Accelerating magnetic induction tomography‐based imaging through heterogeneous parallel computing

Magnetic Induction Tomography (MIT) is a non‐invasive imaging technique, which has applications in both industrial and clinical settings. In essence, it is capable of reconstructing the electromagnetic parameters of an object from measurements made on its surface. With the exploitation of parallelism, it is possible to achieve high quality inexpensive MIT images for biomedical applications on clinically relevant time scales. In this paper we investigate the performance of different parallel implementations of the forward eddy current problem, which is the main computational component of the inverse problem through which measured voltages are converted into images. We show that a heterogeneous parallel method that exploits multiple CPUs and GPUs can provide a high level of parallel scaling, leading to considerably improved runtimes. We also show how multiple GPUs can be used in conjunction with deal.II, a widely‐used open source finite element library

3, 3′-Diindolylmethane Exhibits Antileukemic Activity In Vitro and In Vivo through a Akt-Dependent Process

3,3′-diindolylmethane (DIM), one of the active products derived from Brassica plants, is a promising antitumor agent. The present study indicated that DIM significantly induced apoptosis in U937 human leukemia cells in dose- and time-dependent manners. These events were also noted in other human leukemia cells (Jurkat and HL-60) and primary human leukemia cells (AML) but not in normal bone marrow mononuclear cells. We also found that DIM-induced lethality is associated with caspases activation, myeloid cell leukemia-1 (Mcl-1) down-regulation, p21cip1/waf1 up-regulation, and Akt inactivation accompanied by c-jun NH2-terminal kinase (JNK) activation. Enforced activation of Akt by a constitutively active Akt construct prevented DIM-mediated caspase activation, Mcl-1 down-regulation, JNK activation, and apoptosis. Conversely, DIM lethality was potentiated by the PI3K inhibitor LY294002. Interruption of the JNK pathway by pharmacologic or genetic approaches attenuated DIM-induced caspases activation, Mcl-1 down-regulation, and apoptosis. Lastly, DIM inhibits tumor growth of mouse U937 xenograft, which was related to induction of apoptosis and inactivation of Akt, as well as activation of JNK. Collectively, these findings suggest that DIM induces apoptosis in human leukemia cell lines and primary human leukemia cells, and exhibits antileukemic activity in vivo through Akt inactivation and JNK activation

Multiple Roles for the Non-Coding RNA SRA in Regulation of Adipogenesis and Insulin Sensitivity

Peroxisome proliferator-activated receptor-γ (PPARγ) is a master transcriptional regulator of adipogenesis. Hence, the identification of PPARγ coactivators should help reveal mechanisms controlling gene expression in adipose tissue development and physiology. We show that the non-coding RNA, Steroid receptor RNA Activator (SRA), associates with PPARγ and coactivates PPARγ-dependent reporter gene expression. Overexpression of SRA in ST2 mesenchymal precursor cells promotes their differentiation into adipocytes. Conversely, knockdown of endogenous SRA inhibits 3T3-L1 preadipocyte differentiation. Microarray analysis reveals hundreds of SRA-responsive genes in adipocytes, including genes involved in the cell cycle, and insulin and TNFα signaling pathways. Some functions of SRA may involve mechanisms other than coactivation of PPARγ. SRA in adipocytes increases both glucose uptake and phosphorylation of Akt and FOXO1 in response to insulin. SRA promotes S-phase entry during mitotic clonal expansion, decreases expression of the cyclin-dependent kinase inhibitors p21Cip1 and p27Kip1, and increases phosphorylation of Cdk1/Cdc2. SRA also inhibits the expression of adipocyte-related inflammatory genes and TNFα-induced phosphorylation of c-Jun NH2-terminal kinase. In conclusion, SRA enhances adipogenesis and adipocyte function through multiple pathways

Diffusion MRI fiber tractography of the brain

The ability of fiber tractography to delineate non-invasively the white matter fiber pathways of the brain raises possibilities for clinical applications and offers enormous potential for neuroscience. In the last decade, fiber tracking has become the method of choice to investigate quantitative MRI parameters in specific bundles of white matter. For neurosurgeons, it is quickly becoming an invaluable tool for the planning of surgery, allowing for visualization and localization of important white matter pathways before and even during surgery. Fiber tracking has also claimed a central role in the field of “connectomics,” a technique that builds and studies comprehensive maps of the complex network of connections within the brain, and to which significant resources have been allocated worldwide. Despite its unique abilities and exciting applications, fiber tracking is not without controversy, in particular when it comes to its interpretation. As neuroscientists are eager to study the brain's connectivity, the quantification of tractography-derived “connection strengths” between distant brain regions is becoming increasingly popular. However, this practice is often frowned upon by fiber-tracking experts. In light of this controversy, this paper provides an overview of the key concepts of tractography, the technical considerations at play, and the different types of tractography algorithm, as well as the common misconceptions and mistakes that surround them. We also highlight the ongoing challenges related to fiber tracking. While recent methodological developments have vastly increased the biological accuracy of fiber tractograms, one should be aware that, even with state-of-the-art techniques, many issues that severely bias the resulting structural “connectomes” remain unresolved