Directing and Combining Multiple Queries for Exploratory Search by Visual Interactive Intent Modeling

In interactive information-seeking, a user often performs many interrelated queries and interactions covering multiple aspects of a broad topic of interest. Especially in difficult information-seeking tasks the user may need to find what is in common among such multiple aspects. Therefore, the user may need to compare and combine results across queries. While methods to combine queries or rankings have been proposed, little attention has been paid to interactive support for combining multiple queries in exploratory search. We introduce an interactive information retrieval system for exploratory search with multiple simultaneous search queries that can be combined. The user is able to direct search in the multiple queries, and combine queries by two operations: intersection and difference, which reveal what is relevant to the user intent of two queries, and what is relevant to one but not the other. Search is directed by relevance feedback on visualized user intent models of each query. Operations on queries act directly on the intent models inferring a combined user intent model. Each combination yields a new result (ranking) and acts as a new search that can be interactively directed and further combined. User experiments on difficult information-seeking tasks show that our novel system with query operations yields more relevant top-ranked documents in a shorter time than a baseline multiple-query system.Peer reviewe

Patient appointment scheduling system: with supervised learning prediction

Large waiting times at hospital outpatient clinics are a cause of dissatisfaction to patients, cause additional stress to hospital staff, increase the risk of contagion and add complications for patients with medical conditions. Reducing waiting times and surgeon idle time improves the quality of service and efficiency of a hospital: this is a recently growing focus in healthcare. Oulu hospital wants to identify and reduce large waiting times at their out-patient clinic. For the past few years the clinic has used a self-service system whereby patients register on arrival and hospital staff use a patient call-in system. The past schedules are analyzed using this data: information visualizations and performance measures are provided. The worst performing clinic sessions are the subject of the scheduling optimization prototype system. The scheduling optimization focuses on predicting the duration of an appointment and the late arrival of the surgeon. These two factors have been identified as causes of long patient waiting times. The variance of the duration is identified to be high, therefore supervised-learning regression is used for both simple inference and prediction. The features that are good predictors and the results of the prediction accuracy are reported. With the predicted appointment durations, and surgeon arrival times, a scheduling optimization approach is used to improve the existing schedule; a simple greedy hill-climbing approach is evaluated. It is found that using the historical data to simulate a real day, appointment rules and scheduling optimization the patient waiting time is reduced with this method. Showing the system to be potentially promising

Cotranscriptional Set2 Methylation of Histone H3 Lysine 36 Recruits a Repressive Rpd3 Complex

SummaryThe yeast histone deacetylase Rpd3 can be recruited to promoters to repress transcription initiation. Biochemical, genetic, and gene-expression analyses show that Rpd3 exists in two distinct complexes. The smaller complex, Rpd3C(S), shares Sin3 and Ume1 with Rpd3C(L) but contains the unique subunits Rco1 and Eaf3. Rpd3C(S) mutants exhibit phenotypes remarkably similar to those of Set2, a histone methyltransferase associated with elongating RNA polymerase II. Chromatin immunoprecipitation and biochemical experiments indicate that the chromodomain of Eaf3 recruits Rpd3C(S) to nucleosomes methylated by Set2 on histone H3 lysine 36, leading to deacetylation of transcribed regions. This pathway apparently acts to negatively regulate transcription because deleting the genes for Set2 or Rpd3C(S) bypasses the requirement for the positive elongation factor Bur1/Bur2

Cotranscriptional Set2 Methylation of Histone H3 Lysine 36 Recruits a Repressive Rpd3 Complex

SummaryThe yeast histone deacetylase Rpd3 can be recruited to promoters to repress transcription initiation. Biochemical, genetic, and gene-expression analyses show that Rpd3 exists in two distinct complexes. The smaller complex, Rpd3C(S), shares Sin3 and Ume1 with Rpd3C(L) but contains the unique subunits Rco1 and Eaf3. Rpd3C(S) mutants exhibit phenotypes remarkably similar to those of Set2, a histone methyltransferase associated with elongating RNA polymerase II. Chromatin immunoprecipitation and biochemical experiments indicate that the chromodomain of Eaf3 recruits Rpd3C(S) to nucleosomes methylated by Set2 on histone H3 lysine 36, leading to deacetylation of transcribed regions. This pathway apparently acts to negatively regulate transcription because deleting the genes for Set2 or Rpd3C(S) bypasses the requirement for the positive elongation factor Bur1/Bur2

A Single cis Element Maintains Repression of the Key Developmental Regulator Gata2

