Irradiate-anneal screening of total dose effects in semiconductor devices

An extensive investigation of irradiate-anneal (IRAN) screening against total dose radiation effects was carried out as part of a program to harden the Mariner Jupiter/Saturn 1977 (MJS'77) spacecraft to survive the Jupiter radiation belts. The method consists of irradiating semiconductor devices with Cobalt-60 to a suitable total dose under representative bias conditions and of separating the parts in the undesired tail of the distribution from the bulk of the parts by means of a predetermined acceptance limit. The acceptable devices are then restored close to their preirradiation condition by annealing them at an elevated temperature. IRAN was used when lot screen methods were impracticable due to lack of time, and when members of a lot showed a diversity of radiation response. The feasibility of the technique was determined by testing of a number of types of linear bipolar integrated circuits, analog switches, n-channel JFETS and bipolar transistors. Based on the results of these experiments a number of device types were selected for IRAN of flight parts in the MJS'77 spacecraft systems. The part types, screening doses, acceptance criteria, number of parts tested and rejected as well as the program steps are detailed

Voyager electronic parts radiation program, volume 1

The Voyager spacecraft is subject to radiation from external natural space, from radioisotope thermoelectric generators and heater units, and from the internal environment where penetrating electrons generate surface ionization effects in semiconductor devices. Methods for radiation hardening and tests for radiation sensitivity are described. Results of characterization testing and sample screening of over 200 semiconductor devices in a radiation environment are summarized

Voyager electronic parts radiation program. Volume 2: Test requirements and procedures

Documents are presented outlining the conditions and requirements of the test program. The Appendixes are as follows: appendix A -- Electron Simulation Radiation Test Specification for Voyager Electronic Parts and Devices, appendix B -- Electronic Piece-Part Testing Program for Voyager, appendix C -- Test Procedure for Radiation Screening of Voyager Piece Parts, appendix D -- Boeing In Situ Test Fixture, and appendix E -- Irradiate - Anneal (IRAN) Screening Documents

Unexplained Aspects of Anemia of Inflammation

Anemia of inflammation (AI), also known as anemia of chronic inflammation or anemia of chronic disease was described over 50 years ago as anemia in association with clinically overt inflammatory disease, and the findings of low plasma iron, decreased bone marrow sideroblasts and increased reticuloendothelial iron. Pathogenic features underlying AI include a mild shortening of red cell survival, impaired erythropoietin production, blunted responsiveness of the marrow to erythropoietin, and impaired iron metabolism mediated by inflammatory cytokines and the iron regulatory peptide, hepcidin. Despite marked recent advances in understanding AI, gaps remain, including understanding of the pathogenesis of AI associated with “noninflammatory” or mildly inflammatory diseases, the challenge of excluding iron deficiency anemia in the context of concomitant inflammation, and understanding more precisely the contributory role of hepcidin in the development of AI in human inflammatory diseases

Association of residential mobility over the life course with nonaffective psychosis in 1.4 million young people in Sweden

Importance Residential mobility (changing residence) during childhood and early adolescence is a possible risk factor for several adverse health outcomes, including psychotic disorders. However, it is unclear whether sensitive periods to residential mobility exist over the life course, including in adulthood, or if greater moving distances, which might disrupt social networks, are associated with a greater psychosis risk. Objective To examine the association between residential mobility over the life course and the risk of nonaffective psychosis. Design, Setting, and Participants This prospective cohort study included all people born in Sweden between January 1, 1982, and December 31, 1995, who were alive and resided in Sweden on their 16th birthday who were followed up until up to age 29 years (ending December 2011). Participants were followed until receiving a first diagnosis of an International Statistical Classification of Diseases and Related Health Problems, Tenth Revision (ICD-10) nonaffective psychotic disorder (F20-29), emigration, death, or the end of 2011, whichever was sooner. National register linkage provided exposure, outcome, and covariate data (complete data were available for 1 440 383 participants [97.8%]). Exposures The exposures to distance moved and the number of residential moves were examined for participants at the following periods over the life course: 0 to 6 years, 7 to 15 years, 16 to 19 years, and 20 years and older. Results This study included 1 440 383 participants, of whom 4537 (0.31%) had nonaffective psychotic disorder (median age, 20.9 [interquartile range, 19.0-23.3]). More frequent moves during childhood and adolescence were associated with an increased risk of nonaffective psychosis that showed dose-response associations independent of covariates. The most sensitive period of risk occurred during late adolescence; those who moved during each year between age 16 to 19 years had an increased adjusted hazard ratio (HR) of 1.99 (95% CI, 1.30-3.05) compared with those who never moved. One move during adulthood was not associated with psychosis risk (adjusted HR, 1.04; 95% CI, 0.94-1.14), but moving 4 or more times during adulthood was associated with increased risk (adjusted hazard ratio, 1.82; 95% CI, 1.51-2.23). Independently, moving greater distances before age 16 years was associated with an increased risk (adjusted HR, 1.11; 95% CI, 1.05-1.19), with evidence of a nonlinear threshold effect for moves longer than 30 km. The distance moved after age 20 years was associated with a decreased risk (adjusted HR, 0.67; 95% CI, 0.63-0.71). Conclusions and Relevance Children and adolescents with less disruption in their residential environments are less likely to experience psychotic disorders in early adulthood. Moves that may necessitate changes in school and social networks were most strongly associated with future risk

