VictorJuiz/thesis huggingface dataset:
Reduced complexity robust MIMO transceiver design [electronic resource]

In this thesis, we design receivers and transmitters without the assumption of perfect channel state information (CSI). This is important because in practice, obtaining error-free CSI is impossible due to measurement errors, quantization errors and many other sources of errors. The main bulk of this thesis focuses on the multiple-input multiple-output (MIMO) wireless communication systems, with a chapter being dedicated to the distributed wireless communication systems (DWCS). In the study of the MIMO system, we make use of the estimated CSI and the statistics of the estimation errors to design receiver and to jointly design transmitter-receiver in order to minimize the symbol error rate (SER) performance. Our proposed receiver is known as the robust sphere decoder; it is near-optimal in the SER sense and has significantly reduced complexity when compared to the exact maximum-likelihood (ML) decoder. Our proposed joint transmitter-receiver scheme is an adaptive scheme which adapts to estimated CSI and error statistics. The proposed scheme reduces the computational complexity of decoding whilst improving the SER performance over the best decoding scheme (exact ML decoding) without transmitter CSI. In the study of the DWCS, we consider the problem of minimizing transmit power in the downlink scenario. We account for the power used in both channel estimation and data transmission, We formulate the problem and propose solution strategies for both single-user and multi-user cases. We demonstrate that the proposed schemes significantly outperform the baseline scheme of equal power allocation.

Keywords: Electrical Engineering
Advisor: Boyd Stephen P. primary advisor. Thesis advisor
Goldsmith Andrea
Katti Sachin advisor. Thesis advisor
Paulraj Arogyaswami advisor. Thesis advisor
Regularity theory for the symmetric minimal surface equation [electronic resource]

We consider the solutions of the symmetric minimal surface equation (SME), the geometric significance of which is that such solutions have symmetric graphs, which are minimal hypersurfaces. The SME has been previously studied by Dierkes, Huisken, and Simon. Using the uniform Holder continuity estimate for positive bounded solutions proved by Simon, we are able to define a singular solution of the SME as local uniform limits of sequences of positive solutions of the SME. Next, we study the existence of singular solutions, beginning with the observation that, by standard ODE theory, one-dimensional singular solutions do not exist. However we will show, via a Leray-Schauder argument, that in all dimensions greater than one there is rich class of singular solutions. Having established an existence theory for the SME, we focus on studying the regularity and singularity properties of singular solutions of the SME. More or less standard quasilinear elliptic theory shows that for any bounded positive solution of the SME there are local gradient bounds, and for positive solutions defined on the closure of a smooth convex domain there is a global gradient bound, depending only on the supremum and infimum of the solution and the domain. For singular solutions (or classes of positive solutions without a uniform positive lower bound), it will be shown that there is a local gradient estimate in a neighborhood of any singular point, depending only on the supremum of the solution and the distance of the singular point and the boundary of the domain. To establish these latter gradient estimates, we will use a modification of Simon's blow up of the Jacobi field argument together with the work of Ilmanen. As a consequence of gradient estimates, we are then able to show, via an application of the Federer dimension reducing argument, that the Hausdorff dimension of the singular set of an n-dimensional SME is at most n-2.

Keywords: Mathematics
Advisor: Brendle Simon
Simon L. (Leon)
Schoen Richard (Richard M.) advisor. Thesis advisor
White Brian
Regularization methods and algorithms for noisy output signals and high-dimensional input vectors [electronic resource]

Input-output models with high-dimensional input vectors arise in many applications, such as microarray technology and portfolio risk management, where the dimensionality of the input vectors far exceeds the sample size. Noise in the output signals further complicates the fitting of these models. There has been a large literature to address the computational and statistical difficulties in fitting these models by using regularization methods. After a brief review of the regularization methods in the literature, we develop a new hybrid of L1 and L2 penalties and demonstrate its advantages over a previous proposal, the elastic net, to combine the L1 and L2 penalties. The statistical theory underlying the hybrid penalty is used to show when and how it can provide improvement over existing methods. We use recent advances in convex optimization to implement the proposed method and carry out simulation studies to compare its performance with other methods.

