Integrity protection for code-on-demand mobile agents in e-commerce

The mobile agent paradigm has been proposed as a promising solution to facilitate distributed computing over open and heterogeneous networks. Mobility, autonomy, and intelligence are identified as key features of mobile agent systems and enabling characteristics for the next-generation smart electronic commerce on the Internet. However, security-related issues, especially integrity protection in mobile agent technology, still hinder the widespread use of software agents: from the agent’s perspective, mobile agent integrity should be protected against attacks from malicious hosts and other agents. In this paper, we present Code-on-Demand(CoD) mobile agents and a corresponding agent integrity protection scheme. Compared to the traditional assumption that mobile agents consist of invariant code parts, we propose the use of dynamically upgradeable agent code, in which new agent function modules can be added and redundant ones can be deleted at runtime. This approach will reduce the weight of agent programs, equip mobile agents with more flexibility, enhance code privacy and help the recoverability of agents after attack. In order to meet the security challenges for agent integrity protection, we propose agent code change authorization protocols and a double integrity verification scheme. Finally, we discuss the Java implementation of CoD mobile agents and integrity protection

ACER eNews Issue 04 April 2013

Cell mechanics, in particular mechanical properties, has been suggested as a new biomarker indicative of cell state and phenotype. Acute myeloid leukemia (AML) is characterized by the abnormal increase of myeloblasts in blood and bone marrow. While AML has been extensively studied from the perspectives of biochemical and genetic aspects, little is known about its cellular biophysical properties. In this study, optical tweezer technology was used to examine the micromechanical properties of myeloblasts from bone marrow of AML patients at single cell level. The myeloblasts were separately analyzed according to their expression of CD34 +, a marker of primitive hematopoietic cells. To extract the intrinsic properties from the relationship between the stretching force and the induced deformation, a theoretical approach was developed to model the mechanical responses of cells and further characterize their mechanical properties. The preliminary results show that the area compressibility modulus of CD34 + myeloblasts was significantly less than that of CD34 - cells, which indicate that micromechanical properties are unique features of myeloblasts and provide us with an insight into the cell mechanics of primitive AML cells. © 2010 IEEE.published_or_final_versio

Thermoresponsive block copolymers of increasing architecture complexity: a review on structure-property relationships

Thermogels are an exciting class of stimuli responsive materials with many promising applications ranging from the medical field to additive manufacturing. This review focuses on the structure–property relationship of thermoresponsive block copolymers, with emphasis on the effect of architecture. Polymers based on Pluronic®, N-isopropylacrylamide, oligo(ethylene glycol) (meth)acrylate units, and 2-oxazoline units, which are amongst the most studied thermoresponsive units, are discussed. The effect of the polymer's architecture is crucial for controlling the thermoresponsive properties, such as cloud point and gelation temperature

Orphan receptor GPR110, an oncogene overexpressed in lung and prostate cancer

<p>Abstract</p> <p>Background</p> <p>GPR110 is an orphan G protein-coupled receptor--a receptor without a known ligand, a known signaling pathway, or a known function. Despite the lack of information, one can assume that orphan receptors have important biological roles. In a retroviral insertion mutagenesis screen in the mouse, we identified GPR110 as an oncogene. This prompted us to study the potential isoforms that can be gleaned from known GPR110 transcripts, and the expression of these isoforms in normal and transformed human tissues.</p> <p>Methods</p> <p>Various epitope-tagged isoforms of GPR110 were expressed in cell lines and assayed by western blotting to determine cleavage, surface localization, and secretion patterns. GPR110 transcript and protein levels were measured in lung and prostate cancer cell lines and clinical samples, respectively, by quantitative PCR and immunohistochemistry.</p> <p>Results</p> <p>We found four potential splice variants of GPR110. Of these variants, we confirmed three as being expressed as proteins on the cell surface. Isoform 1 is the canonical form, with a molecular mass of about 100 kD. Isoforms 2 and 3 are truncated products of isoform 1, and are 25 and 23 kD, respectively. These truncated isoforms lack the seven-span transmembrane domain characteristic of GPR proteins and thus are not likely to be membrane anchored; indeed, isoform 2 can be secreted. Compared with the median gene expression of ~200 selected genes, GPR110 expression was low in most tissues. However, it had higher than average gene expression in normal kidney tissue and in prostate tissues originating from older donors. Although identified as an oncogene in murine T lymphomas, GPR110 is greatly overexpressed in human lung and prostate cancers. As detected by immunohistochemistry, GPR110 was overexpressed in 20 of 27 (74%) lung adenocarcinoma tissue cores and in 17 of 29 (59%) prostate adenocarcinoma tissue cores. Additionally, staining with a GPR110 antibody enabled us to differentiate between benign prostate hyperplasia and potential incipient malignancy.</p> <p>Conclusion</p> <p>Our work suggests a role for GPR110 in tumor physiology and supports it as a potential therapeutic candidate and disease marker for both lung and prostate cancer.</p

