GraphVite: A High-Performance CPU-GPU Hybrid System for Node Embedding

Learning continuous representations of nodes is attracting growing interest in both academia and industry recently, due to their simplicity and effectiveness in a variety of applications. Most of existing node embedding algorithms and systems are capable of processing networks with hundreds of thousands or a few millions of nodes. However, how to scale them to networks that have tens of millions or even hundreds of millions of nodes remains a challenging problem. In this paper, we propose GraphVite, a high-performance CPU-GPU hybrid system for training node embeddings, by co-optimizing the algorithm and the system. On the CPU end, augmented edge samples are parallelly generated by random walks in an online fashion on the network, and serve as the training data. On the GPU end, a novel parallel negative sampling is proposed to leverage multiple GPUs to train node embeddings simultaneously, without much data transfer and synchronization. Moreover, an efficient collaboration strategy is proposed to further reduce the synchronization cost between CPUs and GPUs. Experiments on multiple real-world networks show that GraphVite is super efficient. It takes only about one minute for a network with 1 million nodes and 5 million edges on a single machine with 4 GPUs, and takes around 20 hours for a network with 66 million nodes and 1.8 billion edges. Compared to the current fastest system, GraphVite is about 50 times faster without any sacrifice on performance.Comment: accepted at WWW 201

Roles of Rho small GTPase in zebrafish development

Ph.DDOCTOR OF PHILOSOPH

K-ras/PI3K-Akt Signaling Is Essential for Zebrafish Hematopoiesis and Angiogenesis

The RAS small GTPases orchestrate multiple cellular processes. Studies on knock-out mice showed the essential and sufficient role of K-RAS, but not N-RAS and H-RAS in embryonic development. However, many physiological functions of K-RAS in vivo remain unclear. Using wild-type and fli1:GFP transgenic zebrafish, we showed that K-ras-knockdown resulted in specific hematopoietic and angiogenic defects, including the impaired expression of erythroid-specific gene gata1 and ße3-hemoglobin, reduced blood circulation and disorganized blood vessels. Expression of either K-rasC40 that links to phosphoinositide 3-kinase (PI3K) activation, or Akt2 that acts downstream of PI3K, could rescue both hematopoietic and angiogenic defects in the K-ras knockdown. Consistently, the functional rescue by k-ras mRNA was significantly suppressed by wortmannin, a PI3K-specific inhibitor. Our results provide direct evidence that PI3K-Akt plays a crucial role in mediating K-ras signaling during hematopoiesis and angiogenesis in vivo, thus offering new targets and alternative vertebrate model for studying these processes and their related diseases

Clinical and Prognostic Value of PET/CT Imaging with Combination of 68

Background. To evaluate the clinical and prognostic value of PET/CT with combination of 68Ga-DOTATATE and 18F-FDG in gastroenteropancreatic neuroendocrine neoplasms (GEP-NENs). Method. 83 patients of GEP-NENs who underwent 68Ga-DOTATATE and 18F-FDG PET/CT were enrolled between June 2013 and December 2016. Well-differentiated (WD) NETs are divided into group A (Ki-67 < 10%) and group B (Ki-67 ≥ 10%), and poorly differentiated (PD) NECs are defined as group C. The relationship between PET/CT results and clinicopathological characteristics was retrospectively investigated. Result. For groups A/B/C, the sensitivities of 68Ga-DOTATATE and 18F-FDG were 78.8%/83.3%/37.5% and 52.0%/72.2%/100.0%. A negative correlation between Ki-67 and SUVmax of 68Ga-DOTATATE (R = −0.415; P ≤ 0.001) was observed, while a positive correlation was noted between Ki-67 and SUVmax of 18F-FDG (R = 0.683; P ≤ 0.001). 62.5% (5/8) of patients showed significantly more lesions in the bone if 68Ga-DOTATATE was used, and 22.7% (5/22) of patients showed more lymph node metastases if 18F-FDG was used. Conclusions. The sensitivity of dual tracers was correlated with cell differentiation, and a correlation between Ki-67 and both SUVmax of PET-CTs could be observed. 68Ga-DOTATATE is suggested for WD-NET and 18F-FDG is probably suitable for patients with Ki-67 ≥ 10%

Di(2-ethylhexyl) phthalate induces apoptosis through mitochondrial pathway in GC-2spd cells

Di(2-ethylhexyl) phthalate (DEHP), a plasticizer of synthetic polymers, is a well-known endocrine disrupting chemical (EDC) and reproductive toxicant. Addressing the unclear mechanism of DEHP-induced reproductive dysfunction, this study used GC-2spd cells to investigate the molecular mechanism involved in the DEHP-induced toxicity in the male reproductive system. The results indicated that the apoptotic cell death was significantly induced by DEHP exposure over 100 μM. Furthermore, DEHP treatment could induce oxidative stress in GC-2spd cells involving in the decrease of superoxide dismutase (SOD) activity (200 μM) and glutathione peroxidase (GSH-Px) activity (50 and 100 μM). In addition, DEHP induction also caused the elevated ratios of Bax/Bcl-2, release of cytochrome c and decomposition of procaspase-3 and procaspase-9 in GC-2spd cells. Taken together, our work provided the evidence that DEHP exposure might induce apoptosis of GC-2spd cells via mitochondria pathway mediated by oxidative stress. © 2016 Wiley Periodicals, Inc. Environ Toxicol, 2016

Synergy between loss of NF1 and overexpression of MYCN in neuroblastoma is mediated by the GAP-related domain

Earlier reports showed that hyperplasia of sympathoadrenal cell precursors during embryogenesis in Nf1-deficient mice is independent of Nf1’s role in down-modulating RAS-MAPK signaling. We demonstrate in zebrafish that nf1 loss leads to aberrant activation of RAS signaling in MYCN-induced neuroblastomas that arise in these precursors, and that the GTPase-activating protein (GAP)-related domain (GRD) is sufficient to suppress the acceleration of neuroblastoma in nf1-deficient fish, but not the hypertrophy of sympathoadrenal cells in nf1 mutant embryos. Thus, even though neuroblastoma is a classical “developmental tumor”, NF1 relies on a very different mechanism to suppress malignant transformation than it does to modulate normal neural crest cell growth. We also show marked synergy in tumor cell killing between MEK inhibitors (trametinib) and retinoids (isotretinoin) in primary nf1a-/- zebrafish neuroblastomas. Thus, our model system has considerable translational potential for investigating new strategies to improve the treatment of very high-risk neuroblastomas with aberrant RAS-MAPK activation. DOI: http://dx.doi.org/10.7554/eLife.14713.00