Keywords: Management Science and Engineering
Advisor: Lai T. L. primary advisor. Thesis advisor
Ye Yinyu primary advisor. Thesis advisor
Saunders Michael
Regulation of adult stem cell function and identity by a histone variant and polycomb group proteins in the drosophila testis [electronic resource]

Many adult tissues with short-lived cells such as blood and skin require a constant replacement of aging cells. This process is often accomplished by adult stem cells, both self-renew and give rise to differentiating progeny. The process of self-renewal and differentiation must be tightly controlled: failure to self-renew results in the loss of the stem cell population, and lack of differentiation impairs tissue function with dire consequences to the organism. The fate decisions of stem cells are guided by the interaction between extracellular signals from the local microenvironment and intrinsic factors that set the state of the cell, many of which are coordinated by transcriptional programs that are, in turn, is controlled by posttranslational modifications of histones or replacement of canonical histones with histone variants. Polycomb group (PcG) proteins partake in the modification of histones and influence the transcriptional state of genes. PcG proteins are involved in transcriptional regulation by inducing the methylation and ubiquitination of histone tails, which maintain the repression of target genes through cell divisions. Emerging evidence indicates that replacement of canonical histones with histone variants is also important in cell fate decisions. Here I show that PcG proteins Psc and Su(z)2 restrict proliferation and maintain the identity of the cyst stem cell (CySC) lineage in the Drosophila testis. Loss of Psc and Su(z)2 gene function in CySC but not in the germline stem cell (GSC) lineage resulted in the formation of a tumor composed of proliferative mutant cells of abnormal identity, likely due to the derepression of the Hox gene Abdominal-B. The resulting formation of tumor-like masses of proliferative cells interfered non-cell autonomously with maintenance of the germline most likely by displacing GSCs from their niche. I also show that the histone variant His2Av is required cell-autonomously for maintenance of adult stem cells in both somatic and germ cell lineages. GSCs lacking His2Av function were lost over time. Surprisingly, GSCs null mutant for His2Av gave rise to germ cells that underwent normal transit amplification divisions and differentiation to spermatocytes and spermatids. Similarly, CySCs lacking His2Av were also lost over time, but were able to give rise to differentiated cyst cells. My results indicate that His2Av and Stat92E likely maintain GSCs and CySCs independently. His2Av mutant GSCs expressed Stat92E and had properly oriented centrosomes, while Stat92E mutant GSCs expressed His2Av. My results expand knowledge chromatin states required for adult stem cell function, showing, for the first time, that a histone variant has a unique role in maintaining stem cells.

Keywords: Developmental Biology.
Advisor: Brown Bryan
Fuller Margaret
Lipsick Joseph Steven
Villeneuve Anne
Wysocka Joanna
Regulation of meiotic recombination [electronic resource] : DNA double-strand break formation and repair in C. elegans

Sexually reproducing organisms undergo meiotic recombination to increase genetic diversity and to ensure correct segregation of chromosomes at the first meiotic division. During meiotic recombination, DNA double-strand breaks (DSBs) are deliberately induced, and a subset of the breaks are repaired as inter-homolog crossovers (COs). Inter-homolog COs provide physical connections between homologous chromosomes that enable them to segregate away from each other. Despite reliance on COs for chromosome segregation, few COs are made per chromosome pair, implying mechanisms for robust CO control. In addition, DNA breaks are potentially dangerous lesions, therefore DSB formation and repair must be tightly regulated, both to ensure the formation of COs, but also to protect against deleterious effects. This thesis provides new insights into mechanisms that regulate DSB formation and repair, using the nematode Caenorhabditis elegans as a model organism. CO regulation mechanisms were probed by monitoring the repair outcome of a DSB induced at a defined site at different stages of meiotic progression, in WT and mutant situations. This analysis uncovered a previously unappreciated level of control in restricting CO number, which is to limit the duration of access to the homolog as a repair template. In addition, this work showed that when no competing breaks are present, a single induced DSB is converted to a CO with high efficiency. This feature helps achieve CO assurance. Insights into regulation of DSB formation were uncovered from the identification and characterization of novel protein DSB-2. DSB-2 is required for break formation, but is dispensable for later steps of meiotic recombination. DSB-2 localizes to chromatin during the time of break formation, suggesting it acts to promote competence for DSB formation. Both approaches presented in this thesis uncovered evidence for negative feedback regulatory mechanisms, suggesting a model wherein formation of CO-eligible recombination intermediates signals shutdown of DSB formation as well as shutdown of inter-homolog access. The proposed regulatory networks provide a mechanism to both ensure sufficient breaks and COs are made, and to shut down these processes to prevent deleterious effects as meiosis progresses.

