic tumor animal model and to study the mechanism underlying tumorigenesis. METHODS： A mammary gland expression vector containing SV40Tag DNA was generated. Transgene fragments were microinjeted into fertilized eggs of FVB mice. The genetically manipulated embryos were transferred into the oviducts of pseudo-pregnant female mice. PCR and Northern blot analysis were used for genotype analysis of F1 and F2 mice. Transgene expression was detected by RT-PCR and immunohistochemistry. RESULTS： SV40Tag gene was detected in two lines of transgenic mice. One of them delivered the transgene to F1 and a tumor was found in the pancreas of these mice. RT-PCR and immunohistochemistry showed that SV40Tag gene was expressed in the tumor. Pathological characterization of the transgenic mice demonstrated that the tumor belonged to pancreatic cystic neoplasm. CONCLUSION： SV40Tag transgenic mouse model can be successfully established. The transgenic mice develop a pancreatic tumor, which can be used for investigation of the molecular mechanism of tumorigenesis in vivo.

Effects of nuclei ambiguus and dorsal motor nuclei of vagus on gastric H^+ and HCO_3^- secretion in rats

AIM: To determine the effects of electrical stimulation of nucleus ambiguus (NA) and dorsal motor nuclei of vagus (DMV) on gastric acid and bicarbonate secretion in rats. METHODS: NA and DMV in rats were electrically stimulated. Pylorus ligation or esophagus perfusion was used to collect the gastric secretion. The titratable H+ quantum, H+ concentration, HCO3- secretion quantum were measured. RESULTS: Electrical stimulation of NA had no effects on the volume of gastric juice, titratable acidity and acid concentration, but elicited a pronounced increase in the total bicarbonate. However, electrical stimulation of DMV significantly increased the titratable acidity, the volume of gastric juice and the acid concentration. Similarly, electrical stimulation of either NA or DMV decreased the respiratory frequency and sinus bradycardia. CONCLUSION: NA in rats can not control the secretion of gastric acid but the secretion of bicarbonate in gastric juice, while DMV controls the secretion of gastric acid.

Kinetic method for enzymatic analysis by predicting background with uricase reaction as model

Objective：To investigate the reliability for kinetic assay of substance with background predicted by the integrated method using uricase reaction as model. Methods： Absorbance before uricase action （Δ0） was estimated by extrapolation with given lag time of steady-state reaction. With Km fixed at 12.5μmol/L, background absorbance （Δb） was predicted by nonlinearly fitting integrated Michaelis-Menten equation to Candida utilis uricase reaction curve. Uric acid in reaction solution was determined by the difference （ΔA） between Δ0 and Δb. Results .Ab usually showed deviation 〈3% from direct assay with residual substrate done fifth of initial substrate for analysis. ΔA showed CV 〈5% with resistance to common interferences except xanthine, and it linearly responded to uric acid with slope consistent to the absorptivity of uric acid. The lower limit was 2.0 μmol/L and upper limit reached 30 μmol/L in reaction solution with data monitored within 8 min reaction at 0. 015 U/ml uricase. Preliminary application to serum and urine gave better precision than the direct equilibrium method without the removal of proteins before analysis. Conclusion .This kinetic method with background predicted by the integrated method was reliable for enzymatic analysis, and it showed resistance to common interferences and enhanced efficiency at much lower cost.

Doppler study of hepatic vein in cirrhotic patients:Correlation with liver dysfunction and hepatic hemodynamics

AIM: To elucidate the significance of Doppler measurements of hepatic vein in cirrhotic patients and to correlate with liver dysfunction and hepatic hemodynamics. METHODS: One hundred patients with liver cirrhosis and 60 non-cirrhotic controls were studied. Doppler waveforms were obtained from right hepatic vein and flow velocity measured during quiet respiration. Doppler measurements were also obtained from portal trunk, right portal vein and proper hepatic artery. RESULTS: Hepatic vein waveforms were classified into three classical patterns. Flat waveform was uncommon. Mean hepatic vein velocity was significantly higher in cirrhotic patients (12.7 ± 6.4 vs 5.1 ± 2.1 and 6.2 ± 3.2 cm/s; P < 0.0001). The poorer the grade of cirrhosis, the higher was the mean velocity. Maximum forward velocity was never greater than 40 cm/s in controls. Degree of ascites was found to be highly correlated with mean velocity. “Very high” group (≥ 20 cm/s) presented clinically with moderate to massive ascites. Correlations between right portal flow and mean velocity was significant (P < 0.0001, r = 0.687). CONCLUSION: Doppler waveforms of hepatic vein, which is independent of liver dysfunction, should be obtained during normal respiration. Mean hepatic vein velocity reflects the change in hepatic circulation associated with progression of liver cirrhosis. It can be used as a new parameter in the assessment of liver cirrhosis.

