FPGA-PLC-based multi-channel position measurement system.

The existing Programmable Logic Controller (PLC) based on microprocessors (µp) or micro-controllers (µc) are commonly used in the industry for various instrumentation and control applications. PLC exhibits limitations such as less flexibility, poor scanning time, slower speed, and degraded response for high-speed industrial applications due to its fixed hardware and serial execution mechanism. A new Field Programmable Gate Array (FPGA) based PLC multi-channel High Speed Counter (HSC) module has been proposed, enhancing performance and flexibility compared to the existing PLC-HSC module. The proposed FPGA-PLC-HSC module has a 2-phase 2-Input counter with resolutions of 1X, 2X, and 4X which improve performance in terms of accuracy for position speed, and direction measurement applications. The FPGA-PLC-HSC module is implemented with the feedback node method and the shift register method inside LabVIEW FPGA along with device utilization. The simulation results show that the FPGA-PLC-HSC module has faster scanning time, good linearity, better resolution, maximum supporting input frequency, and counting frequency. For experimental purposes, an optical encoder M110960 (E8P-512-118-S-D-M-B) with a signal conditioning circuit is connected to the NI-myRIO-1900 FPGA platform. The experimental results point out that the proposed FPGA-PLC-HSC module offers faster scanning time, better accuracy and linearity in 1X, 2X, and 4X resolution.

Endothelial metallothionein expression and intracellular free zinc levels are regulated by shear stress.

We examined the effects of fluid shear stress on metallothionein (MT) gene and protein expression and intracellular free zinc in mouse aorta and in human umbilical vein endothelial cells (HUVECs). Immunostaining of the endothelial surface of mouse aorta revealed increased expression of MT protein in the lesser curvature of the aorta relative to the descending thoracic aorta. HUVECs were exposed to high steady shear stress (15 dyn/cm(2)), low steady shear stress (1 dyn/cm(2)), or reversing shear stress (mean of 1 dyn/cm(2), 1 Hz) for 24 h. Gene expression of three MT-1 isoforms, MT-2A, and zinc transporter-1 was upregulated by low steady shear stress and reversing shear stress. HUVECs exposed to 15 dyn/cm(2) had increased levels of free zinc compared with cells under other shear stress regimes and static conditions. The increase in free zinc was partially blocked with an inhibitor of nitric oxide synthesis, suggesting a role for shear stress-induced endothelial nitric oxide synthase activity. Cells subjected to reversing shear stress in zinc-supplemented media (50 µM ZnSO(4)) had increased intracellular free zinc, reduced surface intercellular adhesion molecule-1 expression, and reduced monocyte adhesion compared with cells exposed to reversing shear stress in normal media. The sensitivity of intracellular free zinc to differences in shear stress suggests that intracellular zinc levels are important in the regulation of the endothelium and in the progression of vascular disease.

Effect of zinc and nitric oxide on monocyte adhesion to endothelial cells under shear stress.

This study describes the effect of zinc on monocyte adhesion to endothelial cells under different shear stress regimens, which may trigger atherogenesis. Human umbilical vein endothelial cells were exposed to steady shear stress (15 dynes/cm(2) or 1 dyne/cm(2)) or reversing shear stress (time average 1 dyne/cm(2)) for 24 h. In all shear stress regimes, zinc deficiency enhanced THP-1 cell adhesion, while heparinase III reduced monocyte adhesion following reversing shear stress exposure. Unlike other shear stress regimes, reversing shear stress alone enhanced monocyte adhesion, which may be associated with increased H(2)O(2) and superoxide together with relatively low levels of nitric oxide (NO) production. L-N(G)-Nitroarginine methyl ester (L-NAME) treatment increased monocyte adhesion under 15 dynes/cm(2) and under reversing shear stress. After reversing shear stress, monocyte adhesion dramatically increased with heparinase III treatment followed by a zinc scavenger. Static culture experiments supported the reduction of monocyte adhesion by zinc following endothelial cell cytokine activation. These results suggest that endothelial cell zinc levels are important for the inhibition of monocyte adhesion to endothelial cells, and may be one of the key factors in the early stages of atherogenesis.