Keywords: Genetics
Advisor: Villeneuve Anne
Cimprich Karlene advisor. Thesis advisor
Fire Andrew Zachary advisor. Thesis advisor
Lipsick Joseph Steven
Regulation of stem cell self-renewal by microRNAs [electronic resource]

Stem cell self-renewal is dynamically regulated in response to extrinsic stimuli, but the intrinsic mechanisms that mediate the effects of these stimuli remain elusive. Emerging evidence suggests that miRNAs, an abundant class of ~22-nt small regulatory RNAs, play key roles in controlling the post-transcriptional genetic programs in stem and progenitor cells. We systematically examined miRNA expression profiles in various normal and aberrant adult tissue-specific stem and progenitor cells. Delineation of miRNAs whose expression correlated with changes in the self-renewal properties during normal development and as the result of mutant perturbations permitted the identification of miRNAs that marked stem to progenitor transition, termed SPT-miRNAs. Expression of SPT-miRNAs correlated with the exit from a self-renewing state as well as reduced self-renewal capacity in various normal and leukemia stem cells, suggesting that they may play a role in post-transcriptional gene silencing of key mediators of stem cell self-renewal. Consistent with this hypothesis, premature expression of a subset of these miRNAs could diminish the reconstitution potential of hematopoietic stem cells (HSCs) and the self-renewal of embryonic stem cells (ESCs). Furthermore, SPT-miRNAs targeted genes necessary for the self-renewal of HSCs, suggesting that up-regulation of these miRNAs permitted the efficient silencing of self-renewal programs during the stem to progenitor transition. Given the functional overlap of SPT-miRNAs in both embryonic and adult stem cells, we hypothesized that the expression of some SPT-miRNAs may be actively repressed by extrinsic signaling cues in stem cells at multiple developmental stages to potentiate their self-renewal. By subjecting ESCs to various culture conditions that diminished their self-renewal efficiency, we observed an up-regulation of a subset of SPT-miRNAs; in particular, members of the miR-181 family. Ectopic expression of this miRNA reduced ESC self-renewal whereas its deletion augmented ESC self-renewal in serum-free medium. These changes in self-renewal were attributable to simultaneous modulation of ESC proliferation and lineage commitment via target interactions with Lin28A, Spry4, and Dusp6. Finally, we found that the BMP-signaling pathway, necessary for the efficient self-renewal of ESCs, played a key role in the suppression of miR-181a. Collectively, these results reveal how extrinsic signaling cues mediate the quantitative post-transcriptional regulation of stem cell self-renewal programs via the modulation of miRNAs. Our study demonstrated one approach to identify and investigate the role of intrinsic regulators and provided novel insight into how to uncover the intrinsic regulators of stem cell self-renewal with implications on manipulation of stem cell expansion ex vivo.