Analysis of the mechanisms of rabbit's brainstem hemorrhage complicated with irritable changes in the alvine mucous membrane

AIM: To explore the dynamic changes in the pressure of the lateral ventricle during acute brainstem hemorrhage and the changes of neural discharge of vagus nerve under the load of intracranial hypertension, so as to analyze their effects on the congestive degree of intestinal mucous membrane and the morphologic changes of intestinal mucous membrane.METHODS: An operation was made to open the skull to obtain an acute brainstem hemorrhage animal model.Microcirculatory microscope photography device and video recording system were used to determine the changes continuously in the caliber of jejunal mesenteric artery during brainstem hemorrhage and the changes with time in the congestion of jejunal mucosal villi. We used HE stain morphology to analyze the changes of duodenal mucosal villi. A recording electrode was used to calculate and measure the electric discharge activities of cervical vagus nerve.RESULTS: (1) We observed that the pressure of lateral cerebral ventricle increased transiently during acute brainstem hemorrhage; (2) The caliber of the jejunal mesenteric artery increased during brainstem hemorrhage.Analysis of red color coordinate values indicated transient increase in the congestion of jejunal mucous membrane during acute brainstem hemorrhage; (3) Through the analysis of the pathologic slice, we found enlarged blood vessels, stagnant blood, and transudatory red blood cells in the duodenal submucous layer; (4) Electric discharge of vagus nerve increased and sporadic hemorrhage spots occurred in duodenal mucous and submucous layer, when the lateral ventricle was under pressure.CONCLUSION: Brainstem hemorrhage could causeintracranial hypertension, which would increase the neural discharge of vagus nerve and cause the transient congestion of jejunal mucous membrane. It could cause hyperemia and diffused hemorrhage in the duodenal submucous layer 48 h after brainstem hemorrhage.

Microcirculation disturbance affects rats with acute severe pancreatitis following lung injury

AIM: To study the effects of microcirculation disturbance(MD) on rats with acute severe pancreatitis (ASP).METHODS: We developed ASP rat models, and anatomized separately after 1, 3, 5, 7, and 9 h. We took out blood and did hemorrheologic examination and erythrocyte osmotic fragility test, checked up the water content, capillary permeability, and genetic expression of intercellular adhesion molecule-1 (ICAM-1) in lung tissues, examined the apoptosis degree of blood vessel endothelium while we tested related gene expression of Bax and Bcl-2in lung tissues. We did the same examination in control group.RESULTS: The viscosity of total blood and plasma, the hematocrit, and the erythrocyte osmotic fragility were all increased. Fibrinogen was decreased. The water content in lung tissues and capillary permeability were increased.Apoptosis degree of blood vessel endothelium was increased too. ICAM-1 genetic expression moved up after1 h and reached its peak value after 9 h.CONCLUSION: MD plays an important role in ASP following acute lung injury (ALI). The functional damage of blood vessel endothelium, the apoptosis of capillary vessel endothelium, WBC edging-concentration and the increasing of erythrocyte fragility are the main reasons of ALI.

Financial Rogue Waves

We analytically give the financial rogue waves in the nonlinear option pricing model due to Ivancevic,which is nonlinear wave alternative of the Black-Scholes model.These rogue wave solutions may be used to describe thepossible physical mechanisms for rogue wave phenomenon in financial markets and related fields.

Smad3 knock-out mice as a useful model to study intestinal fibrogenesis

AIM： To evaluate the possible differences in morphology and immunohistochemical expression of CD3, transforming growth factor 131（TGF-131）, Smad7, α-smooth muscle actin （α-Sma）, and collagen types Ⅰ-Ⅶ of small and large intestine in Smad3 null and wild-type mice. METHODS： Ten null and ten wild-type adult mice were sacrificed at 4 mo of age and the organs （esophagus, small and large bowel, ureters） were collected for histology（hematoxylin and eosin, Masson thrichrome, silver staining）, morphometry and immunohistochemistry analysis. TGF-β1 levels of intestinal tissue homogenates were assessed by ELISA. RESULTS： No macroscopic intestinal lesions were detected both in null and wild-type mice. Histological and morphometric evaluation revealed a significant reduction in muscle layer thickness of small and large intestine in null mice as compared to wild-type mice. Immunohistochemistry evaluation showed a significant increase of CD3＋T cell, TGF-β1 and Smad7 staining in the small and large intestine mucosa of Smad3 null mice as compared to wild-type mice. α-Sma and collagen Ⅰ-Ⅶ staining of small and large intestine did not differ between the two groups of mice. TGF-β1 levels of colonic tissue homogenates were significantly higher in null mice than in wildtype mice. In preliminary experiments a significant reduction of TNBS-induced intestinal fibrosis was observed in null mice as compared to wild-type mice.