Intervention effects of Ganoderma lucidum spores on epileptiform discharge hippocampal neurons and expression of Neurotrophin-4 and N-Cadherin

Epilepsy can cause cerebral transient dysfunctions. Ganoderma lucidum spores (GLS), a traditional Chinese medicinal herb, has shown some antiepileptic effects in our previous studies. This was the first study of the effects of GLS on cultured primary hippocampal neurons, treated with Mg2+ free medium. This in vitro model of epileptiform discharge hippocampal neurons allowed us to investigate the anti-epileptic effects and mechanism of GLS activity. Primary hippocampal neurons from <1 day old rats were cultured and their morphologies observed under fluorescence microscope. Neurons were confirmed by immunofluorescent staining of neuron specific enolase (NSE). Sterile method for GLS generation was investigated and serial dilutions of GLS were used to test the maximum non-toxic concentration of GLS on hippocampal neurons. The optimized concentration of GLS of 0.122 mg/ml was identified and used for subsequent analysis. Using the in vitro model, hippocampal neurons were divided into 4 groups for subsequent treatment i) control, ii) model (incubated with Mg2+ free medium for 3 hours), iii) GLS group I (incubated with Mg2+ free medium containing GLS for 3 hours and replaced with normal medium and incubated for 6 hours) and iv) GLS group II (neurons incubated with Mg2+ free medium for 3 hours then replaced with a normal medium containing GLS for 6 hours). Neurotrophin-4 and N-Cadherin protein expression were detected using Western blot. The results showed that the number of normal hippocampal neurons increased and the morphologies of hippocampal neurons were well preserved after GLS treatment. Furthermore, the expression of neurotrophin-4 was significantly increased while the expression of N-Cadherin was decreased in the GLS treated group compared with the model group. This data indicates that GLS may protect hippocampal neurons by promoting neurotrophin-4 expression and inhibiting N-Cadherin expression

Nanoparticles of Block Ionomer Complexes from Double Hydrophilic Poly(acrylic acid)-b-poly(ethylene oxide)-b-poly(acrylic acid) Triblock Copolymer and Oppositely Charged Surfactant

The novel water-dispersible nanoparticles from the double hydrophilic poly(acrylic acid)-b-poly(ethylene oxide)-b-poly(acrylic acid) (PAA-b-PEO-b-PAA) triblock copolymer and oppositely charged surfactant dodecyltrimethyl ammonium bromide (DTAB) were prepared by mixing the individual aqueous solutions. The structure of the nanoparticles was investigated as a function of the degree of neutralization (DN) by turbidimetry, dynamic light scattering (DSL),ζ-potential measurement, and atomic force microscope (AFM). The neutralization of the anionic PAA blocks with cationic DTAB accompanied with the hydrophobic interaction of alkyl tails of DTAB led to formation of core–shell nanoparticles with the core of the DTAB neutralized PAA blocks and the shell of the looped PEO blocks. The water-dispersible nanoparticles with negative ζ-potential were obtained over the DN range from 0.4 to 2.0 and their sizes depended on the DN. The looped PEO blocks hindered the further neutralization of the PAA blocks with cationic DTAB, resulting in existence of some negative charged PAA-b-PEO-b-PAA backbones even when DN > 1.0. The spherical and ellipsoidal nature of these nanoparticles was observed with AFM

Tau in cerebrospinal fluid induces neuronal hyperexcitability and alters hippocampal theta oscillations

Alzheimer’s disease (AD) and other tauopathies are characterized by the aggregation of tau into soluble and insoluble forms (including tangles and neuropil threads). In humans, a fraction of both phosphorylated and non-phosphorylated N-terminal to mid-domain tau species, are secreted into cerebrospinal fluid (CSF). Some of these CSF tau species can be measured as diagnostic and prognostic biomarkers, starting from early stages of disease. While in animal models of AD pathology, soluble tau aggregates have been shown to disrupt neuronal function, it is unclear whether the tau species present in CSF will modulate neural activity. Here, we have developed and applied a novel approach to examine the electrophysiological effects of CSF from patients with a tau-positive biomarker profile. The method involves incubation of acutely-isolated wild-type mouse hippocampal brain slices with small volumes of diluted human CSF, followed by a suite of electrophysiological recording methods to evaluate their effects on neuronal function, from single cells through to the network level. Comparison of the toxicity profiles of the same CSF samples, with and without immuno-depletion for tau, has enabled a pioneering demonstration that CSF-tau potently modulates neuronal function. We demonstrate that CSF-tau mediates an increase in neuronal excitability in single cells. We then observed, at the network level, increased input–output responses and enhanced paired-pulse facilitation as well as an increase in long-term potentiation. Finally, we show that CSF-tau modifies the generation and maintenance of hippocampal theta oscillations, which have important roles in learning and memory and are known to be altered in AD patients. Together, we describe a novel method for screening human CSF-tau to understand functional effects on neuron and network activity, which could have far-reaching benefits in understanding tau pathology, thus allowing for the development of better targeted treatments for tauopathies in the future. Graphical Abstract: [Figure not available: see fulltext.