Electronic Commerce Fraud: Towards an Understanding of the Phenomenon

The objective of this paper is to determine the factors that contribute to electronic commerce fraud. We present a model that identifies five causes: the incentives of criminals, the characteristics of victims, the role of technology, the role of enforcement, and system related factors. The Internet has lowered the barriers to entry for criminal enterprises. Victims are unable to determine which sites are real and which ones are fraudulent and lack of reporting further facilitates this type of crime. The lack of enforcement, resulting from inadequate resources and laws, contributes to the lowering of entry barriers to fraudulent businesses. An analysis of FTC cases shows that most crimes are not technologically sophisticated and that greater awareness and experience with this type of schemes people will avoid being victimized

Evaluasi Padang Penggembalaan Alami Maronggela Di Kabupaten Ngada Provinsi Nusa Tenggara Timur

 Evaluasi terhadap padang penggembalaan alami untuk memperbaiki kualitas hijauan merupakan salah satustrategi penting dalam peningkatan produksi ternak ruminansia. Penelitian ini bertujuan untuk menyediakandatabase tentang kondisi padang penggembalaan serta pengelolaan padang penggembalaan yang baik di KabupatenNgada. Kabupateng Ngada merupakan daerah yang sangat potensial bagi pengembangan ternak sapi karenamemiliki padang penggembalaan yang luas. Penelitian dilakukan di padang penggembalaan alami MaronggelaKabupaten Ngada, Provinsi Nusa Tenggara Timur, yang berlangsung selama 2 musim, yaitu pada akhir musimhujan (bulan Maret) dan akhir musim kemarau (bulan Oktober). Peubah yang diamati pada penelitian ini adalahkomposisi botani dan kualitas hijauan. Padang penggembalaan alami Maronggela didominasi oleh hijauan jenisImperata cylindrica dan Themeda aguens, produksi dan kualitas hijauan tertinggi di akhir musim hujan, sertaproduksi dan kualitas terendah di akhir musim kemarau. Daya tampung padang penggembalaan alami Maronggeladalam satu tahun adalah 1,5 satuan ternak. Kata kunci: database, padang pengembalaan, sap

(-)-Epigallocatechin-3-gallate (EGCG) maintains k-casein in its pre-fibrillar state without redirecting its aggregation pathway

The polyphenol (-)-epigallocatechin-3-gallate (EGCG) has recently attracted much research interest in the field of protein-misfolding diseases because of its potent anti-amyloid activity against amyloid-beta, alpha-synuclein and huntingtin, the amyloid-fibril-forming proteins involved in Alzheimer\u27s, Parkinson\u27s and Huntington\u27s diseases, respectively. EGCG redirects the aggregation of these polypeptides to a disordered off-folding pathway that results in the formation of non-toxic amorphous aggregates. whether this anti-fibril activity is specific to these disease-related target proteins or ismore generic remains to be established. In addition, the mechanism by which EGCG exerts its effects, as with all anti-amyloidogenic polyphenols, remains unclear. To address these aspects, we have investigated the ability of EGCG to inhibit amyloidogenesis of the generic model fibril-forming protein RCMkappa-CN (reduced and carboxymethylated kappa-casein) and thereby protect pheochromocytoma-12 cells from RCMkappa-CN amyloid-induced toxicity. We found that EGCG potently inhibits in vitro fibril formation byRCMkappa-CN [the IC50 for 50 uM RCMkappa-CN is 1 uM]. Biophysical studies reveal that EGCG prevents RCMkappa-CN fibril formation by stabilising RCMkappa-CN in its nativelike state rather than by redirecting its aggregation to the disordered, amorphous aggregation pathway. Thus, while it appears that EGCG is a generic inhibitor of amyloid-fibril formation, the mechanism by which it achieves this inhibition is specific to the target fibril-forming polypeptide. It is proposed that EGCG is directed to the amyloidogenic sheet-turn-sheet motif of monomeric RCMkappa-CN with high affinity by strong non-specific hydrophobic associations. Additional non-covalent pi-pi stacking interactions between the polyphenolic and aromatic residues common to the amyloidogenic sequence are also implicated

(-)-Epigallocatechin-3-gallate (EGCG) maintains k-casein in its pre-fibrillar state without redirecting its aggregation pathway

