Welcome! The seminars are held at Rice and we meet usually on Fridays from 2:00 pm to 3:00 pm in Duncan Hall. All times and dates are given below. A Google Calendar of events has also been included below to see future events that might not be posted yet. If you have any questions, please feel free to contact Stephanie Hicks at sch1@rice.edu .
20 November 2009 
2:15pm
	in 1042 DH
Dennis Cox 
Title:
	
Abstract: 
For more information, contact:
	dcox@rice.edu 
	
6 November 2009 
2:15pm
	in 1042 DH
Roberto Bertolusso 
Title:
	
Abstract: 
For more information, contact:
	roberto.bertolusso@rice.edu 
	
16 October 2009 
2:15pm
	in 1042 DH
Bo Peng 
Title:
	
Abstract: 
For more information, contact:
	bpeng@mdanderson.org 
	
18 September 2009 
2pm
	in 1049 DH
Billy Hered 
Title: Using Celltracker
	
Abstract: Celltracker is a program designed to extract intensity data from a series of cell images.  Although the program is able to provide useful information about the relative intensities 
	of the nucleus and cytoplasm over time, gathering the data is a very time intensive task.  This is due mainly to problems with cell boundary detection and declaring the Region of Interest.  When the relative 
	intensities of the nucleus and the cytoplasm were plotted against time, a clear periodic oscillation could be observed in most of the trials.  However, a fair amount of noise was also observed in the data.
	
For more information, contact:
	wah1@rice.edu 
	
4 September 2009 
2:15pm
	in 1042 DH
Marta Iwanaszko 
Title:
	Evolutionary Conservation of Transcription Factor Binding Site in
	the Promoter Regions of NF-KB-dependent Genes 
Abstract:
	N-FKB family plays a prominent role in innate (early) immune
	response and have impact on other processes as cell cycle activation
	or cell apoptosis. Upon stimulation by pathogens such as viral RNA a
	kinase cascade is activated, which eventually strips the NF-KB of
	its inhibitor IKBα molecule and allows it to translocate into the
	nucleus. Once in the nucleus, it activates transcription of
	approximately 90genes, some of which trigger further stages of the
	immune response. NF-KB-dependent genes can be categorized, based on
	the timing of their activation counted from N-FKB translocation into
	the nucleus, as early, middle and late genes.. It is not obvious
	what mechanism is responsible for segregation of the genes’ timing
	of transcriptional response. One likely hypothesis might be that the
	later the gene is, the more co-factors are required to activate it,
	but late response maybe also connected with need of chromatin
	remodeling. It is likely that the differences in timing are
	reflected in differences in the structure of promoter regions of
	genes in different categories. Specifically, this might concern
	differences in number and type of transcription factor binding
	motifs, required for NF-KB itself as well as for the putative
	co-factors. This issue is best considered in the evolutionary
	framework, first, since functional binding sites are likely to be
	conserved in evolution, and second, since the patterns of
	evolutionary change of promoter regions are not very well-known and
	are of serious interest. 
 
For more information, contact:
	miwanaszko@gmail.com 
	
28 August 2009 
2:15
	pm in 1042 DH
Dajiang Liu 
Title:
	Statistical Genomics of Rare Variants 
Abstract: There is
	strong support that quantitative phenotypes can be due to rare
	variants. Next generation sequencing makes it possible to identify
	rare variants, which is the first step to carry-out direct mapping
	association studies of quantitative trait loci (QTL). In designing
	association studies to identify rare variant QTL (rvQTL), sampling
	individuals with extreme quantitative trait values (QTVs) can be
	used to enrich for rare causal variants. In particular rare causal
	variants are more likely to be aggregated in related individuals
	with extreme phenotypes. Although extreme trait ascertainment in
	related individuals has had only limited success in linkage and
	association studies, this design is highly advantageous in the
	analysis of rare variants, because the success of rvQTL mapping is
	highly dependent on causal rare variant enrichment. Collecting a
	specific family type (e.g. discordant sib-pairs) can be difficult
	therefore it is desirable to be able to combine different family
	structures as well as unrelated individuals in the analysis of
	rvQTL. Although methods do exist to analyze QTL due to common
	variants, these methods are underpowered when applied to the
	analysis of rvQTL data, and inflexible for modeling relative
	phenotype correlations due to multiple shared rare variants.
	Additionally these methods cannot combine the analysis of QTL data
	from related and unrelated individuals. We propose a flexible
	likelihood framework with mixed effects for modeling extreme trait
	genetic associations with rvQTL (MEGA-rvQTL) for the analysis of
	related and unrelated individuals with extreme QTVs. MEGA-rvQTL
	detects associations with rvQTL through likelihood ratio tests. A
	unique feature of MEGA-rvQTL is that parameters of genetic interests
	such as heritability and sibling residual correlation can be
	efficiently estimated. We investigated the power of the MEGA-rvQTL
	method, for 7 commonly used prospective selective sampling
	strategies. Simulation was carried out via coalescence theory using
	parameters estimated from population genetic data and heritabilities
	from clinically relevant quantitative traits. We demonstrate that
	analyzing sibpairs with extreme QTVs or using one sib per sibpair
	with extreme QTVs are consistently more powerful than using
	unrelated individuals with extreme QTVs. In conclusion, MEGA-rvQTL
	is a powerful approach to analyze next generation sequence data to
	map QTL due to rare variants by combining data from related and
	unrelated individuals with extreme phenotypes. 
For more
	information, contact: dajiang.liu@gmail.com 
	
