Evaluating the usability of natural language query languages and interfaces to Semantic Web knowledge bases

The need to make the contents of the Semantic Web accessible to end-users becomes increasingly pressing as the amount of information stored in ontology-based knowledge bases steadily increases. Natural language interfaces (NLIs) provide a familiar and convenient means of query access to Semantic Web data for casual end-users. While several studies have shown that NLIs can achieve high retrieval performance as well as domain independence, this paper focuses on usability and investigates if NLIs and natural language query languages are useful from an end-user's point of view. To that end, we introduce four interfaces each allowing a different query language and present a usability study benchmarking these interfaces. The results of the study reveal a clear preference for full natural language query sentences with a limited set of sentence beginnings over keywords or formal query languages. NLIs to ontology-based knowledge bases can, therefore, be considered to be useful for casual or occasional end-users. As such, the overarching contribution is one step towards the theoretical vision of the Semantic Web becoming reality.     

Consensus statement on the diagnosis of multiple system atrophy

We report the results of a consensus conference on the diagnosis of multiple system atrophy (MSA). We describe the clinical features of the disease, which include four domains: autonomic failure/urinary dysfunction, parkinsonism and cerebellar ataxia, and corticospinal dysfunction. We set criteria to define the relative importance of these features. The diagnosis of possible MSA requires one criterion plus two features from separate other domains. The diagnosis of probable MSA requires the criterion for autonomic failure/urinary dysfunction plus poorly levodopa responsive parkinsonism or cerebellar ataxia. The diagnosis of definite MSA requires pathological confirmation.     

Chromosomal instability is correlated with telomere erosion and inactivation of G2 checkpoint function in human fibroblasts expressing human papillomavirus type 16 E6 oncoprotein

Cell cycle checkpoints and tumor suppressor gene functions appear to be required for the maintenance of a stable genome in proliferating cells. In this study chromosomal destabilization was monitored in relation to telomere structure, lifespan control and G2 checkpoint function. Replicative senescence was inactivated in secondary cultures of human skin fibroblasts by expressing the human papillomavirus type 16 (HPV-16) E6 oncoprotein to inactivate p53. Chromosome aberrations were enumerated during in vitro aging of isogenic control (F5neo) and HPV-16E6-expressing (F5E6) fibroblasts. We found that structural and numerical aberrations in chromosomes were significantly increased in F5E6 cells during aging in vitro and fluorescence in situ hybridization (FISH) analysis using chromosome-specific probes demonstrated the occurrence of rearrangements involving chromosome 4 and 6 in genetically unstable F5E6 cells. Flow cytometry and karyotypic analyses revealed increased polyploidy and aneuploidy in F5E6 cells only at passages > 16, although these cells displayed defective mitotic spindle checkpoint function associated with inactivation of p53 at passages 5 and 16. G2 checkpoint function was confirmed to be gradually but progressively inactivated during in vitro aging of E6-expressing cells. Aging of F5neo fibroblasts was documented during in vitro passaging by induction of a senescence-associated marker, pH 6.0 lysosomal beta-galactosidase. F5E6 cells displayed extension of in vitro lifespan and did not induce beta-galactosidase at high passage. Erosion of telomeres during in vitro aging of telomerase-negative F5neo cells was demonstrated by Southern hybridization and by quantitative FISH analysis on an individual cell level. Telomeric signals diminished continuously as F5neo cells aged in vitro being reduced by 80% near the time of replicative senescence. Telomeric signals detected by FISH also decreased continuously during aging of telomerase-negative F5E6 cells, but telomeres appeared to be stabilized at passage 34 when telomerase was expressed. Chromosomal instability in E6-expressing cells was correlated (P < 0.05) with both loss of telomeric signals and inactivation of G2 checkpoint function. The results suggest that chromosomal stability depends upon a complex interaction among the systems of telomere length maintenance and cell cycle checkpoints.     

