Which User Interaction for Cross-Language Information Retrieval? Design Issues and Reflections

A novel and complex form of information access is cross-language information retrieval: searching for texts written in foreign languages based on native language queries. Although the underlying technology for achieving such a search is relatively well understood, the appropriate interface design is not. This paper presents three user evaluations undertaken during the iterative design of Clarity, a cross-language retrieval system for rare languages, and shows how the user interaction design evolved depending on the results of usability tests. The first test was instrumental to identify weaknesses in both functionalities and interface; the second was run to determine if query translation should be shown or not; the final was a global assessment and focussed on user satisfaction criteria. Lessons were learned at every stage of the process leading to a much more informed view of what a cross-language retrieval system should offer to users

Which user interaction for cross-language information retrieval? Design issues and reflections

A novel and complex form of information access is cross-language information retrieval: searching for texts written in foreign languages based on native language queries. Although the underlying technology for achieving such a search is relatively well understood, the appropriate interface design is not. The authors present three user evaluations undertaken during the iterative design of Clarity, a cross-language retrieval system for low-density languages, and shows how the user-interaction design evolved depending on the results of usability tests. The first test was instrumental to identify weaknesses in both functionalities and interface; the second was run to determine if query translation should be shown or not; the final was a global assessment and focused on user satisfaction criteria. Lessons were learned at every stage of the process leading to a much more informed view of what a cross-language retrieval system should offer to users

Hypertrophic Cardiomyopathy Complicated by Left Ventricular Apical Necrosis and Aneurysm in a Young Man: FDG-PET Findings

A 29-year old male was transferred to our hospital with an abnormal chest X-ray finding diagnosed as hypertrophic cardiomyopathy with apical necrosis and aneurysm formation. Four years after the initial hospitalization, we confirmed the aneurysm and necrosis using both integrated positron emission tomography (PET) and computed tomography (CT) scanning. The F-18 2-fluoro-2-deoxy-D-glucose (FDG) PET/CT enabled precise localization of the aneurysm, which was found to be composed of semi-lunar calcification of non-metabolic myocardium. A contrast-enhanced CT angiography showed an hour-glass appearance of the left ventricular cavity. The integrated PET/CT fusion scanner is a novel multimodality technology that allows for a comprehensive analysis of the anatomical and functional status of complex heart disease. Based on these findings, long standing mechanical and physiologic abnormalities may have led to chronic ischemia in the hypertrophied myocardium, induced necrosis and calcification at the cardiac apex

Trends in primary total hip arthroplasty in Spain from 2001 to 2008: Evaluating changes in demographics, comorbidity, incidence rates, length of stay, costs and mortality

<p>Abstract</p> <p>Background</p> <p>Hip arthroplasties is one of the most frequent surgical procedures in Spain and are conducted mainly in elderly subjects. We aim to analyze changes in incidence, co-morbidity profile, length of hospital stay (LOHS), costs and in-hospital mortality (IHM) of patients undergoing primary total hip arthroplasty (THA) over an 8-year study period in Spain.</p> <p>Methods</p> <p>We selected all surgical admissions in individuals aged ≥40 years who had received a primary THA (ICD-9-CM procedure code 81.51) between 2001 and 2008 from the National Hospital Discharge Database. Age- and sex-specific incidence rates, LOHS, costs and IHM were estimated for each year. Co-morbidity was assessed using the Charlson comorbidity index.</p> <p>Multivariate analysis of time trends was conducted using Poisson regression. Logistic regression models were conducted to analyze IHM.</p> <p>Results</p> <p>We identified a total of 161,791 discharges of patients having undergone THA from 2001 to 2008. Overall crude incidence had increased from 99 to 105 THA per 100.000 inhabitants from 2001 to 2008 (p < 0.001). In 2001, 81% of patients had a Charlson Index of 0, 18.4% of 1-2, and 0.6% > 2 and in 2008, the prevalence of 1-2 or >2 had increased to 20.4% and 1.1% respectively (p < 0.001). The mean LOHS was 13 days in 2001 and decreased to 10.45 days in 2008 (p < 0.001). During the period studied, the mean cost per patient increased from 6,634 to 9,474 Euros. Multivariate analysis shows that from 2001 to 2008 the incidence of THA hospitalizations has significantly increased for both sexes and only men showed a significant reduction in IHM after THA.</p> <p>Conclusions</p> <p>The current study provides clear and valid data indicating increased incidence of primary THA in Spain from 2001 to 2008 with concomitant reductions in LOHS, slight reduction IHM, but a significant increase in cost per patient. The health profile of the patient undergoing a THA seems to be worsening in Spain.</p

Nesfatin-1 in human and murine cardiomyocytes: synthesis, secretion, and mobilization of GLUT-4

