Conversation-Based Assessment (CBA) represents a relatively new method of measuring student cognitive skills(e.g., science reasoning) through adaptive dialogues with automated characters. This approach leverages the openness ofnatural language with the interactivity of spoken dialogue to engage students in verbal reasoning and constructive processes(i.e., cognition). These two dimensions differentiate CBA from other assessment items (e.g., multiple choice and essays) byallowing for more freedom in responses along with the ability to adapt and follow-up on particular threads of information.The conversational exchange affords a rich data stream that can provide additional explanatory evidence of students’ cognitionexhibited through conversational content and dialogue paths. The current work, built on the AutoTutor dialogue engine, willdiscuss the affordances and constraints of CBA along with how this approach may complement and enhance other methods ofmeasuring of cognitive skills.

Conversations with computer agents can be used to measure skills that may be difficult to accomplish using tra-ditional multiple-choice assessments. In order to achieve natural conversations in this form of assessment, we are exploringissues related to how test-takers interact with computer agents, such as what dialogue moves lead to interpretable responses,the influence of “cognitive characteristics” of computer agents, how should the system adapt to test-taker responses, and howthese interactions impact test-taker emotions and affect. In this presentation we will discuss our current research addressingthese questions, illustrating important dimensions that are involved with designing a conversation space and how each designdecision can impact multiple factors within assessment contexts.

Cell-mediated adaptive immunity is critical for host defense, but little is known about T cell behavior during delivery of effector function. Here we investigate relationships among antigen presentation, T cell motility, and local production of effector cytokines by CD4+ T cells within hepatic granulomas triggered by Bacille Calmette-Guérin or Mycobacterium tuberculosis. At steady-state, only small fractions of mycobacteria-specific T cells showed antigen-induced migration arrest within granulomas, resulting in low-level, polarized secretion of cytokines. However, exogenous antigen elicited rapid arrest and robust cytokine production by the vast majority of effector T cells. These findings suggest that limited antigen presentation and/or recognition within granulomas evoke a muted T cell response drawing on only a fraction of the host's potential effector capacity. Our results provide new insights into the regulation of host-protective functions, especially how antigen availability influences T cell dynamics and, in turn, effector T cell function during chronic infection.

Background

There is microscopic spatial and temporal heterogeneity of pathological changes in idiopathic pulmonary fibrosis (IPF) lung tissue, which may relate to heterogeneity in pathophysiological mediators of disease and clinical progression. We assessed relationships between gene expression patterns, pathological features, and systemic biomarkers to identify biomarkers that reflect the aggregate disease burden in patients with IPF.

Methods

Gene expression microarrays (N=40 IPF; 8 controls) and immunohistochemical analyses (N=22 IPF; 8 controls) of lung biopsies. Clinical characterisation and blood biomarker levels of MMP3 and CXCL13 in a separate cohort of patients with IPF (N=80).

Results

2940 genes were significantly differentially expressed between IPF and control samples (|fold change| >1.5, p<0.05). Two clusters of co-regulated genes related to bronchiolar epithelium or lymphoid aggregates exhibited substantial heterogeneity within the IPF population. Gene expression in bronchiolar and lymphoid clusters corresponded to the extent of bronchiolisation and lymphoid aggregates determined by immunohistochemistry in adjacent tissue sections. Elevated serum levels of MMP3, encoded in the bronchiolar cluster, and CXCL13, encoded in the lymphoid cluster, corresponded to disease severity and shortened survival time (p<10(-7) for MMP3 and p<10(-5) for CXCL13; Cox proportional hazards model).

Conclusions

Microscopic pathological heterogeneity in IPF lung tissue corresponds to specific gene expression patterns related to bronchiolisation and lymphoid aggregates. MMP3 and CXCL13 are systemic biomarkers that reflect the aggregate burden of these pathological features across total lung tissue. These biomarkers may have clinical utility as prognostic and/or surrogate biomarkers of disease activity in interventional studies in IPF.

We study the process e+e-→ψ(2S)π+π- with initial-state-radiation events produced at the PEP-II asymmetric-energy collider. The data were recorded with the BABAR detector at center-of-mass energies at and near the (nS) (n=2,3,4) resonances and correspond to an integrated luminosity of 520fb-1. We investigate the ψ(2S)π+π- mass distribution from 3.95 to 5.95GeV/c2, and measure the center-of-mass energy dependence of the associated e+e-→ψ(2S)π+π- cross section. The mass distribution exhibits evidence of two resonant structures. A fit to the ψ(2S)π+π- mass distribution corresponding to the decay mode ψ(2S)→J/ψπ+π- yields a mass value of 4340±16(stat) ±9(syst)MeV/c2 and a width of 94±32(stat)±13(syst)MeV for the first resonance, and for the second a mass value of 4669±21(stat) ±3(syst)MeV/c2 and a width of 104±48(stat)±10(syst)MeV. In addition, we show the π+π- mass distributions for these resonant regions. © 2014 American Physical Society.

We present updated measurements of the branching fractions for B0 meson decays to ηK0, ηη, ηφ, ηω, η′K0, η′η′, η′φ, and η′ω, and branching fractions and CP-violating charge asymmetries for B+ decays to ηπ+, ηK+, η′π+, and η′K+. The data represent the full data set of 467×106 BB̄ pairs collected with the BABAR detector at the PEP-II asymmetric-energy e+e- collider at the SLAC National Accelerator Laboratory. Besides large signals for the four charged B decay modes and for B0→η′K0, we find evidence for three B0 decay modes at greater than 3.0σ significance. We find B(B0→ηK0)=(1.15-0.38+0. 43±0.09)×10-6, B(B0→ηω)=(0.94-0.30+0.35±0.09) ×10-6, and B(B0→η′ω)=(1.01-0.38+0.46±0.09) ×10-6, where the first (second) uncertainty is statistical (systematic). For the B+→ηK+ decay mode, we measure the charge asymmetry Ach(B+→ηK+)=-0.36±0.11±0.03. © 2009 The American Physical Society.

We report measurements of the branching fractions of neutral and charged B meson decays to final states containing a K1(1270) or K1(1400) meson and a charged pion. The data, collected with the BABAR detector at the SLAC National Accelerator Laboratory, correspond to 454×106 BB̄ pairs produced in e+e- annihilation. We measure the branching fractions B(B0→K1(1270)+π-+K1(1400) +π -)=3.1-0.7+0.8×10-5 and B(B+→ K1(1270) 0π++K1(1400) 0π+)=2.9-1.7+2.9×10 -5 (<8.2×10-5 at 90% confidence level), where the errors are statistical and systematic combined. The B0 decay mode is observed with a significance of 7.5σ, while a significance of 3.2σ is obtained for the B+ decay mode. Based on these results, we estimate the weak phase α=(79±7±11)°from the time-dependent CP asymmetries in B0→a1(1260)±π decays. © 2010 The American Physical Society.