Kuo-Chu Chang

Direct displacement-based design for building with passive energy dissipation systems

This paper presents a seismic displacement-based design method for new and regular buildings equipped with passive energy dissipation systems (EDS). Using the substitute structure approach for the building structure and simulating the mechanical properties of the passive energy dissipation devices (EDD) by the effective stiffness and effective viscous damping ratio, a rational linear iteration method is proposed. A target displacement is at first specified and then the corresponding design force, strength and stiffness are obtained. Comprehensive procedures for displacement-based design of several buildings with passive energy dissipation systems are presented. The results are verified by dynamic inelastic time history analysis. Based on the study, it is found that the proposed displacement-based design method is straightforward and can accurately predict the nonlinear behavior of buildings equipped with passive energy dissipation systems.

Acute effects of nitric oxide blockade with L-NAME on arterial haemodynamics in the rat

1 We employed the technique of impedance spectral analysis to investigate the role of endogenous nitric oxide (NO) in the regulation of steady and pulsatile haemodynamics in Wistar Kyoto rat (WKY). 2 A total of 12 WKYs was anaesthetized with pentobarbitol sodium (40 mg kg−1, i.p.) and artificially ventilated with an animal respirator. The aortic pressure wave was monitored with a high fidelity Millar sensor, and aortic flow wave with an electromagnetic flow probe. The pressure and flow waves were subjected to Fourier transform for the analysis of impedance spectra. 3 The baseline cardiovascular parameters were mean arterial pressure (APm) 95±9 mmHg, heart rate (HR) 338±9 b.p.m., stroke volume (SV) 0.23±0.01 ml, cardiac output (CO) 77.8±1.6 ml min−1, total peripheral resistance (TPR) 98±11 (×103) dyne  s  cm−5, characteristic impedance (Zc) 2046±141 dyne  s  cm−5, arterial compliance at mean AP (Cm) 3.78±0.22 μl mmHg−1 and backward pulse wave (Pb) 12.9±0.6 mmHg. 4 An NO synthase inhibitor, NG‐nitro‐L‐arginine monomethyl ester (L‐NAME) was administered at graded intravenous doses. This agent caused dose‐dependent increases in AP and TPR with decreases in HR. At an accumulative dose of 10 mg kg−1, APm was increased by 29±3 mmHg (+31%) and TPR by 49±6 (×103) dyne  s  cm−5 (+50%), while HR was reduced by 37±5 b.p.m. (−11%) and CO by 10.4±0.8 ml min−1 (−14%). The pulsatile haemodynamics including Zc and Pb were slightly increased by 14–15%. Cm was decreased by 1.09 μl mmHg−1 (−29%). L‐NAME also did not significantly affect the ventricular work including the steady, oscillatory and total work. 5 Aminoguanidine, a specific inhibitor for inducible NO synthase (iNOS), in dose 10–60 mg kg−1 i.v. did not alter the AP, HR and other parameters. The result indicated that blockade of constitutive NOS, but not iNOS is involved in these changes. 6 Angiotensin II (Ang) in various infusion doses was used to produce a profile of AP increase similar to that caused by L‐NAME. Ang remarkably increased Zc, while TPR was moderately elevated. The pattern of haemodynamic changes was different from that following L‐NAME. 7 The results suggest that blockade of the endogenous NO affects predominantly the arterial pressure and peripheral resistance. The Windkessel functions such as arterial impedance and pulse wave reflection are slightly increased. Ventricular works are not significantly altered.

Seismic behaviour of reinforced concrete frame with added viscoelastic dampers

Abstract This paper summarizes an experimental and analytical study on the seismic retrofit of a 1 3 - scale reinforced concrete frame using viscoelastic dampers. After the frame had been damaged in the laboratory under simulated strong earthquake ground motions, two sets of viscoelastic dampers were designed and implemented to the structure, and the frame was subjected to further simulated seismic excitations. Test results show that viscoelastic dampers are very effective in reducing the seismic response of reinforced concrete structures. In addition, the equivalent structural damping ratio can easily be predicted by the modal strain energy method with some modification. Therefore, seismic design of reinforced concrete structures with added viscoelastic dampers can be carried out similarly to conventional structural design procedures.

Aminoguanidine prevents arterial stiffening in a new rat model of type 2 diabetes

Background  Formation of advanced glycation end‐products (AGEs) on collagen within the arterial wall may be responsible for the development of diabetic vascular injury. This study focused on investigating the role of aminoguanidine (AG), an inhibitor of AGE formation, in the prevention of noninsulin‐dependent diabetes mellitus (NIDDM)‐derived arterial stiffening and cardiac hypertrophy in rats.

Arterial stiffening and cardiac hypertrophy in a new rat model of type 2 diabetes

Background  We determined the effects of NIDDM on haemodynamic parameters describing arterial wall elasticity and cardiac hypertrophy in rats administered streptozotocin (STZ) and nicotinamide (NA), using the aortic impedance analysis.