21 August 2009 
2pm
	in 1044 DH 
Stephanie Hicks 
Title:
	Predicting Functionality of Missense Mutations with Varying Levels
	of Evolutionary Depth 
Abstract: We investigate three
	computational algorithms, SIFT, Polyphen, and Align-GVGD, that
	predict the impact of missense mutations on protein structure and
	function. Past research has shown a high predictive value for
	methods that use evolutionary sequence conservation, surprisingly
	with or without protein structural information. The goal of the
	study is to investigate the prediction accuracy of functionality of
	missense mutations by using both curated and uncurated alignments of
	varying evolutionary depth. 
For more information, contact:
	sch1@rice.edu 
	
14 August 2009 
3pm
	in 3076 DH 
Kevin Dehoff 
Title:Image
	Processing and Live Cell Tracking 
Abstract: An
	introduction to image processing techniques, object tracking, and
	how these methods are implemented in the Cell Profiler and Cell
	Tracker programs. 
For more information, contact:
	kdhoff@rice.edu 
	
7 August 2009 
2pm
	in 3076 DH 
Biao Li 
Title:
	
Abstract: Theory of multi-type age dependent branching
	process with immigration. Review of techniques in stathmokinetic
	experiments and discussion of its application in estimate of cell
	cycle length parameters in neurogenic system. 
For more
	information, contact: lb4@rice.edu 
	
3 August 2009 
11am
	in 1044 DH 
Rosa Banuelos 
Title:
	
Abstract: 
For more information, contact:
	banuelos@rice.edu 
	
13 July 2009 
2pm
	in 1044 DH
Deborah Goldwasser 
Title:
	Stochastic Modeling of Lung Cancer Screening 
Abstract: We
	evaluate data on tumor size and stage from two data-sets on lung
	cancer screening, namely the Mayo Lung Project and the Mayo CT
	study, in order to examine evidence for and against the bipartite
	model of lung cancer progression. An initial homogeneity analysis of
	the two data-sets suggests the presence of two or more clusters
	having distinct expected mean size at stage transitions. We use a
	model that parameterizes tumor growth and stage transition by the
	evolutionary parameters of branching fraction (f) and the cell
	mutation rate (u) in order to simulate likelihoods for cancers from
	both the MLP and the Mayo CT study. Clustering of MLP cancers based
	on a likelihood-derived similarity matrix indicates the presence of
	two distinct clusters (A and B) having expected mean size at stage
	transition of 94 mm (CI: 64,100) and 6.1 mm (CI: 5,20) respectively.
	The tumor stage and size distribution evident in the Mayo CT results
	are consistent with a reduction in representation of Cluster A
	cancers due to higher sensitivity of the prevalence CT screen and
	detection of Cluster B cancers at smaller sizes. These results
	indicate that a reduction in lung cancer mortality attributable to
	CT may require a lower detection threshold than previously believed.
	
