A Study of Very Short Intermittent DDoS Attacks on the Performance of Web Services in Clouds

Distributed Denial-of-Service (DDoS) attacks for web applications such as e-commerce are increasing in size, scale, and frequency. The emerging elastic cloud computing cannot defend against ever-evolving new types of DDoS attacks, since they exploit various newly discovered network or system vulnerabilities even in the cloud platform, bypassing not only the state-of-the-art defense mechanisms but also the elasticity mechanisms of cloud computing. In this dissertation, we focus on a new type of low-volume DDoS attack, Very Short Intermittent DDoS Attacks, which can hurt the performance of web applications deployed in the cloud via transiently saturating the critical bottleneck resource of the target systems by means of external attack HTTP requests outside the cloud or internal resource contention inside the cloud. We have explored external attacks by modeling the n-tier web applications with queuing network theory and implementing the attacking framework based-on feedback control theory. We have explored internal attacks by investigating and exploiting resource contention and performance interference to locate a target VM (virtual machine) and degrade its performance

Management and Deployment of Scientific Applications with SIMULOCEAN Science Gateway

SIMULOCEAN is a web-based scientific application and visualization framework for the management and deployment of software serving the coastal modeling community. The framework helps to collect observational data, schedule modeling codes for execution, manage data transfer, and visualize both observational and numerical results. With all the information collected, SIMULOCEAN can also provide direct validation and verification for models, and generate high quality technical reports. As part of the SIMULOCEAN framework, we developed the Coastal Model Repository (CMR) which is targeting cloud and cloud-like architectures to enable quick deployment of coastal models and their working environments. CMR will serve as a community repository for precompiled open source models that are widely used by coastal researchers. While source code for various executables and libraries will be available, CMR will also introduce distribution of containerized coastal models, which can run on any cloud-like architecture directly, and with negligible system overhead. The idea of containerization of cloud-ready applications is not new, but it has become a viable solution given the rapid development of kernel-level virtualization technologies. One such technology, Docker, is an open platform allowing developers to build, ship, and run distributed applications in self-contained environments. Docker enables executable applications to be quickly assembled from components then run by a user without the need to rebuild or satisfy any external dependencies. As a result, a Docker-enabled app can be reliably executed in a known operating system environment on any system that supports Docker containers. With the help of CMR, a coastal researcher can start running state-of-the-art models on the latest cloud-ready computing systems in minutes. The SIMULOCEAN science gateway can take advantage of CMR to quickly deploy coastal models on academic and commercial cloud platforms, in addition to traditional HPC systems. This work is supported by NSF Award CCF-1539567 and in part by HPC computing resources at LSU. We acknowledge the assistance and support of the CSDMS Integration Facility and XSEDE Extended Collaborative Support Service (ECSS) program

REJ-C1G3 triggers the release of P-TEFb from 7SK snRNP.

<p><b>(A and B)</b> WCE of J-Lat A2 (A) HeLa cells (B) that were either untreated (-) or treated (+) with REJ-C1G3 (20 μM) were analyzed by Western blotting for the indicated proteins (left panels). Anti-CDK9 immunoprecipitates (IP) derived from WCE were tested by Western blotting for presence of the indicated proteins (right panels). The amounts of the CDK9-bound proteins were quantified by densitometry and shown at the bottom. CDK9 in untreated cells (lane 1) was artifically set at 100%.</p

REJ-C1G3 preferentially stimulates the Tat-dependent HIV transcription.

<p><b>(A)</b> The HeLa-based based NH1 and NH2 cells were treated with REJ-C1G3 or DMSO as indicated. WCE were prepared and tested for luciferase activities (top panel) and the celluar tubulin levels detected by Western blotting (bottom panel). The activity detected in cells treated with DMSO was set to 1. The error bars represent mean ± SD from three independent experiments. <b>(B)</b> NH1 cells were transciently transfected with an empty vector (-) or the Tat-expressing construct (+; 10 ng/well) and then treated with REJ-C1G3 or DMSO (-) as indicated. WCE were prepared and tested for luciferase activities as in A. (C) mRNAs transcribed from the integrated HIV-1 LTR-luciferase reporter gene were analyzed by qRT-PCR with primers that hybridize to the three marked locations along the DNA template and then normalized to the levels of GAPDH mRNA. The error bars represent the mean ± SD from three independent measurements.</p

REJ-C1G3 synergizes with prostratin or JQ1 to reactivate latent HIV.

<p><b>(A and B)</b> J-Lat A2 cells were treated with REJ-C1G3 (20 μM) alone or in combination with prostratin (0.25 μM) or JQ1 (1 μM) for 12 hr and then analyzed by flow cytometry for the percentages of EGFP-positive cells in the total cell population. DMSO was used as a negative control. The error bars represent mean ± SD from three independent experiments.</p

A Natural Product from <i>Polygonum cuspidatum</i> Sieb. Et Zucc. Promotes Tat-Dependent HIV Latency Reversal through Triggering P-TEFb’s Release from 7SK snRNP

<div><p>The latent reservoirs of HIV represent a major impediment to eradication of HIV/AIDS. To overcome this problem, agents that can activate latent HIV proviruses have been actively sought after, as they can potentially be used in combination with the highly active antiretroviral therapy (HAART) to eliminate the latent reservoirs. Although several chemical compounds have been shown to activate latency, they are of limited use due to high toxicity and poor clinical outcomes. In an attempt to identify natural products as effective latency activators from traditional Chinese medicinal herbs that have long been widely used in human population, we have isolated procyanidin C-13,3',3"-tri-O-gallate (named as REJ-C1G3) from <i>Polygonum cuspidatum</i> Sieb. et Zucc., that can activate HIV in latently infected Jurkat T cells. REJ-C1G3 preferentially stimulates HIV transcription in a process that depends on the viral encoded Tat protein and acts synergistically with prostratin (an activator of the NF-κB pathway) or JQ1 (an inhibitor of Brd4) to activate HIV latency. Our mechanistic analyses further show that REJ-C1G3 accomplishes these tasks by inducing the release of P-TEFb, a host cofactor essential for Tat-activation of HIV transcription, from the cellular P-TEFb reservoir 7SK snRNP.</p></div

Determination of the purity and structure of REJ-C1G3 and its impact on cell viability.

<p><b>(A)</b> High performance liquid chromatography (HPLC) was performed to confirm the purity of REJ-C1G3. <b>(B)</b> Chemical tructure of REJ-C1G3. <b>(C and D)</b> J-Lat A2 (C) and HeLa cells (D) were exposed to REJ-C1G3 (20 μM) for 5 days and then assayed for cell viability. The error bars represent mean ± SD from three independent experiments.</p

Extracts of <i>Polygonum cuspidatum</i> Sieb. et Zucc. contain an activity that promotes HIV-1 LTR-driven EGFP expression.

<p><b>(A)</b> A flow chart depicting the purification of the active product REJ-C1G3 from the extracts of <i>Polygonum cuspidatum</i> Sieb. et Zucc.. <b>(B-E)</b> During the purification of REJ-C1G3, individual fractions obtained after each chromotography step were tested for their abilities to activate EGFP expression in J-Lat A2 cells. The indicated concentrations of these fractions or 2.5 μM prostratin as a positive control were incubated with J-Lat A2 cells for 12 hr, and the EGFP-positive cells detected by flow cytometry. The percentages of EGFP-expressing cells in the entire viable cell population were shown, with the error bars in all panels indicating mean ± SD from three independent experiments.</p