The position invariant geometric inaccuracies of a machine tool are the ®rst to in¯uence the quality of machined parts. A systematic approach is presented to identify some of these errors on a ®ve-axis machine tool. The methodology is applied to the link error parameters such as joint misalignments, angular o set and rotary axis separation distance. A method based on the mathematical analysis of singularities of linear systems is used to assist in selecting a minimal but su cient set of link error parameters for the calibration of a machine tool. A number of criteria are proposed in order to verify that the identi®ed parameters accurately predict the positioning errors of the true machine. Finally, the numerical e ectiveness of this method is shown through simulations.
To elucidate the relationship between microscopic red blood cell (RBC) interactions and macroscopic rheological behavior, we propose a two-dimensional particle model capable of mimicking the main characteristics of RBC aggregation kinetics. The mechanical model of RBCs sheared in Couette flow is based on Newton law. We assumed a hydrodynamic force to move particles, a force to describe aggregation and an elasticity force. The role of molecular mass and concentration of neutral polymers on aggregation [Neu, B., and H. J. Meiselman. Biophys. J. 83:2482-2490, 2002] could be mimicked. Specifically, it was shown that for any shear rate (SR), the mean aggregate size (MAS) grew with time until it reached a constant value, which is consistent with in vitro experiments. It was also demonstrated that we could mimic the modal relationship between MAS and SR and the occurrence of maximum aggregation at about 0.1 s(-1). As anticipated, simulations indicated that an increase in aggregation force augmented MAS. Further, augmentation of the depletion layer thickness influenced MAS only for SR close to zero, which is a new finding. To conclude, our contribution reveals that the aggregation force intensity and SR influence the steady state MAS, and that the depletion and layer thickness affect the aggregation speed.
Abstract-Preeclampsia is the major cause of maternal and fetal mortality/morbidity. Because hypertension is an important risk factor for preeclampsia, we investigated whether hypertensive mice that overexpress human renin and angiotensinogen develop superimposed preeclampsia. Given that the mechanisms underlying this disease are still poorly understood, animal models are of great use for elucidatation. Blood pressure and proteinuria were measured by telemetry and ELISA, respectively. Heart function was evaluated by echocardiography, whereas pathological cardiac hypertrophy-related genes were assessed by real-time PCR. Soluble fms-like tyrosine kinase 1 plasma concentrations were quantitated by ELISA and placental expression by real-time PCR. Transgenic mice develop de novo proteinuria during gestation and marked blood pressure elevation, which are hallmarks of superimposed preeclampsia on chronic hypertension. Abnormal placentation present in these mothers produced a significant decrease in pup and placental weight and was associated with an increased placental expression of soluble fms-like tyrosine kinase 1. We also found heightened circulating levels of this receptor, when adjusted for placental mass, as has been observed in women who suffer from preeclampsia. Cardiac hypertrophy could be observed in the transgenic mice and was exacerbated by gestation. As a result, heart function was significantly decreased, and markers of pathological hypertrophy were increased. Our data, thus, confirm the characterization of a new model of superimposed preeclampsia on chronic hypertension. Because chronically hypertensive women are at risk of developing the pathology, our model reflects a clinical reality and is, thus, an excellent tool to elucidate the molecular mechanisms triggering this disease. Key Words: preeclampsia Ⅲ mouse model Ⅲ renin-angiotensin system Ⅲ cardiac hypertrophy Ⅲ hypertension P reeclampsia (PE) has been studied extensively in the last 2 decades, because it is the most common cause of fetal and maternal mortality and morbidity. 1 However, thus far, apart from delivery, there are no available treatments, because antihypertensive medications are deleterious to the fetus. 2 This human pregnancy-associated syndrome is characterized by the new occurrence of proteinuria and hypertension, in previously normotensive women, or a progression of chronic hypertension to superimposed PE (SPE). 3 Other symptoms that can also be associated with this disease are placental pathology and cardiac hypertrophy. 1,4 Because it is difficult to predict disease onset, studies in humans are challenging and require a tremendous number of subjects to be of any significance. Moreover, few animal models develop PE spontaneously. [5][6][7] Because it has been suggested that PE may not be a homogenous disease, similar to essential hypertension, many different animal models may be required to characterize the different faces of this pathology that is still so poorly understood.The renin-angiotensin system (RAS) is postulated to be ...
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