For more information, contact: dlg2004@rice.edu 
	
19 June 2009 
2pm
	in 3110 DH 
Xing Chen 
Title:
	Correlation of tumor size and epidemiological characteristics in
	patients with non-small cell lung cancer: a preliminary study of
	tumor size data 
Abstract: Background: Tumor size at
	diagnosis is not only an indicator for the treatment and prognosis
	of lung cancer, but also an important predictor for the tumor
	growth, metastasis and survival in patients. To our knowledge, the
	distribution of tumor size at diagnosis may reveal the nature
	history of lung cancer. So it’s of great importance to find out
	what factors would influence the tumor size at diagnosis. 
Material
	and methods: Recently, we reviewed the electronic medical records of
	about 1400 patients in M.D. Anderson Cancer Center to collect the
	information about tumor characteristics (with the tumor size of
	radiology and pathology) and patient characteristics (including
	smoking history and vital status with last contact date). We used
	T-test and Kruskal-Wallis test method to explore the relationship
	between the tumor size at diagnosis and the epidemiological
	factors.
Results: Smoking may affect the tumor size at the time
	of diagnosis which leads to larger tumor at presentation (P<0.05).
	There was a difference in tumor size by gender and age (Male 4.40cm
	VS female 3.61cm, mean, P<0.01; Age>65 3.83cm VS age<65
	4.26cm, mean, P<0.01). Besides, lung cancer with emphysema always
	have smaller tumor at presentation than those whom don’t have this
	condition (3.62cm of emphysema VS 4.15cm of non-emphysema, mean,
	P<0.01). The tumor histological results such as cancer cell type
	(Adenocarcinoma 3.40cm VS squamous cell carcinoma 4.45cm, mean,
	P<0.01) and degrees of differentiation (Poorly to not
	differentiated 4.28cm VS moderately to well 3.71cm, mean, P<0.01)
	have relationship with tumor size at presentation. With the
	limitation of ethnic groups (only 147 black compared to 974 white),
	the Africa American have significant larger tumor (P<0.01) at
	diagnose.
Conclusions: According to the data set, tumor size at
	the time of diagnosis is associated with smoking, gender, age,
	ethnicity, tumor histology, and presence of emphysema. 
For
	more information, contact: XChen6@mdanderson.org 
	
8 June 2009 
2pm
	in 1044 DH 
Xiaowei Wu 
Title:
	Bayesian Analysis of Array CGH Data 
Abstract: We propose
	a Bayesian approach to analyze array comparative genomic
	hybridization (CGH) data. Different from most currently available
	methods, this new approach builds a Bayesian hierarchical model for
	the data and use a reversible jump Markov chain Monte Carlo (MCMC)
	algorithm for posterior sampling. The estimated parameters are used
	to identify copy number changes (gains/losses) in the target DNA
	sequence. This method is computationally efficient and is flexible
	to model various covariance structures of the data. Moreover, it
	also has great advantage in analyzing recurrent copy number
	alterations (CNAs) in multiple arrays. Simulation study shows a good
	performance of the proposed method. As a real data analysis example,
	we apply the method to publicly available Corriel cell lines data
	and obtain satisfying results. 
For more information,
	contact: xwwu@rice.edu 
	
22 May 2009 
3:15
	in 1044 DH 
Pawel Paszek 
Title:
	Oscillations and feedback regulation in the NF-KB signaling
	
Abstract: Feedback regulation is a common structural
	motif controlling dynamics of genetic networks. Here we discuss how
	negative and positive feedbacks contribute to the control of
	temporal and spatial activity of transcription factor NF-KappaB in
	immune response and inflammation. We theoretically explore how the
	NF-KB system achieves an intricate level of control by using
	redundant negative feedback loops due to IKBalpha and IKBesilon
	synthesis. We show that the transcriptional time-delay between
	activation of IKBalpha and IKBepsilon feedback loops increases the
	total level of intrinsic noise in the system and thus modulates the
	heterogeneity of NF-KB oscillation timing between individual cells.
	Redundancy in IKB feedback was predicted to allow the system
	achieving more robust responses, through decreasing the sensitivity
	to parameter variation. These data suggest a general mechanism for
	signalling system robustness and control which may also be important
	in other signalling networks. 
For more information, contact:
	paszek@liv.ac.uk 
Centre for Cell Imaging, School of
	Biological Sciences, The Biosciences Building, University of
	Liverpool, Crown St., Liverpool L69 7ZB, UK, Tel: 0151 795 4029 
	
15 May 2009 
2pm
	in 1044 DH 
Biao Li 
Title:
	Review of Branching stochastic processes with immigration in
	analysis of renewing cell populations by Dr. Andrei Yakovlev
	
Abstract: The talk will present and review a paper,
	Branching stochastic processes with immigration in analysis of
	renewing cell populations, which is written by Dr. Andrei Yakovlev.
	The abstract is available on this webpage.
	I will also summarize recent work on computation and programming of
	model of differentiating neuron stem cells. 
Presentation
	
