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In this study, we address how people respond to a robotic trashcan initiating interactions and offering its service. We show that considerable coordination and negotiation work takes place both between human and robot and between humans who are involved in a joint activity when the robot approaches. While in this scenario attention getting was no problem, the interactions posed significant problems to people who did not want the robot's service. The unwillingness to interact with the robot was mostly communicated by withholding social signals, which means that human-robot interaction designers not only need to build in ways to respond to human social signals in a timely and appropriate manner, but also a representation of what kinds of signals could be expected in order to interpret the ostensive lack of such signals adequately.

The TEI-community is based a various paradigms. We believe that the community matures by scrutinising these different paradigms and unravelling the consequences for designing for tangible, embedded and embodied interaction. In this paper we explore the consequences and possibilities of phenomenology-inspired embodied theory, and more specifically the concept of embodied sensemaking, i.e. human sensemaking using sensorimotor couplings to support social coordination between people. Based on our theoretical setting, we introduce seven design principles for developing face-to-face embodied sensemaking technology. We show in this paper how we used these principles to develop a mobile design and sensemaking studio for the encounter between two persons to sketch a future at the cross-section of their disciplines. By explaining these principles, we aim to show what embodied theory can bring the TEI-community, and invite others to do the same.

Warfarin is an oral anticoagulant that requires frequent therapeutic drug monitoring due to a narrow therapeutic window, considerable interindividual variability in drug response, and susceptibility to drug-drug and drug-diet interactions. Enantiomeric separation and quantification of warfarin enantiomers and clinically important major hydroxylation metabolites are essential for drug interaction studies and phenotypic characterization of CYP2C9 and CYP3A4, the major cytochrome P450 (CYP) enzymes involved in warfarin metabolism. Here, we describe the development and validation of a chiral high performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS)-based quantification of R-warfarin, S-warfarin, S-7-hydroxywarfarin (the major CYP2C9 metabolite) and (9R;10S)-10-hydroxywarfarin (the CYP3A4 metabolite) in human plasma. Simple protein precipitation-based extraction showed good recovery of analytes (82.9 – 96.9%). The developed method exhibited satisfactory intra-day and inter-day accuracy and precision. The lower limits of detection were 0.25 nM (or ~0.08 ng/mL) for the warfarin enantiomers and 0.1 nM (or ~0.04 ng/mL) for S-7-hydroxywarfarin and (9R;10S)-10-hydroxywarfarin using only 50 µL plasma during extraction. The validated method was successfully applied to analyze plasma samples obtained from a healthy human subject who enrolled in a clinical drug interaction study involving warfarin.

The seventh annual ARVO/Pfizer Ophthalmic Research Institute conference was held Friday and Saturday, April 29 and 30, 2011, at the Fort Lauderdale Hyatt Regency Pier 66, Fort Lauderdale, Florida. The conference, funded by The ARVO Foundation for Eye Research through a grant from Pfizer Ophthalmics, provided an opportunity to gather experts from within and outside ophthalmology to determine the state of knowledge pertaining to molecular biomarkers associated with glaucoma, as well as the methods to identify and validate them to predict (a) those who would be susceptible to development of glaucoma; (b) markers that will enable prediction of glaucoma progression; and (c) markers that will predict efficacy of treatment of glaucoma. Identification of such biomarkers will aid in prevention of glaucoma-related vision loss and blindness. The conference focused on an evaluation of glaucoma molecular biomarkers and progress needed for future validation of glaucoma biomarkers. A working group of 21 glaucoma researchers, 7 scientists focused on diseases other than glaucoma and with expertise in areas such as proteomic biomarkers or molecular mechanisms for neurodegeneration, and 60 observers from ARVO, Pfizer, and clinical and basic ophthalmic research convened to evaluate current understanding of the molecular biomarkers of glaucoma. The meeting format emphasized discussion and concentrated on questions within areas of glaucoma molecular biomarker research: Session I: How to define a biomarker in medicine? Current knowledge about biomarkers in human health and in glaucoma Session II: Genetic biomarkers in glaucoma Session III: Proteomic biomarkers in glaucoma Session IV: Pre-immune and immune events: Immunoproteomics and its possible applications in glaucoma Session V: From bench to bedside: How can a translational approach be successful? Each session began with a 10-minute overview by a glaucoma researcher followed by a 30-minute presentation by an outside expert, with parallels between their fields of expertise and the eye included. Invited outside experts covered several areas of research, including proteomic biomarker discovery in cancer (Emanuel Petricoin, PhD, George Mason University, Maryland; and Akhilesh Pandey, MD, PhD, Johns Hopkins University, Maryland) and astroglial cells in neurodegeneration (Stephen D. Miller, PhD, Northwestern University, Illinois).

