A Java based software solution for efficient pairing cryptography.

This thesis is concerned with applying software Engineering techniques to pairing based cryptographic systems. In particular we evolve our existing cryptographic system to incorporate new cryptographic concepts that strengthen the system. We discuss the design approach taken to allow an advanced mathematically based cryptographic concept to be developed in a maintainable manner. We present the integration process and evolutionary impacts on the existing system. We provide some testing data on the resulting system and give an indication of its performance. The language chosen is Java and the objective is that the Java developer can easily use the resulting system with minimal knowledge of the underlying machinery. Specifically, we present, implement, and evaluate alternative approaches to the use of a standard implementation of Tate pairing in a Java-based biometric identity verification tool

A Java based software solution for efficient pairing cryptography.

This thesis is concerned with applying software Engineering techniques to pairing based cryptographic systems. In particular we evolve our existing cryptographic system to incorporate new cryptographic concepts that strengthen the system. We discuss the design approach taken to allow an advanced mathematically based cryptographic concept to be developed in a maintainable manner. We present the integration process and evolutionary impacts on the existing system. We provide some testing data on the resulting system and give an indication of its performance. The language chosen is Java and the objective is that the Java developer can easily use the resulting system with minimal knowledge of the underlying machinery. Specifically, we present, implement, and evaluate alternative approaches to the use of a standard implementation of Tate pairing in a Java-based biometric identity verification tool

Estrogen Receptor (ER)-α36 Is Involved in Estrogen- and Tamoxifen-Induced Neuroprotective Effects in Ischemic Stroke Models

<div><p>The neuroprotection by estrogen (E2) and tamoxifen is well documented in experimental stroke models; however, the exact mechanism is unclear. A membrane-based estrogen receptor, ER-α36, has been identified. Postmenopausal-levels of E2 act through ER-α36 to induce osteoclast apoptosis due to a prolonged activation of the mitogen-activated protein kinase (MAPK)/extracellular signal-related kinase (ERK) signaling. We hypothesized that ER-α36 may play a role in the neuroprotective activities of estrogen and tamoxifen. Here, we studied ER-α36 expression in the brain, as well as its neuroprotective effects against oxygen and glucose deprivation (OGD) in PC12 cells. We found that ER-α36 was expressed in both rat and human brain. In addition, OGD-induced cell death was prevented by l nmol/L 17β-estradiol (E2β). E2β activates the MAPK/ERK signaling pathway in PC12 cells under basal and OGD conditions by interacting with ER-α36 and also induces ER-α36 expression. Low-dose of tamoxifen up-regulated ER-α36 expression and enhanced neuronal survival in an ovariectomized ischemic stroke model. Furthermore, low-dose of tamoxifen enhanced neuroprotective effects by modulating activates or suppress ER-α36. Our results thus demonstrated that ER-α36 is involved in neuroprotective activities mediated by both estrogen and tamoxifen.</p></div

Expression of ER-α36 and caveolin-1 protein in the human cerebral cortex.

<p>Immunocytochemical staining of ER-α36 (green), caveolin-1 (red), and nuclei (blue) in brain slices at different magnifications. Scale bars = 75 μm/10 μm.</p

Estrogen receptor (ER)-α36 expression in the rat hippocampus.

<p>(<b>A</b>) Hyperfluorescence of ER-α36 expressed in the CA1 and CA3 regions of the rat hippocampus, and co-staining of ER-α36 with the neuronal marker, NeuN. (<b>B</b>) Nissl staining of the hippocampus. (<b>C</b>) Statistical analysis of ER-α36 expression. Scale bar = 200 μm (200×), <i>n</i> = 3. *<i>p</i> < 0.05, **<i>p</i> < 0.01.</p

The ischemic brain of the MCAO model.

<p>Ischemia-reperfusion produced infarcts in the rat hippocampus, cortex and striatum. Red arrows show that ATP activity was decreased in the injured hippocampal CA1 region, as revealed by ATPase staining.</p

ER-α36 is involved in mitogen-activated protein kinase (MAPK) signaling pathway activation.

<p>(<b>A</b>) Low-dose E2β-induced activation of MAPK in PC12 cells under non-injury conditions. (B) Low-dose E2β induced activation of the ER-α36 promoter. The results represent a percentage of the control values (no exposure to OGD), expressed as mean ± standard deviation (<i>s</i>.<i>d</i>.; n = 3). *<i>p</i> < 0.05 vs. control.</p

Diagram of the neuroprotective effects of estrogen and TAM.

<p>Diagram of the neuroprotective effects of estrogen and TAM.</p