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A new normally open valve is presented. A polydimethylsiloxane (PDMS) cavity with two microchannels were fabricated using soft lithography technology. The one end of the cavity is arc-shaped at the joint with the microchannel. A steel ball is placed into the PDMS cavity mounted on a piezoelectric substrate with an interdigital transducer (IDT). Surface acoustic wave excited by the IDT is used for driving the steel ball to the arc area, leading to blocking the inlet of the microchannel. The microvalve was then closed. The switching characteristics were experimentally demonstrated using red ink solution. [ABSTRACT FROM AUTHOR]

A new method for dispatching microfluid is presented. A steel ball of 2mm diameter is placed on a 128 degrees YX LiNbO3 substrate. A PDMS frame is mounted on the piezoelectric substrate for defining the movement trajectory of the steel ball. Paper testing zone is fixed on a PDMS block for the target of the microfluidic dispatch. The steel ball is driven by surface acoustic wave, and carried microfluid at the outlet of the PDMS microchannel to the paper testing zone. Red ink solution is used to demonstrate the fluid dispatch. [ABSTRACT FROM AUTHOR]

A new paper-based microfluidic device is fabricated on a piezoelectric substrate. A polydimethylsiloxane channel filled with cotton threads is mounted on the piezoelectric substrate with an interdigital transducer. A testing filter paper with dried reaction solution is coated on the end of the cotton thread. Sample solution is driven to the cotton thread channel and transported to testing area for microfluidic analysis. Red ink solution and color development reaction of starch are demonstrated for microfluidic operation and analysis. Results show that the linear velocity of microfluidic transportation in the cotton thread channel is 4.558 mm/s, and color development reaction of starch is successfully implemented. [ABSTRACT FROM AUTHOR]

A new method for heating microfluid in a polydimethylsiloxane (PDMS) array chip is presented. Interdigital transducers are fabricated on a 128° YX-LiNbO3substrate. A 4 × 4 polydimethylsiloxane array chip is placed on the piezoelectric substrate, where a heat transfer pillar with a heat transfer sheet is connected with every reaction zone in the PDMS array chip. An oil droplet is driven for selecting special heat transfer pillar to heat the microfluid in the special reaction zone. Theoretical calculation of heat transfer is finished. At equilibrium state, the emitted energy per second during heat transfer is 7.436 mJ at 30.0 dBm electric signal power. [ABSTRACT FROM AUTHOR]

Grape seed procyanidin B2 (GSPB2) exerts a variety of potent protective pharmacological effects on diabetic complications. The renal protective effects of GSPB2 and the target protein mimecan regulated by GSPB2, discovered in a previous quantitative proteomic analysis, were assessed in mice with diabetic nephropathy Twenty-four db/db mice were divided into 2 groups of the vehicle-treated and GSPB2-treated (30 mg/kg/d) diabetic groups. All animals were observed for 10 weeks. Treatment with GSPB2 resulted in an improvement in body weight increase and serum levels of triglyceride, total cholesterol, advanced glycation end products, and urinary albumin excretion in comparison with the vehicle-treated diabetic mice (P < .05), although these levels were still higher than those in the control group. Treatment with GSPB2 significantly reduced the extent of glomerular basement membranes thickening, mesangial expansion, and glomerular area as well. Mimecan protein expressions in diabetes mellitus were decreased approximately by 28% when compared with those in the control group (P < .05), and restored remarkably after GSPB2 treatment (P < .05). The expression of nuclear factor-κB (NF-κB) p65 in nuclear extracts, markedly higher in the diabetic mice than in the controls, was significantly suppressed by GSPB2. The findings of this study revealed that mimecan might become a new therapeutic target in the future and indicated that GSPB2 had beneficial effects not only on oxidative stress, but also on renal fibrosis, particularly in the diabetic kidney. [ABSTRACT FROM AUTHOR]

Abstract: Microvascular changes in the brain are significant causes of cerebral edema and ischemia injury. A number of studies suggest that angiotensin (Ang) II may be involved in the initiation and regulation of processes occurring in brain ischemia. We recently reported that Ang II injures brain microvascular endothelial cells (BMEC) partially via stimulating intercellular adhesion molecule-1 (ICAM-1) expression. However, the signaling cascade leading to Ang II-induced ICAM-1 expression in BMEC was unclear. The present study tested the hypothesis that Ang II induces ICAM-1 expression via an AT1 receptor/nuclear factor-κB (NF-κB) pathway in BMEC. Ang II directly stimulated the expression of ICAM-1 mRNA and protein in primary cultured BMEC. Ang II treatment also resulted in the degradation of IκBα and increase of NF-κB p65 subunit in the nucleus as well as the DNA binding activity of nuclear NF-κB. These effects were abolished by pretreatment with the selective AT1 receptor antagonists, losartan and compound EXP-2528, or losartan plus the AT2 receptor antagonist PD123319, but not by PD123319 alone. Moreover, there were no significant differences between the losartan and losartan plus PD123319 groups. These findings indicate that Ang II-induced ICAM-1 upregulation in brain microvascular endothelial cells may be mediated via an AT1 receptor/NF-κB pathway. [Copyright &y& Elsevier]