Ursodeoxycholic acid improves gastrointestinal motility defects in gallstone patients

AIM: To simultaneously evaluate the presence of defects in gallbladder and gastric emptying, as well as in intestinal transit in gallstone patients (GS) and the effect of chronic ursodeoxycholic acid (UDCA) administration on these parameters and on serum bile acids and clinical outcome in GS and controls (CTR). METHODS: After a standard liquid test meal, gallbla-dder and gastric emptying (by ultrasound), oroileal transit time (OITT) (by an immunoenzymatic technique) and serum bile acids (by HPLC) were evaluated before and after 3 mo of UDCA (12 mg/kg bw/d) or placebo administration in 10 symptomatic GS and 10 matched healthy CTR. RESULTS: OITT was longer in GS than in CTR (P < 0.0001); UDCA significantly reduced OITT in GS (P < 0.0001), but not in CTR. GS had longer gastric half-emptying time (t1/2) than CTR (P < 0.0044) at baseline; after UDCA, t1/2 significantly decreased (P < 0.006) in GS but not in CTR. Placebo administration had no effect on gastric emptying and intestinal transit in both GS and CTR. CONCLUSION: The gallstone patient has simultaneous multiple impairments of gallbladder and gastric emptying, as well as of intestinal transit. UDCA administration restores these defects in GS, without any effect in CTR. These results confirm the pathogenetic role of gastrointestinal motility in gallstone disease and suggest an additional mechanism of action for UDCA in reducing bile cholesterol supersaturation.

Effect of emodin on small intestinal peristalsis of mice and relevant mechanism

AIM: To investigate the effect of emodin on small intestinal peristalsis of mice and to explore its relevant mechanisms.METHODS: The effect of emodin on small intestinal peristalsis of mice was observed by charcoal powder propelling test of small intestine. The contents of motilin and somatostatin in small intestine of mice were determinated by radioimmunoassay. The electrical potential difference (PD) related to Na+ and glucose transport was measured across the wall of reverted intestinal sacs. Na+-K+-ATPase activity of small intestinal mucosa was measured by spectroscopic analysis.RESULTS: Different dosages of emodin can improve small intestinal peristalsis of mice. Emodin increased the content of motilin, while reduced the content of somatostatin in small intestine of mice significantly. Emodin 0.2, 0.4, 0.8, and 1.6 g/L decreased PD when there was glucose. However, emodin had little effect when glucose was free. The Na+-K+-ATPase activity of small intestinal mucosa of mice in emodin groups was inhibited obviously. CONCLUSION: Emodin can enhance the function of small intestinal peristalsis of mice by mechanisms of promoting secretion of motilin, lowering the content of somatostatin and inhibiting Na+-K+-ATPase activity of small intestinal mucosa.

Apopotic gene Bax expression in carotid plaque

The expression of BAX in carotid atherosclerosis and its regulation is far from defined. Objectives To investigate BAX expression in stable/fibrous and instable/vulnerable carotid plaque and its clinical significance. Methods 25 cases of carotid plaque specimens obtained from endarterectomy were divided into two groups, stable/fibrous 14 cases, vulnerable/instable 11 cases; aortic artery and its branches from hepatic transplantation donors 6 case as control The expression of proapoptotic BAX was detected by immunohistochemistry （IHC）, in situ hybridization （ISH） and in situ TdT dUTP nick end labeling （TUNEL）. Results 5 cases of BAX （ ＋ ） were detected by ICH and ISH, 4 case of TUNEL （ ＋ ） were detected by TUNEL in stable/fibrous carotid plaque , while 10 cases were BAX （ ＋ ）by IHC（P 〈 0.05 ） , 11 case by ISH and 9 case by TUNEL were detected in instable/vulnerable carotid plaque （P 〈0.01 ）, respectively. The intensity of BAX （ ＋ ） cells by IHC and ISH was 8.63±2.62 and 10.32 ± 3.12 in fibrous plaques,whereas 122 ±21.64 and 152 ± 23.35 in vulnerable plaques, respectively. No expression of BAX was found in controlled group. Conclusion The higher expression of Bax in vulnerable carotid plaque may be one mechanisms in molecular pathogenesis of carotid atherosclerosis which affect plaque stability and be the cause of higher incidence of stroke than fibrous carotid plaques, the regulation of BAX expression in different stage of atherosclerosis may provide targets in gene therapy for carotid atherosclerosis.