Keywords: Immunology.
Advisor: Chen Chang-Zheng primary advisor. Thesis advisor
Cleary Michael L. advisor. Thesis advisor
Fuller Margaret
Longaker Michael T.
Sage Julien advisor. Thesis advisor
Reprogramming of fibroblasts to a neural fate [electronic resource]

Cellular differentiation and lineage commitment are considered to be robust and irreversible processes during development. However, recent work has shown that mouse and human fibroblasts can be reprogrammed to a pluripotent state with a combination of four transcription factors. This raised the question of whether transcription factors could directly induce other defined somatic cell fates, and not only an undifferentiated state. We hypothesized that combinatorial expression of neural-lineage-specific transcription factors could directly convert fibroblasts into neurons. Starting from a pool of nineteen candidate genes, we identified a combination of only three factors, Ascl1, Brn2 (also called Pou3f2) and Myt1l that suffice to rapidly and efficiently convert mouse embryonic and postnatal fibroblasts into functional neurons in vitro. These induced neuronal (iN) cells express multiple neuron-specific proteins, generate action potentials and form functional synapses. Similar methods can also convert human fibroblasts to functional iN cells, by forced expression of Ascl1, Brn2, Myt1l and NeuroD1. Generation of iN cells from non-neural lineages could have important implications for studies of neural development, neurological disease modelling and regenerative medicine.

Advisor: Wernig Marius primary advisor. Thesis advisor
Beachy Philip Arden advisor. Thesis advisor
Chang Howard
Wysocka Joanna
Responding to the Monetary Superpower Investigating the Behavioral Spillovers of U.S. Monetary Policy

Between 2002 and 2006, the United States Federal Reserve set interest rates significantly below the rates suggested by well-known monetary policy rules. There is a growing body of research suggesting that this helped fuel an excess of liquidity in the U.S. that contributed to the 2008 worldwide financial crash. What is less well known is that a number of other central banks also lowered interest rates during this period. An important question, then, is what role the Federal Reserve played in influencing other central banks to alter their own monetary policies, which could have magnified the Fed’s actions in creating global liquidity. This paper addresses the issue by showing how spillovers in central bank behavior occur in theoretical rational expectations models. It then establishes empirically how U.S. monetary policy actions affect the actions of other major central banks, particularly in terms of interest rates and currency interventions. The data suggest that the U.S. lowering its policy rate, in general or in reference to a specific monetary policy rule, influences other central banks to lower their own policy rates and intervene in currency markets, even when controlling for worldwide macroeconomic trends. Finally, this paper shows that spillovers from U.S. actions are partially responsible for the worldwide lowering of interest rates and the increase in currency reserves in the early 2000’s that may have contributed to the subsequent worldwide liquidity boom.

Keywords:  Department of Economics
Stanford Department of Economics
United States
Federal Reserve
interest rates
monetary policy
excess liquidity
2008 financial crash
spillover effects
rational expectations
Thesis
Advisor: Taylor John B.
Resting networks in primary insomnia [electronic resource]

Insomnia is a prevalent and costly disorder of sleep-related distress, yet little is known about its etiology. To better understand the neurobiology underlying insomnia, we examined resting state and directed sleep brain activity in insomniacs and healthy controls using simultaneous blood oxygen level-dependent (BOLD) signal functional magnetic resonance imaging (fMRI) and electroencephalography (EEG). Using dual regression analysis of BOLD signal brain networks derived from independent component analysis, we found increased coactivation of the insula in salience networks in insomniacs compared to healthy controls. This increase was accompanied by altered EEG power in insomniacs compared to healthy controls, as well as altered BOLD connectivity signatures of EEG frequency bands. These results suggest that aberrant connectivity of the insula and salience networks contribute to neural dysfunction in insomnia.

Keywords: Psychology
Advisor: Gotlib Ian H. primary advisor. Thesis advisor
Knutson Brian advisor. Thesis advisor
Wagner Anthony David advisor. Thesis advisor
The rilp-like proteins and ciliary trafficking [electronic resource]

