Improving Recall of Regular Expressions for Information Extraction

Learning or writing regular expressions to identify instances of a specific
concept within text documents with a high precision and recall is challenging.
It is relatively easy to improve the precision of an initial regular expression
by identifying false positives covered and tweaking the expression to avoid the
false positives. However, modifying the expression to improve recall is difficult
since false negatives can only be identified by manually analyzing all documents,
in the absence of any tools to identify the missing instances. We focus on partially
automating the discovery of missing instances by soliciting minimal user
feedback. We present a technique to identify good generalizations of a regular
expression that have improved recall while retaining high precision. We empirically
demonstrate the effectiveness of the proposed technique as compared to
existing methods and show results for a variety of tasks such as identification of
dates, phone numbers, product names, and course numbers on real world datasets

Following instructions from working memory: Why does action at encoding and recall help?

Two experiments investigated the consequences of action at encoding and recall on the ability to follow sequences of instructions. Children aged 7–9 years recalled sequences of spoken action commands under presentation and recall conditions that either did or did not involve their physical performance. In both experiments, recall was enhanced by carrying out the instructions as they were being initially presented and also by performing them at recall. In contrast, the accuracy of instruction-following did not improve above spoken presentation alone, either when the instructions were silently read or heard by the child (Experiment 1), or when the child repeated the spoken instructions as they were presented (Experiment 2). These findings suggest that the enactment advantage at presentation does not simply reflect a general benefit of a dual exposure to instructions, and that it is not a result of their self-production at presentation. The benefits of action-based recall were reduced following enactment during presentation, suggesting that the positive effects of action at encoding and recall may have a common origin. It is proposed that the benefits of physical movement arise from the existence of a short-term motor store that maintains the temporal, spatial, and motoric features of either planned or already executed actions.

Vasodilator-Stimulated Phosphoprotein (VASP)-dependent and -independent pathways regulate thrombin-induced activation of Rap1b in platelets

Background: Vasodilator-Stimulated Phosphoprotein (VASP) is involved in the inhibition of agonist-induced platelet aggregation by cyclic nucleotides and the adhesion of platelets to the vascular wall. αIIbβ3 is the main integrin responsible for platelet activation and Rap1b plays a key role in integrin signalling. We investigated whether VASP is involved in the regulation of Rap1b in platelets since VASP-null platelets exhibit augmented adhesion to endothelial cells in vivo.

Methods: Washed platelets from wild type and VASP-deficient mice were stimulated with thrombin, the purinergic receptors agonist ADP, or the thromboxane A2 receptor agonist U46619 and Rap1b activation was measured using the GST-RalGDS-RBD binding assay. Interaction of VASP and Crkl was investigated by co-immunoprecipitation, confocal microscopy, and pull-down assays using Crkl domains expressed as GST-fusion proteins.

Results: Surprisingly, we found that activation of Rap1b in response to thrombin, ADP, or U46619 was significantly reduced in platelets from VASP-null mice compared to platelets from wild type mice. However, inhibition of thrombin-induced activation of Rap1b by nitric oxide was similar in platelets from wild type and VASP-null mice indicating that the NO/cGMP/PKG pathway controls inhibition of Rap1b independently from VASP. To understand how VASP regulated Rap1b, we investigated association between VASP and the Crk-like protein (Crkl), an adapter protein which activates the Rap1b guanine nucleotide exchange factor C3G. We demonstrated the formation of a Crkl/VASP complex by showing that: 1) Crkl co-immunoprecipitated VASP from platelet lysates; 2) Crkl and VASP dynamically co-localized at actin-rich protrusions reminiscent of focal adhesions, filopodia, and lamellipodia upon platelet spreading on fibronectin; 3) recombinant VASP bound directly to the N-terminal SH3 domain of Crkl; 4) PKA-mediated VASP phosphorylation on Ser157 abrogated the binding of Crkl.

Conclusions: We identified Crkl as a novel protein interacting with VASP in platelets. We propose that the C3G/Crkl/VASP complex plays a role in the regulation of Rap1b and this explains, at least in part, the reduced agonist-induced activation of Rap1b in VASP-null platelets. In addition, the fact that PKA-dependent VASP phosphorylation abrogated its interaction with Crkl may provide, at least in part, a rationale for the PKA-dependent inhibition of Rap1b and platelet aggregation.