Cholecystokinin B-type receptor signaling is involved in human pancreatic cancer cell growth

Cholecystokinin (CCK) is known to stimulate pancreatic cancer cell growth, but no detailed CCK receptor subtype characterization and investigation of CCK receptor-mediated cellular responses in human pancreatic cancer cells have been reported thus far. In this study, CCK binding sites were identified in human pancreatic cancer cells (MIA-PaCa-2) using radioligand binding studies. Pharmacological characterization demonstrated a single class of high-affinity CCK sites on MIA-PaCa-2 cells (326 +/- 18 pM, receptor density 16.9 +/- 2.3 fmol/mg protein). These CCK binding sites displayed a typical CCKB binding profile as shown in competition studies by using different CCK-related compounds and non-peptide CCK antagonists discriminating between CCKA and CCKB sites. CCKB receptor-connected effector systems have been characterized in MIA-PaCA-2 cells, and their involvement in CCK-8S-induced proliferative effects on MIA-PaCa-2 cells has been demonstrated.     

On Triangulating Planar Graphs under the Four-Connectivity Constraint

Triangulation of planar graphs under constraints is a fundamental problem in the representation of objects. Related keywords are graph augmentation from the field of graph algorithms and mesh generation from the field of computational geometry. We consider the triangulation problem for planar graphs under the constraint to satisfy 4-connectivity. A 4-connected planar graph has no separating triangles, i.e., cycles of length 3 which are not a face. We show that triangulating embedded planar graphs without introducing new separating triangles can be solved in linear time and space. If the initial graph had no separating triangle, the resulting triangulation is 4-connected. If the planar graph is not embedded, then deciding whether there exists an embedding with at most k separating triangles is NP-complete. For biconnected graphs a linear-time approximation which produces an embedding with at most twice the optimal number is presented. With this algorithm we can check in linear time whether a biconnected planar graph can be made 4-connected while maintaining planarity. Several related remarks and results are included. Received August 1, 1995; revised July 8, 1996, and August 23, 1996.     

Effect of adding the topoisomerase I poison 7-ethyl-10-hydroxycamptothecin (SN-38) to 5-fluorouracil and folinic acid in HCT-8 cells: elevated dTTP pools and enhanced cytotoxicity

Checkpoints maintain the interdependency of cell cycle events by permitting the onset of an event only after the completion of the preceding event. The DNA replication checkpoint induces a cell cycle arrest until the completion of the DNA replication. Similarly, the DNA damage checkpoint arrests cell cycle progression if DNA repair is incomplete. A number of genes that play a role in the two checkpoints have been identified through genetic studies in yeasts, and their homologues have been found in fly, mouse, and human. They form signaling cascades activated by a DNA replication block or DNA damage and subsequently generate the negative constraints on cell cycle regulators. The failure of these signaling cascades results in producing offspring that carry mutations or that lack a portion of the genome. In humans, defects in the checkpoints are often associated with cancer-prone diseases. Focusing mainly on the studies in budding and fission yeasts, we summarize the recent progress.     

Syncope. A neurologist's viewpoint

Syncope is caused by a global reversible reduction of blood flow to the brain. Three hemodynamic abnormalities can cause syncope: (1) a fall in systemic blood pressure because of ineffective control of peripheral vascular resistance, (2) an acute decrease in cardiac output, and (3) an acute increase in cerebrovascular resistance. Complicating the differential diagnosis of syncope are other causes of loss of consciousness, such as seizures, metabolic disorders, and psychiatric disorders, which may simulate syncope.     

The effect of caffeine on the serum insulin level during intravenous glucose tolerance test in patients with chemical diabetes

A small but significant number of tritiated thymidine labelled cells were found, by autoradiography, in the glomeruli of rats with Masugi nephritis or chronic serum sickness nephritis. There were no labelled glomerular cells in sections of untreated animals. The findings favour the contention that in proliferative glomerulonephritis, glomerular hypercellularity is due to infiltration of monocytic cells into the tufts where they divide.     

An extension of the Boyer-Moore Theorem Prover to support first-order quantification

We describe an implementation of an extension to the Boyer-Moore Theorem Prover and logic that allows first-order quantification. The extension retains the capabilities of the Boyer-Moore system while allowing the increased flexibility in specification and proof that is provided by quantifiers. The idea is to Skolemize in an appropriate manner. We demonstrate the power of this approach by describing three successful proof-checking experiments using the system, each of which involves a theorem of set theory as translated into a first-order logic. We also demonstrate the soundness of our approach.This research was supported in part by ONR Contract N00014-88-C-0454. The views and conclusions contained in this document are those of the author and should not be interpreted as representing the official policies, either expressed or implied, of Computational Logic, Inc., the Office of Naval Research or the U.S. Government.