Aminoguanidine prevents arterial stiffening and cardiac hypertrophy in streptozotocin-induced diabetes in rats

The formation of advanced glycation endproducts (AGEs) on collagen within the arterial wall may be responsible for the development of diabetic vascular injury. This study was to examine the role of aminoguanidine (AG), an inhibitor of AGEs formation, in the prevention of arterial stiffening and cardiac hypertrophy in streptozotocin (STZ) induced diabetes in rats. Diabetes was induced in animals by a single tail vein injection with 65 mg kg−1 STZ. After confirmation of the development of hyperglycemia (2 days later), rats were treated for 8 weeks with AG (daily peritoneal injections of 50 mg kg−1) and compared with the age‐matched untreated diabetic controls. After exposure to AG, the STZ‐diabetic rats showed no alterations in cardiac output, aortic pressure profiles, total peripheral resistance, and aortic characteristic impedance. By contrast, treatment of this experimental diabetes with AG resulted in a significant increase in wave transit time (τ), from 20.4±0.6 to 24.7±0.5 ms (P<0.05) and a decrease in wave reflection factor (Rf), from 0.78±0.04 to 0.53±0.02 (P<0.05). The decreased Rf associated with the increased τ suggest that AG may retard the diabetes‐induced augmentation in systolic load of the left ventricle coupled to its arterial system. Meanwhile, the diminished ratio of left ventricular weight to body weight suggests that prevention of the diabetes‐related cardiac hypertrophy by AG may correspond to the drug‐induced decline in aortic stiffening. Glycation‐derived modification on aortic collagen was also found to be enhanced in rats with diabetes (+65.3%, P<0.05) and the advanced glycation process was retarded by AG treatment. We conclude that long‐term administration of AG to the STZ‐treated rats imparts significant protection against the diabetes‐derived deterioration in vascular dynamics, at least partly through inhibition of the AGEs accumulation on collagen in the arterial wall.

Prevention of arterial stiffening by pyridoxamine in diabetes is associated with inhibition of the pathogenic glycation on aortic collagen

Background and purpose:  Our team previously demonstrated that diabetes induces a deterioration in vascular dynamics, in parallel with the enhanced formation of advanced glycation end products. The aim of this study was to determine whether prevention of the arterial stiffening by pyridoxamine in diabetes is associated with inhibition of the pathogenic glycation on aortic collagen.

Aminoguanidine prevents the impairment of cardiac pumping mechanics in rats with streptozotocin and nicotinamide‐induced type 2 diabetes

Aminoguanidine (AG), an inhibitor of advanced glycation endproducts, has been shown to prevent arterial stiffening and cardiac hypertrophy in streptozotocin (STZ) and nicotinamide (NA)‐induced type 2 diabetes in rats. Our aims were to examine whether AG produced benefits on cardiac pumping mechanics in the STZ and NA‐treated animals in terms of maximal systolic elastance (Emax) and theoretical maximum flow (Qmax).

Composite damping ratio of seismically isolated regular bridges

In this paper seismically isolated regular bridges are modelled as two-degree-of-freedom systems in the longitudinal or transverse direction. The equivalent linear characteristics, including the effective stiffness and equivalent viscous damping ratio of isolation bearings, are used to formulate the equivalent linear theory of the seismically isolated regular bridge. The system composite damping ratio, attributed to the equivalent viscous damping ratio of isolation bearing and the viscous damping ratio of bridge column bents or piers, is obtained both by classical damping and nonclassical damping assumptions. The parametric influences including those of the mass ratio, stiffness ratio, viscous damping ratio of bridge column bents and equivalent viscous damping ratio of isolation bearings on the composite damping ratio are investigated. The composite damping ratio formulated in the study is compared with that obtained from the modal strain energy method. In addition, the parametric influences on the system composite damping ratio of isolated bridges are compared with those of isolated buildings.

The correlation of cardiac mass with arterial haemodynamics of resistive and capacitive load in rats with normotension and established hypertension

In hypertensive animals and humans, cardiac hypertrophy may occur as a consequence of an external load on the heart. Several studies have suggested that the non-pulsatile components of arterial haemodynamics, such as arterial pressure and vascular resistance, do not adequately represent the ventricular afterload and are not well correlated with the degree of cardiac hypertrophy (CH). The present study was undertaken to analyse the correlation between the degree of CH and various haemodynamic parameters in the spontaneously hypertensive rat (SHR) with established hypertension. A total of 36 SHRs (6–8 months) with a tail-cuff pressure above 190 mm Hg were used. Control data were obtained from 32 age-matched normotensive Wistar Kyoto rats (WKY). Animals were anaesthetized with pentobarbitone sodium (40 mg/kg i.p.) and artificially ventilated with a respirator. A Millar catheter with a high-fidelity pressure sensor was used to record the aortic pressure and an electromagnetic flow transducer to monitor the aortic flow. The pressure and flow signals were subjected to Fourier transformation for the analysis of the arterial impedance spectrum. The left ventricular weight-to-body weight ratio (LVW/BW) was taken as a measure of the degree of CH. The measured haemodynamic parameters in these anaesthetized, open-chest SHRs were systolic pressure (SP) (mean ± SE) 172±4 mm Hg, diastolic pressure (DP), 120±3 mm Hg, pulse pressure (PP) 52±2 mm Hg, peripheral resistance (Rp) 344,032±8,012 dyne · s · cm−5, characteristic impedance (Zc) 6,442±313 dyne · s · cm−5, the impedance modulus at the first harmonic (Z1) 26,611±1,061 dyne · s · cm−5, mean arterial compliance (Cm) 0.87 ±0.04 μl/mm Hg and LVW/BW 3.092±0.026 mg/g. These parameters were significantly greater than the corresponding values in WKY, except that Cm was much decreased. In SHR, the LVW/BW was not significantly correlated with the SP, DP, Rp and steady external power. In contrast, the degree of CH was positively correlated with Zc (r=0.66, P<0.001), Z1 (r=0.62, P<0.001) and pulsatile external work (r=0.41, P<0.05). It was also positively correlated with the backward pressure wave (r=0.42, P<0.05) and negatively correlated with Cm (r=-0.72, P<0.01). Such correlations of LVW/BW with pulsatile haemodynamics were not found in the normotensive WKY. The results indicate that the degree of cardiac hypertrophy in hypertensive rats, with a high blood pressure and increased stiffness of the arterial tree, is more closely related to pulsatile arterial haemodynamics than to the nonpulsatile components.