Comparisons of Our Scheme with the Main References.

<p>Comparisons of Our Scheme with the Main References.</p

Flowchart of attack model 2.

<p>Flowchart of attack model 2.</p

The performance of CP-ABE.

<p>The performance of CP-ABE.</p

Comparisons of Computational Complexity.

<p>Comparisons of Computational Complexity.</p

System model of the proposed scheme.

<p>System model of the proposed scheme.</p

File Storage Format in CS.

<p>File Storage Format in CS.</p

Flowchart of Our Proposed Scheme.

<p>Flowchart of Our Proposed Scheme.</p

Understanding individual-level protective responses to air pollution warning: A case study of Beijing, China

<p>Air pollution is harmful to human health; effective interventions are therefore, needed for health protection. The aim of this study was to explore the main protective measures taken by residents under air pollution warnings, and the factors that affect warning response and mode of intervention. Descriptive statistics, independent sample <i>t</i>-tests, and binary logit models were used to analyze the data obtained from the respondents. The results demonstrate the different levels of air pollution warning were correctly understood, but that the warning response rate was nevertheless low. Television and the Internet were the primary sources for receiving warnings and related information about protective measures. Major measures taken by respondents included wearing smog masks, modifying diet, using air filters, and reducing the time spent outdoors. Warning response is associated with knowledge of warning, perception of health risks of air pollution, and gender of respondents. The research also revealed that protective measures taken by male and female respondents were influenced by different sets of factors. This study clarify the factors that determine whether residents take protective measures in response to warnings, and the strategic interventions necessary to warn people effectively. Policy makers can use this research to improve the effectiveness of air pollution warnings.</p

Islet Amyloid Polypeptide Membrane Interactions: Effects of Membrane Composition

Amyloid formation by islet amyloid polypeptide (IAPP) contributes to β-cell dysfunction in type 2 diabetes. Perturbation of the β-cell membrane may contribute to IAPP-induced toxicity. We examine the effects of lipid composition, salt, and buffer on IAPP amyloid formation and on the ability of IAPP to induce leakage of model membranes. Even low levels of anionic lipids promote amyloid formation and membrane permeabilization. Increasing the percentage of the anionic lipids, 1-palmitoyl-2-oleoyl-<i>sn</i>-glycero-3-phospho-l-serine (POPS) or 1,2-dioleoyl-<i>sn</i>-glycero-3-phospho­(1′-<i>rac</i>-glycerol), enhances the rate of amyloid formation and increases the level of membrane permeabilization. The choice of zwitterionic lipid has no noticeable effect on membrane-catalyzed amyloid formation but in most cases affects leakage, which tends to decrease in the following order: 1,2-dioleoyl-<i>sn</i>-glycero-3-phosphocholine > 1-palmitoyl-2-oleoyl-<i>sn</i>-glycero-3-phosphocholine > sphingomyelin. Uncharged lipids that increase the level of membrane order weaken the ability of IAPP to induce leakage. Leakage is due predominately to pore formation rather than complete disruption of the vesicles under the conditions used in these studies. Cholesterol at or below physiological levels significantly reduces the rate of vesicle-catalyzed IAPP amyloid formation and decreases the susceptibility to IAPP-induced leakage. The effects of cholesterol on amyloid formation are masked by 25 mol % POPS. Overall, there is a strong inverse correlation between the time to form amyloid and the extent of vesicle leakage. NaCl reduces the rate of membrane-catalyzed amyloid formation by anionic vesicles, but accelerates amyloid formation in solution. The implications for IAPP membrane interactions are discussed, as is the possibility that the loss of phosphatidylserine asymmetry enhances IAPP amyloid formation and membrane damage <i>in vivo</i> via a positive feedback loop

Analysis of the Role of the Conserved Disulfide in Amyloid Formation by Human Islet Amyloid Polypeptide in Homogeneous and Heterogeneous Environments

Human islet amyloid polypeptide (hIAPP) is a hormone secreted from β-cells in the Islets of Langerhans in response to the same stimuli that lead to insulin secretion. hIAPP plays an adaptive role in glucose homeostasis but misfolds to form insoluble, fibrillar aggregates in type II diabetes that are associated with the disease. Along the misfolding pathway, hIAPP forms species that are toxic to β-cells, resulting in reduced β-cell mass. hIAPP contains a strictly conserved disulfide bond between residues 2 and 7, which forms a small loop at the N-terminus of the molecule. The loop is located outside of the cross β-core in all models of the hIAPP amyloid fibrils. Mutations in this region are rare, and the disulfide loop plays a role in receptor binding; however, the contribution of this region to the aggregation of hIAPP is not well understood. We define the role of the disulfide by analyzing a collection of analogues that remove the disulfide, by mutation of Cys to Ser, by reduction and modification of the Cys residues, or by deletion of the first seven residues. The cytotoxic properties of hIAPP are retained in the Cys to Ser disulfide-free mutant. Removal of the disulfide bond accelerates amyloid formation in all constructs, both in solution and in the presence of model membranes. Removal of the disulfide weakens the ability of hIAPP to induce leakage of vesicles consisting of POPS and POPC. Smaller effects are observed with vesicles that contain 40 mol % cholesterol, although N-terminal truncation still reduces the extent of leakage