IgG immunoreactivity to Malassezia pachydermatis was compared in atopic and non-atopic dogs. Malassezia pachydermatis proteins with a molecular weight of 98 kDa were recognized at a significantly higher frequency in the sera of atopic dogs. Most of the atopic dogs with Malassezia dermatitis had a greater IgG response than did normal dogs.

Purpose: This study was conducted to determine whether elevated hydrostatic pressure alters mitochondrial structure, triggers release of the dynamin-related guanosine triphosphatase (GTPase) optic atrophy type 1 (OPA1) or cytochrome C from mitochondria, alters OPA1 gene expression, and can directly induce apoptotic cell death in cultured retinal ganglion cell (RGC)-5 cells. Methods: Differentiated RGC-5 cells were exposed to 30 mmHg for three days in a pressurized incubator. As a control, differentiated RGC-5 cell cultures were incubated simultaneously in a conventional incubator. Live RGC-5 cells were then labeled with MitoTracker Red and mitochondrial morphology was assessed by fluorescence microscopy. Mitochondrial structural changes were also assessed by electron microscopy and three-dimenstional (3D) electron microscope tomography. OPA1 mRNA was measured by Taqman quantitative PCR. The cellular distribution of OPA1 protein and cytochrome C was assessed by immunocytochemistry and western blot. Caspase-3 activation was examined by western blot. Apoptotic cell death was evaluated by the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) method. Results: Mitochondrial fission, characterized by the conversion of tubular fused mitochondria into isolated small organelles, was triggered after three days exposure to elevated hydrostatic pressure. Electron microscopy confirmed the fission and noted no changes to mitochondrial architecture, nor outer membrane rupture. Electron microscope tomography showed that elevated pressure depleted mitochondrial cristae content by fourfold. Elevated hydrostatic pressure increased OPA1 gene expression by 35±14% on day 2, but reduced expression by 36±4% on day 3. Total OPA1 protein content was not changed on day 2 or 3. However, pressure treatment induced release of OPA1 and cytochrome C from mitochondria to the cytoplasm. Elevated pressure also activated caspase-3 and induced apoptotic cell death. Conclusions: Elevated hydrostatic pressure triggered mitochondrial changes including mitochondrial fission and abnormal cristae depletion, alteration of OPA1 gene expression, and release of OPA1 and cytochrome C into the cytoplasm before the onset of apoptotic cell death in differentiated RGC-5 cells. These results suggest that sustained moderate pressure elevation may directly damage RGC cell integrity by injuring mitochondria. © 2009 Molecular Vision.

A zero voltage switching (ZVS) three level auxiliary resonant commutated pole inverter (ARCPI) is presented for high power GTO inverters. The concept of ARCP for a two level inverter is extended to the three level inverter. The proposed auxiliary commutation circuit consists of one resonant inductor and two bi-directional switches, which provides ZVS condition to the main devices without increasing device voltage or current stresses. The auxiliary device operates with zero current switching (ZCS) which enables use of the low cost thyristors. The proposed ARCPI can handle higher voltage and higher power (1-10 MVA) compared to the two level one. Operation and analysis of the ARCPI are illustrated and the features are compared to those of the snubber circuit incorporated three level inverter. Experimental results with 10 kW, 4 kHz prototype are presented to verify the principle of operation.

To determine whether there is an association of polymorphic variants of the serotonin transporter (5-HTT) gene-linked polymorphic region (5-HTTLPR) and autistic spectrum disorders, we analyzed the 5-HTTLPR genotypes of 72 autistic subjects, 11 fragile X syndrome patients with autistic behavior, 43 normal subjects, and 49 fragile X syndrome non-autistic subjects. The distribution frequency of 5-HTTLPR long allele (L) and the short allele (S) variants showed no differences between subjects. Our findings do not support the hypothesis that polymorphic 5-HTTLPR variants are a susceptibility factor for autistic disorders.