The polyphenol (-)-epigallocatechin-3-gallate (EGCG) has recently attracted much research interest in the field of protein-misfolding diseases because of its potent anti-amyloid activity against amyloid-beta, alpha-synuclein and huntingtin, the amyloid-fibril-forming proteins involved in Alzheimer\u27s, Parkinson\u27s and Huntington\u27s diseases, respectively. EGCG redirects the aggregation of these polypeptides to a disordered off-folding pathway that results in the formation of non-toxic amorphous aggregates. whether this anti-fibril activity is specific to these disease-related target proteins or ismore generic remains to be established. In addition, the mechanism by which EGCG exerts its effects, as with all anti-amyloidogenic polyphenols, remains unclear. To address these aspects, we have investigated the ability of EGCG to inhibit amyloidogenesis of the generic model fibril-forming protein RCMkappa-CN (reduced and carboxymethylated kappa-casein) and thereby protect pheochromocytoma-12 cells from RCMkappa-CN amyloid-induced toxicity. We found that EGCG potently inhibits in vitro fibril formation byRCMkappa-CN [the IC50 for 50 uM RCMkappa-CN is 1 uM]. Biophysical studies reveal that EGCG prevents RCMkappa-CN fibril formation by stabilising RCMkappa-CN in its nativelike state rather than by redirecting its aggregation to the disordered, amorphous aggregation pathway. Thus, while it appears that EGCG is a generic inhibitor of amyloid-fibril formation, the mechanism by which it achieves this inhibition is specific to the target fibril-forming polypeptide. It is proposed that EGCG is directed to the amyloidogenic sheet-turn-sheet motif of monomeric RCMkappa-CN with high affinity by strong non-specific hydrophobic associations. Additional non-covalent pi-pi stacking interactions between the polyphenolic and aromatic residues common to the amyloidogenic sequence are also implicated

Broadband, picosecond two-stage optical parametrical chirped pulse amplification system at 100 Hz

We report on a broadband, picosecond two-stage optical parametrical chirped pulse amplification system, pumped at 515 nm by a frequency doubled Yb regenerative amplifier. The system, designed to be part of the new petawatt picosecond front end, delivers 30  μJ pulses at a central wavelength of 870 nm with about 200 nm bandwidth at 100 Hz. The overall efficiency of the system (pump signal) is 8% while the second stage presents ∼17% conversion efficiency

Kranc: a Mathematica application to generate numerical codes for tensorial evolution equations

We present a suite of Mathematica-based computer-algebra packages, termed "Kranc", which comprise a toolbox to convert (tensorial) systems of partial differential evolution equations to parallelized C or Fortran code. Kranc can be used as a "rapid prototyping" system for physicists or mathematicians handling very complicated systems of partial differential equations, but through integration into the Cactus computational toolkit we can also produce efficient parallelized production codes. Our work is motivated by the field of numerical relativity, where Kranc is used as a research tool by the authors. In this paper we describe the design and implementation of both the Mathematica packages and the resulting code, we discuss some example applications, and provide results on the performance of an example numerical code for the Einstein equations.Comment: 24 pages, 1 figure. Corresponds to journal versio

In vitro studies of the neuroprotective activities of astaxanthin and fucoxanthin against amyloid beta (Aβ1-42) toxicity and aggregation

Crown Copyright © 2019 Published by Elsevier Ltd. This manuscript version is made available under the CC-BY-NC-ND 4.0 license: http://creativecommons.org/licenses/by-nc-nd/4.0/ This author accepted manuscript is made available following 12 month embargo from date of publication (January 2019) in accordance with the publisher’s archiving policyAmyloid beta (Aβ) can aggregate and form plaques, which are considered as one of the major hallmarks of Alzheimer's disease. This study aims to directly compare the neuroprotective activities in vitro of two marine-derived carotenoids astaxanthin and fucoxanthin that have shown a spectrum of biological activities, including neuroprotection. The in vitro neuroprotective activities were investigated against Aβ1-42-mediated toxicity in pheochromocytoma (PC-12) neuronal cells using the MTT cell viability assay, anti-apoptotic, antioxidant and neurite outgrowth activities; as well as inhibition against Aβ1-42 fibrillization in the Thioflavin T (ThT) assay of fibril kinetics and via transmission electron microscopic (TEM) evaluation of fibril morphology. The results demonstrated that both astaxanthin and fucoxanthin exhibited multi-neuroprotective effects favouring fucoxanthin over astaxanthin supporting neuroprotective roles of marine-derived carotenoids as potential novel dementia prevention or therapeutic strategies

New reactivity at the silicon bridge in sila[1]ferrocenophanes

Two new types of reactivity involving silicon-bridged [1]ferrocenophanes are described.</p