University of Zurich

About: University of Zurich is a education organization based out in Zurich, Switzerland. It is known for research contribution in the topics: Population & Medicine. The organization has 50842 authors who have published 124042 publications receiving 5304521 citations. The organization is also known as: UZH & Uni Zurich.

What makes a good bug report

Abstract: In software development, bug reports provide crucial information to developers. However, these reports widely differ in their quality. We conducted a survey among developers and users of APACHE, ECLIPSE, and MOZILLA to find out what makes a good bug report.The analysis of the 466 responses revealed an information mismatch between what developers need and what users supply. Most developers consider steps to reproduce, stack traces, and test cases as helpful, which are at the same time most difficult to provide for users. Such insight is helpful to design new bug tracking tools that guide users at collecting and providing more helpful information.Our CUEZILLA prototype is such a tool and measures the quality of new bug reports; it also recommends which elements should be added to improve the quality. We trained CUEZILLA on a sample of 289 bug reports, rated by developers as part of the survey. In our experiments, CUEZILLA was able to predict the quality of 31--48% of bug reports accurately.

Development and function of human innate immune cells in a humanized mouse model

Abstract: Mice repopulated with human hematopoietic cells are a powerful tool for the study of human hematopoiesis and immune function in vivo. However, existing humanized mouse models cannot support development of human innate immune cells, including myeloid cells and natural killer (NK) cells. Here we describe two mouse strains called MITRG and MISTRG, in which human versions of four genes encoding cytokines important for innate immune cell development are knocked into their respective mouse loci. The human cytokines support the development and function of monocytes, macrophages and NK cells derived from human fetal liver or adult CD34(+) progenitor cells injected into the mice. Human macrophages infiltrated a human tumor xenograft in MITRG and MISTRG mice in a manner resembling that observed in tumors obtained from human patients. This humanized mouse model may be used to model the human immune system in scenarios of health and pathology, and may enable evaluation of therapeutic candidates in an in vivo setting relevant to human physiology.

Molecular Mechanisms of Lymphocyte-Mediated Cytotoxicity and Their Role in Immunological Protection and Pathogenesis In Vivo

Abstract: Studies with perforin-deficient mice have demonstrated that two independent mechanisms account for T cell–mediated cytotoxicity: A main pathway is mediated by the secretion of the pore-forming protein perforin by the cytotoxic T cell, whereas an alternative nonsecretory pathway relies on the interaction of the Fas ligand that is upregulated during T cell activation with the apoptosis-inducing Fas molecule on the target cell. NK cells use the former pathway exclusively. The protective role of the perforin-dependent pathway has been shown for infection with the noncytopathic lymphocytic choriomeningitis virus, for infection with Listeria monocytogenes, and for the elimination of tumor cells by T cells and NK cells. In contrast, perforin-dependent cytotoxicity is not involved in protection against the cytopathic vaccinia virus and vesicular stomatitis virus. LCMV-induced immunopathology and autoimmune diabetes have been found to require perforin-expression. A contribution of perforin-dependent cytotoxicity t...

The association between short sleep duration and obesity in young adults: a 13-year prospective study.

Abstract: STUDY OBJECTIVES: Obesity has become a major health problem with increasing prevalence. Given the limited availability of effective treatment of weight problems, the identification of potentially modifiable risk factors may lead to preventive approaches to obesity. The objective of this study was to test the hypothesis that short sleep duration is associated with obesity and weight gain during young adulthood. DESIGN: Prospective single-age cohort study of young adults. Information was derived from 4 interviews when participants were ages 27, 29, 34, and 40 years. SETTING: Community setting. PARTICIPANTS: 496 young adults. MEASUREMENTS AND RESULTS: Trained health professionals administered a semistructured interview for psychiatric and medical conditions and health habits. This study showed an association between short sleep duration and obesity (at age 27 years, odds ratio: 7.4, 95% confidence interval: 1.3-43.1) and a negative association between sleep duration and body mass index in young adults. These associations persisted after controlling for a variety of potentially confounding variables, including family history of weight problems, levels of physical activity, and demographic variables. Associations between sleep duration and obesity diminished after age 34 years. There was a trend (P =.08) for average change rate of weight gain to be negatively associated with average change rate of sleep duration. CONCLUSIONS: Because sleep duration is a potentially modifiable risk factor, these findings might have important clinical implications for the prevention and treatment of obesity.

TRIM5 is an innate immune sensor for the retrovirus capsid lattice

Abstract: TRIM5 is a RING domain-E3 ubiquitin ligase that restricts infection by human immunodeficiency virus (HIV)-1 and other retroviruses immediately following virus invasion of the target cell cytoplasm. Antiviral potency correlates with TRIM5 avidity for the retrovirion capsid lattice and several reports indicate that TRIM5 has a role in signal transduction, but the precise mechanism of restriction is unknown. Here we demonstrate that TRIM5 promotes innate immune signalling and that this activity is amplified by retroviral infection and interaction with the capsid lattice. Acting with the heterodimeric, ubiquitin-conjugating enzyme UBC13-UEV1A (also known as UBE2N-UBE2V1), TRIM5 catalyses the synthesis of unattached K63-linked ubiquitin chains that activate the TAK1 (also known as MAP3K7) kinase complex and stimulate AP-1 and NFκB signalling. Interaction with the HIV-1 capsid lattice greatly enhances the UBC13-UEV1A-dependent E3 activity of TRIM5 and challenge with retroviruses induces the transcription of AP-1 and NF-κB-dependent factors with a magnitude that tracks with TRIM5 avidity for the invading capsid. Finally, TAK1 and UBC13-UEV1A contribute to capsid-specific restriction by TRIM5. Thus, the retroviral restriction factor TRIM5 has two additional activities that are linked to restriction: it constitutively promotes innate immune signalling and it acts as a pattern recognition receptor specific for the retrovirus capsid lattice.