Hybrid Water Pump

This project seeks to use multiple sources to power a water pump. We will design a system which will combine inputs from solar and wind energy production to ensure the pump will have enough power to run. This will create a system powered by clean energy and will be self-sustained once completed. This will theoretically create a more sustainable source of power for the pump than only one of the sources. Because the power sources don’t require outside inputs (aside from sun and wind), the pump can be placed in a remote area. This could be very helpful in developing communities, where residents may not have a reliable power supply. This system will allow these types of communities to pump water from wells to bring back to their homes. This will also reduce dependence on non-renewable sources of energy. The system will consist of a solar panel, wind turbine, control system to integrate the sources, and the water pump. The system will be made to require minimal user input to run. Inside the control system, two DC-DC buck converters are used to regulate input voltages. Two diodes are used to joint 2 input sources and prevent backflow of energy. This method is selected instead of MISO (Multiple Inputs Single Output) converter due to its simplicity. An Arduino Uno microcontroller powered by AtMega328p microprocessor is used for displaying power reading from the two sources and the load. The microcontroller also control the relay for protection purposes. An adjustable speed drive and motors combination is studied and used for simulating the wind turbine generation. Relays and circuit breakers are also studied for circuit protection in renewable power systems. This project showcase the possibility of having a hybrid renewable system for common electrical appliances as well as pointing out some difficulties in such system

Proteome profiler array of human cytokines/chmokines.

<p>The array is capable of detecting a panel of 36 cytokines, chemokines, and soluble mediators. Top panel shows expression of cytokines/chemokines in resting unstimulated human astrocyrtes, and middle panel shows expression of cytkines/chemokines in human astrocytes stimulated with IL-1β and TNF-α. Items circled in red are newly expressed cytokines in activated astrocytes and ones circled in blue are cytokines changed expression in activated aqstrocytes. In bottom panel, newly expressed cytokines and cytokines changed expression are listed separately.</p

The purity of human astrocytes in culture exceeded 99% glial fibrillary acidic protein (GFAP) immunoreactivity-positive.

<p>Astocytes shown are at the normal non-stimulated resting state. A: Phase contrast microscopy. B: Immunostaning with anti-GFAP antibody.</p

Cytokines expressed in normal resting human astrocytes.

<p>Cytokines expressed in normal resting human astrocytes.</p

Cytokines/chemokines changed their secretion levels in human astrocytes stimulated with IL-1β and TNF-α.

<p>A: Forty five-fold increase in secertion of GM-CSF and twenty-fold increase in secretion of G-CSF are shown here. A minor reduction in expression of MCP-1 and MIF is also shown. B. Among the elevated levels of cytokines/chemokines in human astrocytes stimulated with IL-1β and TNF-α, upregulated expression of RANTES was the most prominent with more than 150-fold increase.</p

Proteome profiler array of human cytokines/chmokines used in the present study.

<p>Proteome profiler array of human cytokines/chmokines used in the present study.</p

Cytokines upregulated in human astrocytes following IL-1β/TNFα treatment.

<p>Cytokines upregulated in human astrocytes following IL-1β/TNFα treatment.</p

The members of the miR-200 family and related differentially expressed mRNA network are implicated in insulin signaling in the cortex of 10-month-old Tg2576 mice.

<p>(A) Volcano plot showing microarray data of significantly upregulated miRNAs in the cortices of 10-month-old (10 mo.) Tg2576 mice as compared to wild-type (WT) mice. The threshold values for fold change were set at > 2 or < 0.5 (outside the vertical lines) and P value < 0.05 (above the horizontal line); red points in the plots represent the significant differentially expressed miRNA. The miRNAs that were upregulated were members of the miR-200 and miR-183 families. (B) qRT-PCR was used to validate the upregulation of miR-200 family members using TaqMan assays. The upregulation of members of this miRNA family was confined to the 10 mo. period, a phase during which Aβ accumulation increases. (C) The top network of differentially expressed mRNA as identified by IPA analysis of the microarray data. Up- and down- regulated genes are colored in yellow and blue, respectively. Solid and dashed arrows indicate direct and indirect connections, respectively. Subscripted numbers indicate fold change. The network involves components of the insulin signaling pathway.</p

Defensive effect of microRNA-200b/c against amyloid-beta peptide-induced toxicity in Alzheimer's disease models

<div><p>MiRNA molecules are important post-transcriptional regulators of gene expression in the brain function. Altered miRNA profiles could represent a defensive response against the pathogenesis of neurodegenerative disorders, such as Alzheimer's disease (AD). Endogenous miRNAs have lower toxic effects than other gene silencing methods, thus enhancing the expression of defensive miRNA could be an effective therapy. However, little is known about the potential of targeting miRNAs for the treatment of AD. Here, we examined the function of the miR-200 family (miR-200a, -141, -429, -200b, -200c), identified using miRNA microarray analysis of cortical tissue from Tg2576 transgenic mice. In murine primary neurons, we found that upregulation of miR-200b or -200c was induced by the addition of amyloid beta (Aβ). Neurons transfected with miR-200b or -200c reduced secretion of Aβ in conditioned medium. Moreover, mice infused with miR-200b/c into the brain were relieved of memory impairments induced by intracerebroventricular injection of oligomeric Aβ, and demonstrated proper spatial learning in the Barnes maze. To gain further understanding of the relationship between miR-200b/c and Aβ, we identified target mRNAs via an RNA-binding protein immunoprecipitation-microarray assay. Western blot analysis showed that expression of ribosomal protein S6 kinase B1 (S6K1), a candidate target, was inhibited by miR-200c. S6K1, a downstream effector of mammalian target of rapamycin (mTOR), serves as a negative feedback mediator that phosphorylates insulin receptor substrate 1 at serine residues (IRS-1pSer). S6K1-dependent IRS-1pSer suppresses insulin signaling leading to insulin resistance, which is frequently observed in AD brains. Notably, miR-200b/c transfection of SH-SY5Y cells reduced the levels of IRS-1pSer. This finding indicates that miR-200b/c has the potential to alleviate insulin resistance via modulation of S6K1. Taken together, miR-200b/c may contribute to reduce Aβ secretion and Aβ-induced cognitive impairment by promoting insulin signaling.</p></div

Additional file 1 of Plasma microRNA biomarker detection for mild cognitive impairment using differential correlation analysis

Supplement A. Scatterplots and ROC curves for each of top 20 pairs of miRNAs selected by differential correlation analysis between Normal and MCI. (PDF 63.2 kb