Proceedings of the 19th ACM SIGKDD international conference on Knowledge discovery and data mining - KDD '13, 2013
We present a novel learning algorithm, DirectRank, which directly and exactly optimizes ranking m... more We present a novel learning algorithm, DirectRank, which directly and exactly optimizes ranking measures without resorting to any upper bounds or approximations. Our approach is essentially an iterative coordinate ascent method. In each iteration, we choose one coordinate and only update the corresponding parameter, with all others remaining fixed. Since the ranking measure is a stepwise function of a single parameter, we propose a novel line search algorithm that can locate the interval with the best ranking measure along this coordinate quite efficiently. In order to stabilize our system in small datasets, we construct a probabilistic framework for document-query pairs to maximize the likelihood of the objective permutation of top-τ documents. This iterative procedure ensures convergence. Furthermore, we integrate regression trees as our weak learners in order to consider the correlation between the different features. Experiments on LETOR datasets and two large datasets, Yahoo challenge data and Microsoft 30K web data, show an improvement over state-of-the-art systems.
Journal of cellular and molecular medicine, Jan 16, 2015
Multiple mechanisms contribute to progressive cardiac dysfunction after myocardial infarction (MI... more Multiple mechanisms contribute to progressive cardiac dysfunction after myocardial infarction (MI) and inflammation is an important mediator. Mast cells (MCs) trigger inflammation after MI by releasing bio-active factors that contribute to healing. c-Kit-deficient (Kit(W/W-v) ) mice have dysfunctional MCs and develop severe ventricular dilatation post-MI. We explored the role of MCs in post-MI repair. Mouse wild-type (WT) and Kit(W/W-v) MCs were obtained from bone marrow (BM). MC effects on fibroblasts were examined in vitro by proliferation and gel contraction assays. MCs were implanted into infarcted mouse hearts and their effects were evaluated using molecular, cellular and cardiac functional analyses. In contrast to WT, Kit(W/W-v) MC transplantation into Kit(W/W-v) mice did not improve cardiac function or scar size post-MI. Kit(W/W-v) MCs induced significantly reduced fibroblast proliferation and contraction compared to WT MCs. MC influence on fibroblast proliferation was Basic ...
After a myocardial infarction, thinning and expansion of the fibrotic scar contribute to progress... more After a myocardial infarction, thinning and expansion of the fibrotic scar contribute to progressive heart failure. The loss of elastin is a major contributor to adverse extracellular matrix remodelling of the infarcted heart, and restoration of the elastic properties of the infarct region can prevent ventricular dysfunction. We implanted cells genetically modified to overexpress elastin to re-establish the elastic properties of the infarcted myocardium and prevent cardiac failure. A full-length human elastin cDNA was cloned, subcloned into an adenoviral vector and then transduced into rat bone marrow stromal cells (BMSCs). In vitro studies showed that BMSCs expressed the elastin protein, which was deposited into the extracellular matrix. Transduced BMSCs were injected into the infarcted myocardium of adult rats. Control groups received either BMSCs transduced with the green fluorescent protein gene or medium alone. Elastin deposition in the infarcted myocardium was associated with preservation of myocardial tissue structural integrity (by birefringence of polarized light; P < 0.05 versus controls). As a result, infarct scar thickness and diastolic compliance were maintained and infarct expansion was prevented (P < 0.05 versus controls). Over a 9-week period, rats implanted with BMSCs demonstrated better cardiac function than medium controls; however, rats receiving BMSCs overexpressing elastin showed the greatest functional improvement (P < 0.01). Overexpression of elastin in the infarcted heart preserved the elastic structure of the extracellular matrix, which, in turn, preserved diastolic function, prevented ventricular dilation and preserved cardiac function. This cell-based gene therapy provides a new approach to cardiac regeneration.
Proceedings of the 19th ACM SIGKDD international conference on Knowledge discovery and data mining - KDD '13, 2013
We present a novel learning algorithm, DirectRank, which directly and exactly optimizes ranking m... more We present a novel learning algorithm, DirectRank, which directly and exactly optimizes ranking measures without resorting to any upper bounds or approximations. Our approach is essentially an iterative coordinate ascent method. In each iteration, we choose one coordinate and only update the corresponding parameter, with all others remaining fixed. Since the ranking measure is a stepwise function of a single parameter, we propose a novel line search algorithm that can locate the interval with the best ranking measure along this coordinate quite efficiently. In order to stabilize our system in small datasets, we construct a probabilistic framework for document-query pairs to maximize the likelihood of the objective permutation of top-τ documents. This iterative procedure ensures convergence. Furthermore, we integrate regression trees as our weak learners in order to consider the correlation between the different features. Experiments on LETOR datasets and two large datasets, Yahoo challenge data and Microsoft 30K web data, show an improvement over state-of-the-art systems.
Journal of cellular and molecular medicine, Jan 16, 2015
Multiple mechanisms contribute to progressive cardiac dysfunction after myocardial infarction (MI... more Multiple mechanisms contribute to progressive cardiac dysfunction after myocardial infarction (MI) and inflammation is an important mediator. Mast cells (MCs) trigger inflammation after MI by releasing bio-active factors that contribute to healing. c-Kit-deficient (Kit(W/W-v) ) mice have dysfunctional MCs and develop severe ventricular dilatation post-MI. We explored the role of MCs in post-MI repair. Mouse wild-type (WT) and Kit(W/W-v) MCs were obtained from bone marrow (BM). MC effects on fibroblasts were examined in vitro by proliferation and gel contraction assays. MCs were implanted into infarcted mouse hearts and their effects were evaluated using molecular, cellular and cardiac functional analyses. In contrast to WT, Kit(W/W-v) MC transplantation into Kit(W/W-v) mice did not improve cardiac function or scar size post-MI. Kit(W/W-v) MCs induced significantly reduced fibroblast proliferation and contraction compared to WT MCs. MC influence on fibroblast proliferation was Basic ...
After a myocardial infarction, thinning and expansion of the fibrotic scar contribute to progress... more After a myocardial infarction, thinning and expansion of the fibrotic scar contribute to progressive heart failure. The loss of elastin is a major contributor to adverse extracellular matrix remodelling of the infarcted heart, and restoration of the elastic properties of the infarct region can prevent ventricular dysfunction. We implanted cells genetically modified to overexpress elastin to re-establish the elastic properties of the infarcted myocardium and prevent cardiac failure. A full-length human elastin cDNA was cloned, subcloned into an adenoviral vector and then transduced into rat bone marrow stromal cells (BMSCs). In vitro studies showed that BMSCs expressed the elastin protein, which was deposited into the extracellular matrix. Transduced BMSCs were injected into the infarcted myocardium of adult rats. Control groups received either BMSCs transduced with the green fluorescent protein gene or medium alone. Elastin deposition in the infarcted myocardium was associated with preservation of myocardial tissue structural integrity (by birefringence of polarized light; P < 0.05 versus controls). As a result, infarct scar thickness and diastolic compliance were maintained and infarct expansion was prevented (P < 0.05 versus controls). Over a 9-week period, rats implanted with BMSCs demonstrated better cardiac function than medium controls; however, rats receiving BMSCs overexpressing elastin showed the greatest functional improvement (P < 0.01). Overexpression of elastin in the infarcted heart preserved the elastic structure of the extracellular matrix, which, in turn, preserved diastolic function, prevented ventricular dilation and preserved cardiac function. This cell-based gene therapy provides a new approach to cardiac regeneration.
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Papers by Lily Guo