For more information, contact: lb4@rice.edu 
	
8 May 2009 
10am
	in 1075 DH 
Millena Foy 
Title:
	Lung Carcinogenesis Modeling and it's Application 
Abstract:
	Lung cancer is the second leading cancer in terms of incidence for
	both men and women. However, because of its serious health
	implications, lung cancer is the leading cancer killer for both men
	and women. It is well known that smoking is a major risk factor for
	lung cancer. The two-stage clonal expansion (TSCE) will be fit to
	data to determine the effects of smoking on the risk of developing
	lung cancer. This model is then used in the Smoking Base Case
	project, and in an analysis of the effectiveness of CT screening in
	the reduction of lung cancer mortality. 
The TSCE model is
	traditionally fit to prospective cohort data. A new method is
	introduced that allows for the reconstruction of cohort data from
	the combination of risk factor data from a case-control data, and
	tabled incidence/mortality rate data. Simulation study reveals that
	the results of fitting the model using this new method are
	reasonable. The method is used to fit a TSCE model based on smoking
	history. 
The model is then applied to the smoking base case
	project in conjunction with the Smoking Base Case project of the
	CISNET lung group. The results of simulations show that the model
	reasonably reconstructs US mortality. 
Lung carcinogenesis
	modeling provides a framework for simulating lung cancer mortality
	to serve as a surrogate for a control arm in the analyses of the
	effectiveness of lung cancer screening in studies missing a control
	comparison. A previously fit model was used to simulate lung cancer
	mortality in individuals in the absence of screening given their
	particular smoking histories, ages, and genders. The model was used
	to create a pseudo-control arm that is missing from the lung cancer
	screening trial and allowed for a comparison of lung cancer
	mortality. The model shows that CT screening does reduce LC
	mortality. (Due to confidentiality, no actual data will be shown on
	the screening study.) 
For more information, contact:
	mfoy@rice.edu 
	
13 April 2009 
1pm
	in 107 Keck Hall 
Roberto Bertolusso 
Title:
	
Abstract: 
For more information, contact:
	Roberto.Bertolusso@rice.edu 
	
6 April 2009 
1pm
	in 119 HZ 
Xiaowei Wu 
Title:
	Markovian paths to extinction 
Abstract: Subcritical and
	critical Markov branching processes die out sooner or later. This
	talk summarizes some known results about the survival probability,
	the limiting distribution conditional on non-extinction, and
	demonstrates the asymptotic behavior of the time to extinction and
	the path to extinction. These results are verified by simulations.
	
For more information, contact: xwwu@rice.edu 
	
27 March 2009 
1pm
	in 1042 DH 
Elizabeth Jones 
Title:
	Single-cell characterization of heterogeneity of Androgen Receptor
	Activity 
Abstract: Single-cell based studies on nuclear
	receptor (NR) mediated gene activation and regulation demonstrate a
	range of responses to environmental and physiological stimuli not
	previously appreciated by population-based studies. Utilizing
	imaging modalities, including deconvolution, confocal, and automated
	microscopy we can visualize single cells and measure distinct
	cellular responses in an androgen receptor (AR) system. During the
	transcriptional activation process, AR changes spatial organization,
	a microscopically visible process, including nuclear translocation
	and organization into subnuclear speckles. To examine the
	ligand-based population shifts and the variation within the AR
	subcellular trafficking and synthesis of target gene mRNA we
	developed a quantitative biological approach utilizing a
	stably-expressing GFP-AR HeLa cell line. We identify and categorize
	subpopulations of AR-responsive cells during a time- and
	concentration-based series defining measurements that are linked to
	responsive vs. non-responsive cells, and may indicate factors, for
	example cell cycle stage, that could influence sensitivity to
	ligands. Further analysis, both experimentally and mathematically,
	of this data will allow us to quantify individual cellular responses
	and the variation between these responses from a seemingly
	homogenous population. 
For more information, contact:
	edjones@bcm.tmc.edu 
	
20 March 2009 
1:30pm
	in 3092 DH 
Krzysztof Fujarewicz
	
Title: Planning identification experiments for cell
	signaling pathways 
Abstract: Mathematical modeling of
	cell signaling pathways becomes very important and challenging
	problem in recent years. Fitting of the parameters of the model is
	not a trivial problem because of the nature of measurements. The
	blotting techniques usually give only semi-quantitative observations
	which are very noisy and they are collected only at limited number
	of time moments. The accuracy of parameter estimation may be
	significantly improved by proper experiment design. The talk will
	concern the optimal sampling design - one of the aspects of optimal
	experiment design. 
For more information, contact:
	Krzysztof.Fujarewicz@polsl.pl 
	
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