Mechanism of MIR-210 mediated NF-κB pathway on cardiac ischemia-reperfusion injury.

In this study, MicroRNA-210 (miR-210), which was previously proved to be a potential immunomodulator in various disease, attenuated mouse myocardium ischemia/reperfusion (I/R) injury. miR-210 was increased in cardiomyocytes exposed to hypoxia/reoxygenation (H/R). The expression of IL-6 and TNF-α in both serum and supernatant were reduced in miR-210 mimics groups. Mice were randomly divided into four groups, which were pre-treated with saline (sham and ischemia/reperfusion group), miR-210 mimics and miR-210 inhibitor treatments. Three days later, the mouse IR model was established by ischemia for 30 min, followed by reperfusion for 3 h. Myocardium and plasma were harvested and assessed. The myocardium histopathological changes were reduced in miR-210 mimics groups, and serum levels of Creatine kinase isoenzyme (CK-MB) and Lactate dehydrogenase (LDH) were significantly decreased compared with I/R groups. The protein expression of proinflammatory factor interleukin (IL)-1ß and IL-6 were suppressed by the up-regulation of miR-210. The expression of miR-210 was negatively correlated with the expression of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB). In conclusion, our study indicates that miR-210 protects heart from myocardium I/R injury via suppressing NF-κB signal pathway.

Phosphorus removal of rural wastewater by the paddy-rice-wetland system in Tai Lake Basin.

A field experiment was conducted to remove the potential eutrophication effect of P from rural wastewater (RW) during the whole rice growing season of 2007. The experiments consisted of five treatments, namely black water (BW), domestic wastewater (DW), grey water (GW), surface lake water (SW) and surface lake water without P application as a check (CK), with three replicates in a randomized block design. Commercial fertilizer and RW were applied to furnish 40 kg Pha(-1) except CK. Results showed total P (TP) concentration had significantly declined after P application, from October 15 there were no significant increases in TP concentration in the floodwater. TP removal rates from RW was significantly higher (P

Receptor tyrosine kinase inhibitors AG013764 and AG013711 reduce choroidal neovascularization in rat eye.

Age-related macular degeneration (AMD) is the major cause of blindness for people over 60. In the "wet" form of AMD compounds targeting growth factor signaling pathways such as VEGF have been a major focus for therapeutic interventions. In a previously developed rat model of CNV, we utilized two receptor tyrosine kinase inhibitors (RTKi) to block VEGFR-1, VEGFR-2 and PDGFR signaling following the establishment of CNV. AAV-VEGF(165) was injected into the subretinal space of rats at postnatal days 15-17. Six weeks later, a suspension of RTK inhibitors, AG013764 or AG013711, was injected intraperitoneally (IP, twice daily) or intravitreally (every five days) over a two week period. FITC-dextran whole-mounts of RPE-choroid-sclera were prepared after the animals were sacrificed. CNV area was quantified using Neurolucida to measure the hyperfluorescence on FITC-dextran whole-mounts. Histology and immunohistochemistry were performed as described previously. VEGF expression in control and treated eyes was confirmed by immunohistochemistry and histological sections indicated recovery of retinal morphology and CNV reduction in treated eyes. In the animals IP injected with AG013764 or AG013711 the mean CNV level was reduced by 25 to 33% compared to control, but this effect did not achieve statistical significance. Intravitreal injections of AG013764 or AG013711 reduced the level of CNV by approximately 60% compared to control (p<0.005 or p<0.05, respectively). These data show that two RTK inhibitors, AG013764 or AG013711, delivered intravitreally, significantly reduce blood vessel proliferation in this AAV-VEGF(165) model of CNV.

Uniformity of current density under stimulating electrodes.

This work examines all the factors that go into designing, simulating, implementing, and experimentally testing high-current bioelectrodes. It reviews previous work on the properties and risks of electrodes used to interface high currents to the human body. It is a self-contained presentation covering all aspects of the design, test, and implementation of high-current stimulating bioelectrodes. Inherent properties derived from theoretical work are pointed out. The tools to design and evaluate electrodes are introduced and discussed. Analytical methods provide insights into inherent characteristics, but lack generality and are often very difficult to use. Numerical methods overcome the difficulties of analytical procedures and are capable of quantitatively evaluating existing electrode designs, or can be used to find a design that is optimal in certain properties and specific applications. Experimental studies have verified and provided knowledge of the mechanisms that can potentially cause damage to the patient. They are also used to test the validity as well as the limitations of numerical models and their predictions, and to point out which aspects of the numerical methods need to be improved. Experimental measurements are in good agreement with the analytical predictions and simulation results. For example, all three approaches pinpoint that the edge effect (the current density at the electrode-body interface increases toward the perimeter of the electrode) is an inherent property of a low-impedance electrode attached to a body of higher resistivity. Also, several optimal stimulating electrode designs to obtain the uniformity of current density under the electrodes are presented.