Nesfatin-1, a satiety-inducing peptide identified in hypothalamic regions that regulate energy balance, is an integral regulator of energy homeostasis and a putative glucose-dependent insulin coadjuvant. We investigated its production by human cardiomyocytes and its effects on glucose uptake, in the main cardiac glucose transporter GLUT-4 and in intracellular signaling. Quantitative RT-PCR, Western blots, confocal immunofluorescence microscopy, and ELISA of human and murine cardiomyocytes and/or cardiac tissue showed that cardiomyocytes can synthesize and secrete nesfatin-1. Confocal microscopy of cultured cardiomyocytes after GLUT-4 labeling showed that nesfatin-1 mobilizes this glucose transporter to cell peripherals. The rate of 2-deoxy-D-[(3)H]glucose incorporation demonstrated that nesfatin-1 induces glucose uptake by HL-1 cells and cultured cardiomyocytes. Nesfatin-1 induced dose- and time-dependent increases in the phosphorylation of ERK1/2, AKT, and AS160. In murine and human cardiac tissue, nesfatin-1 levels varied with diet and coronary health. In conclusion, human and murine cardiomyocytes can synthesize and secrete nesfatin-1, which is able to induce glucose uptake and the mobilization of the glucose transporter GLUT-4 in these cells. Nesfatin-1 cardiac levels are regulated by diet and coronary health

The σE stress response is required for stress-induced mutation and amplification in Escherichia coli

Pathways of mutagenesis are induced in microbes under adverse conditions controlled by stress responses. Control of mutagenesis by stress responses may accelerate evolution specifically when cells are maladapted to their environments, i.e. are stressed. Stress-induced mutagenesis in the Escherichia coli Lac assay occurs either by ‘point’ mutation or gene amplification. Point mutagenesis is associated with DNA double-strand-break (DSB) repair and requires DinB error-prone DNA polymerase and the SOS DNA-damage- and RpoS general-stress responses. We report that the RpoE envelope-protein-stress response is also required. In a screen for mutagenesis-defective mutants, we isolated a transposon insertion in the rpoE P2 promoter. The insertion prevents rpoE induction during stress, but leaves constitutive expression intact, and allows cell viability. rpoE insertion and suppressed null mutants display reduced point mutagenesis and maintenance of amplified DNA. Furthermore, σE acts independently of stress responses previously implicated: SOS/DinB and RpoS, and of σ32, which was postulated to affect mutagenesis. I-SceI-induced DSBs alleviated much of the rpoE phenotype, implying that σE promoted DSB formation. Thus, a third stress response and stress input regulate DSB-repair-associated stress-induced mutagenesis. This provides the first report of mutagenesis promoted by σE, and implies that extracytoplasmic stressors may affect genome integrity and, potentially, the ability to evolve

Evidence, and replication thereof, that molecular-genetic and environmental risks for psychosis impact through an affective pathway

Background There is evidence that environmental and genetic risk factors for schizophrenia spectrum disorders are transdiagnostic and mediated in part through a generic pathway of affective dysregulation. Methods We analysed to what degree the impact of schizophrenia polygenic risk (PRS-SZ) and childhood adversity (CA) on psychosis outcomes was contingent on co-presence of affective dysregulation, defined as significant depressive symptoms, in (i) NEMESIS-2 (n = 6646), a representative general population sample, interviewed four times over nine years and (ii) EUGEI (n = 4068) a sample of patients with schizophrenia spectrum disorder, the siblings of these patients and controls. Results The impact of PRS-SZ on psychosis showed significant dependence on co-presence of affective dysregulation in NEMESIS-2 [relative excess risk due to interaction (RERI): 1.01, p = 0.037] and in EUGEI (RERI = 3.39, p = 0.048). This was particularly evident for delusional ideation (NEMESIS-2: RERI = 1.74, p = 0.003; EUGEI: RERI = 4.16, p = 0.019) and not for hallucinatory experiences (NEMESIS-2: RERI = 0.65, p = 0.284; EUGEI: -0.37, p = 0.547). A similar and stronger pattern of results was evident for CA (RERI delusions and hallucinations: NEMESIS-2: 3.02, p < 0.001; EUGEI: 6.44, p < 0.001; RERI delusional ideation: NEMESIS-2: 3.79, p < 0.001; EUGEI: 5.43, p = 0.001; RERI hallucinatory experiences: NEMESIS-2: 2.46, p < 0.001; EUGEI: 0.54, p = 0.465). Conclusions The results, and internal replication, suggest that the effects of known genetic and non-genetic risk factors for psychosis are mediated in part through an affective pathway, from which early states of delusional meaning may arise

Association between lifestyle factors and headache

Modification of lifestyle habits is a key preventive strategy for many diseases. The role of lifestyle for the onset of headache in general and for specific headache types, such as migraine and tension-type headache (TTH), has been discussed for many years. Most results, however, were inconsistent and data on the association between lifestyle factors and probable headache forms are completely lacking. We evaluated the cross-sectional association between different lifestyle factors and headache subtypes using data from three different German cohorts. Information was assessed by standardized face-to-face interviews. Lifestyle factors included alcohol consumption, smoking status, physical activity and body mass index. According to the 2004 diagnostic criteria, we distinguished the following headache types: migraine, TTH and their probable forms. Regional variations of lifestyle factors were observed. In the age- and gender-adjusted logistic regression models, none of the lifestyle factors was statistically significant associated with migraine, TTH, and their probable headache forms. In addition, we found no association between headache subtypes and the health index representing the sum of individual lifestyle factors. The lifestyle factors such as alcohol consumption, smoking, physical activity and overweight seem to be unrelated to migraine and TTH prevalence. For a judgement on their role in the onset of new or first attacks of migraine or TTH (incident cases), prospective cohort studies are required