In development, lineage-restricted transcription factors simultaneously promote differentiation while repressing alternative fates. Molecular dissection of this process has been challenging as transcription factor loci are regulated by many trans-acting factors functioning through dispersed cis elements. It is not understood whether these elements function collectively to confer transcriptional regulation, or individually to control specific aspects of activation or repression, such as initiation versus maintenance. Here, we have analyzed cis element regulation of the critical hematopoietic factor Gata2, which is expressed in early precursors and repressed as GATA-1 levels rise during terminal differentiation. We engineered mice lacking a single cis element −1.8 kb upstream of the Gata2 transcriptional start site. Although Gata2 is normally repressed in late-stage erythroblasts, the −1.8 kb mutation unexpectedly resulted in reactivated Gata2 transcription, blocked differentiation, and an aberrant lineage-specific gene expression pattern. Our findings demonstrate that the −1.8 kb site selectively maintains repression, confers a specific histone modification pattern and expels RNA Polymerase II from the locus. These studies reveal how an individual cis element establishes a normal developmental program via regulating specific steps in the mechanism by which a critical transcription factor is repressed

An acetylation-mediated chromatin switch governs H3K4 methylation read-write capability

In nucleosomes, histone N-terminal tails exist in dynamic equilibrium between free/accessible and collapsed/DNA-bound states. The latter state is expected to impact histone N-termini availability to the epigenetic machinery. Notably, H3 tail acetylation (e.g. K9ac, K14ac, K18ac) is linked to increased H3K4me3 engagement by the BPTF PHD finger, but it is unknown if this mechanism has a broader extension. Here, we show that H3 tail acetylation promotes nucleosomal accessibility to other H3K4 methyl readers, and importantly, extends to H3K4 writers, notably methyltransferase MLL1. This regulation is not observed on peptide substrates yet occurs on the cis H3 tail, as determined with fully-defined heterotypic nucleosomes. In vivo, H3 tail acetylation is directly and dynamically coupled with cis H3K4 methylation levels. Together, these observations reveal an acetylation ‘chromatin switch’ on the H3 tail that modulates read-write accessibility in nucleosomes and resolves the long-standing question of why H3K4me3 levels are coupled with H3 acetylation

Negative relevance feedback for exploratory search with visual interactive intent modelling

Peer reviewe

Scalable Probabilistic Matrix Factorization with Graph-Based Priors

In matrix factorization, available graph side-information may not be well suited for the matrix completion problem, having edges that disagree with the latent-feature relations learnt from the incomplete data matrix. We show that removing these $\textit{contested}$ edges improves prediction accuracy and scalability. We identify the contested edges through a highly-efficient graphical lasso approximation. The identification and removal of contested edges adds no computational complexity to state-of-the-art graph-regularized matrix factorization, remaining linear with respect to the number of non-zeros. Computational load even decreases proportional to the number of edges removed. Formulating a probabilistic generative model and using expectation maximization to extend graph-regularised alternating least squares (GRALS) guarantees convergence. Rich simulated experiments illustrate the desired properties of the resulting algorithm. On real data experiments we demonstrate improved prediction accuracy with fewer graph edges (empirical evidence that graph side-information is often inaccurate). A 300 thousand dimensional graph with three million edges (Yahoo music side-information) can be analyzed in under ten minutes on a standard laptop computer demonstrating the efficiency of our graph update.Comment: Under revie

CCR4/NOT complex associates with the proteasome and regulates histone methylation

The proteasome regulates histone lysine methylation and gene transcription, but how it does so is poorly understood. To better understand this process, we used the epistatic miniarray profile (E-MAP) approach to identify factors that genetically interact with proteasomal subunits. In addition to members of the Set1 complex that mediate histone H3 lysine 4 methylation (H3K4me), we found that deleting members of the CCR4/NOT mRNA processing complex exhibit synthetic phenotypes when combined with proteasome mutants. Further biochemical analyses revealed physical associations between CCR4/NOT and the proteasome in vivo. Consistent with the genetic and biochemical interactions linking CCR4/NOT with proteasome and Set1-mediated methylation, we find that loss of Not4 decreases global and gene-specific H3K4 trimethylation (H3K4me3) and decreases 19S proteasome recruitment to the PMA1 gene. Similar to proteasome regulation of histone methylation, loss of CCR4/NOT members does not affect ubiquitinated H2B. Mapping of Not4 identified the RING finger domain as essential for H3K4me3, suggesting a role for ubiquitin in this process. Consistent with this idea, loss of the Not4-interacting protein Ubc4, a known ubiquitin-conjugating enzyme, decreases H3K4me3. These studies implicate CCR4/NOT in the regulation of H3K4me3 through a ubiquitin-dependent pathway that likely involves the proteasome