Primary cilia have critical sensory and signaling roles in development and disease. These functions rely on the proper localization of structural and signaling proteins to the cilium. Ciliary trafficking is the movement of proteins to, within, and from the cilium, processes that are regulated by several classes of proteins, for example: endo- and exocytic machinery, diffusion barriers, and motor proteins. To understand how ciliary trafficking is regulated we used gene expression data from multi-ciliated cells to identify two proteins involved in ciliary trafficking: the Rilp-like proteins Rilpl1 and Rilpl2. We took three approaches to characterizing these proteins: 1) examining localization of Rilpl1 and Rilpl2 in mammalian cells, 2) determining the phenotype of cells depleted of Rilpl1 and/or Rilpl2, and 3) identifying interaction partners. We found that Rilpl2 is up-regulated during ciliogenesis and localizes to the centrosome and primary cilium. Rilpl1 also localizes to the primary cilium and is a distal mother centriole protein with cell-cycle dependent localization. Additionally, Rilp-like proteins form dynamic tubules from the base of the cilium, which are microtubule dependent and induced by disruption of the actin network. Depletion of Rilpl1 and/or Rilpl2 from ciliated cells leads to an accumulation of signaling proteins in the ciliary membrane and disrupts epithelial cell organization in three-dimensional culture. We also determined that both Rilpl1 and Rilpl2 interact with Rab36. Taken together, our data suggest that Rilp-like proteins control ciliary protein content through the regulation of ciliary protein removal.

Advisor: Stearns Tim primary advisor. Thesis advisor
Nelson W. J. (W. James) advisor. Thesis advisor
Oro Anthony
Sage Julien advisor. Thesis advisor
RNA-mediated programming of active chromatin [electronic resource]

Various long noncoding RNAs (lncRNAs) have been recently identified, but their functions remain unknown. To better understand the role of lncRNAs in gene activation, we have characterized a 3.76 kilobase highly conserved lncRNA, called HOTTIP, found at the 5' distal tip of the HoxA locus. HOTTIP is required for the expression of HoxA9 to HoxA13 in human fibroblasts and chicken embryos. This region spans a linear 40 kilobases, but forms a compact three dimensional DNA structure by high throughput chromosome conformation capture. Knockdown of HOTTIP causes loss of the activating histone H3K4 trimethylation mark, as well as lost occupancy of the MLL methylase complex by chromatin immunoprecipitation coupled with tiling microarray analysis. To cause these changes, HOTTIP binds WDR5, a component of the MLL complex, to alter histone H3K4 trimethylation and gene activation. Together, the characterization of HOTTIP demonstrates an example of lncRNA-mediated epigenetic activation. A close examination of the binding interaction between HOTTIP and WDR5 has further revealed a novel pathway of lncRNA-regulated proteolysis. HOTTIP acts as a "molecular switch, " causing increased WDR5 protein levels by preventing proteasomal degradation through thermodynamic stabilization post poly-ubiquitination. Increased WDR5 deposition then causes gene activation. One HOTTIP RNA binds a single WDR5 protein through a direct RNA-protein interaction, and RNA-mediated stabilization requires a specific HOTTIP RNA domain in a long RNA context. Using a small scale alanine scanning mutagenesis screen, the HOTTIP binding interface on WDR5 has been identified as the cleft between blades 5 and 6. WDR5 mutations that abrogate lncRNA binding cannot be stabilized by HOTTIP, and are defective in gene activation, maintenance of histone H3K4 trimethylation, and embryonic stem cell self renewal. By altering protein turnover, lncRNAs may be able to regulate the temporal landscape of proteins in cells, potentially altering epigenetic states and cellular functions.

Advisor: Chang Howard
Khavari Paul A. advisor. Thesis advisor
Kim Seung K. advisor. Thesis advisor
Wysocka Joanna
Robust trajectory optimization and control of a dynamic soaring unmanned aerial vehicle [electronic resource]

A robust trajectory optimization method is formulated using a stochastic collocation based approach and is then applied to the design of periodic dynamic soaring trajectories for unmanned aerial vehicles (UAVs). Repetitive control is proposed and evaluated as a means for reducing tracking error for UAVs flying periodic trajectories both in simulation and experimentally. Experiments conducted in an indoor flying laboratory outfitted with a VICON motion capture system demonstrate significant reductions in tracking error even in the presence of large and unknown disturbances.

Keywords: Aeronautics and Astronautics
Advisor: Kroo Ilan primary advisor. Thesis advisor
Alonso Juan José
Bieniawski Stefan Richard advisor. Thesis advisor
Rock Stephen M. advisor. Thesis advisor