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The design principles, optical configurations, and capabilities of a newly developed advanced vibrometer/interferometer device called AVID are presented. The fundamental principles of this metrology instrument that enables it to have a dc to 20-MHz bandwidth and nanometer resolution are also detailed. The applicability of using laminated one-dimensional piezoelectric plates as testbeds to study some of the fundamental characteristics of piezoelectric actuators and sensors is also examined. Taking advantages of the linear and angular displacement/velocity measurement modes of the vibrometer/interferometer, the performance of distributed piezoelectric sensors, which can measure bending angle and bending displacement at any point of the testbed, is characterized. In addition, the corresponding piezoelectric actuator that can exert bending moment on the testbed is also evaluated. The hysteresis effect and feedback vibration control potential of both piezoelectric polymer polyvinylidene fluoride ([PVF.sub.2]) and piezoelectric ceramic lead, zirconate, and titarate (PZT) are investigated by using a bimorph configuration testbed. Experimental results show that [PVF.sub.2] acts more linearly than PZT during sensing. Furthermore, the influence of the driving sources on the piezoelectric actuators can be verified experimentally. It can be shown that driving PZT by using a current source will have a less severe hysteresis effect than driving it with a traditional voltage source.

Lipoprotein lipase (LPL) plays a crucial role in the regulation of lipoprotein metabolism by hydrolyzing the core triglycerides of circulating chylomicrons and very low-density lipoprotein. Deficiency in this enzyme usually results in disturbances in lipid levels. To understand the molecular defect that leads to a functional deficiency of LPL in patients with hypertriglyceridemia, we looked for mutations of the LPL gene by means of single-strand conformation polymorphism (SSCP) analysis and direct DNA sequencing in 24 patients. A single base C-->G substitution in codon 252 of the LPL gene, encoding a change of a leucine to a valine residue in the mature protein, was found in three women who had hypertriglyceridemia and recurrent pancreatitis. Two of these patients, who were homozygous for the L252V mutation, had variable and occasionally severe hypertriglyceridemia with undetectable or very low LPL activities, respectively. The third woman was heterozygous for this mutation. All three patients had poor post-heparin LPL activity. Site-directed mutagenesis experiments provided in vitro evidence that the mutation of codon 252 was responsible for the loss of LPL activity. In conclusion, we identified a novel LPL mutation that results in decreased LPL activity in Taiwanese patients with hypertriglyceridemia. The assessment of a causative link between the mutation and hyperlipidemia awaits further studies.