Santiago, the Fisherman-Artist: Autobiography and Aesthetics in the Old Man and the Sea

Englis

Monitoring asthma in childhood : symptoms, exacerbations and quality of life

Acknowledgements The Task Force members and their affiliations are as follows. Paul L.P. Brand: Princess Amalia Children’s Centre, Isala Hospital, Zwolle, and UMCG Postgraduate School of Medicine, University Medical Centre and University of Groningen, Groningen, The Netherlands; Mika J. Mäkelä: Skin and Allergy Hospital, Helsinki University Hospital, Helsinki, Finland; Stanley J. Szefler: Children’s Hospital Colorado and University of Colorado Denver School of Medicine, Denver, CO, USA; Thomas Frischer: Dept of Paediatrics and Paediatric Surgery, Wilhelminenspital, Vienna, Austria; David Price: Dept of Primary Care Respiratory Medicine, Academic Primary Care, Division of Applied Health Sciences, University of Aberdeen, Aberdeen, UK; Eugenio Baraldi: Women’s and Children’s Health Dept, Unit of Respiratory Medicine and Allergy, University of Padova, Padova, Italy; Kai-Hakon Carlsen: Dept of Paediatrics, Women and Children’s Division, University of Oslo, and Oslo University Hospital, Oslo, Norway; Ernst Eber: Respiratory and Allergic Disease Division, Dept of Paediatrics and Adolescence Medicine, Medical University of Graz, Graz, Austria; Gunilla Hedlin: Dept of Women’s and Children’s Health and Centre for Allergy Research, Karolinska Institutet, and Astrid Lindgren Children’s hospital, Stockholm, Sweden; Neeta Kulkarni: Leicestershire Partnership Trust and Dept of Infection, Immunity and Inflammation, University of Leicester, Leicester, UK; Christiane Lex: Dept of Paediatric Cardiology and Intensive Care Medicine, Division of Paediatric Respiratory Medicine, University Hospital Goettingen, Goettingen, Germany; Karin C. Lødrup Carlsen: Dept of Paediatrics, Women and Children’s Division, Oslo University Hospital, and Dept of Paediatrics, Faculty of Medicine, University of Oslo, Oslo, Norway; Eva Mantzouranis: Dept of Paediatrics, University Hospital of Heraklion, University of Crete, Heraklion, Greece; Alexander Moeller: Division of Respiratory Medicine, University Children’s Hospital Zurich, Zurich, Switzerland; Ian Pavord: Dept of Respiratory Medicine, University of Oxford, Oxford, UK; Giorgio Piacentini: Paediatric Section, Dept of Life and Reproduction Sciences, University of Verona, Verona, Italy; Mariëlle W. Pijnenburg: Dept Paediatrics/Paediatric Respiratory Medicine, Erasmus MC - Sophia Children’s Hospital, Rotterdam, The Netherlands; Bart L. Rottier: Dept of Pediatric Pulmonology and Allergology, GRIAC Research Institute, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands; Sejal Saglani: Leukocyte Biology and Respiratory Paediatrics, National Heart and Lung Institute, Imperial College London, London, UK; Peter D. Sly: Queensland Children’s Medical Research Institute, The University of Queensland, Brisbane, Australia; Steve Turner: Dept of Paediatrics, University of Aberdeen, Aberdeen, UK; Edwina Wooler: Royal Alexandra Children’s Hospital, Brighton, UK.Peer reviewedPublisher PD

Manipulation of P-TEFb control machinery by HIV: recruitment of P-TEFb from the large form by Tat and binding of HEXIM1 to TAR

Basal transcription of the HIV LTR is highly repressed and requires Tat to recruit the positive transcription elongation factor, P-TEFb, which functions to promote the transition of RNA polymerase II from abortive to productive elongation. P-TEFb is found in two forms in cells, a free, active form and a large, inactive complex that also contains 7SK RNA and HEXIM1 or HEXIM2. Here we show that HIV infection of cells led to the release of P-TEFb from the large form. Consistent with Tat being the cause of this effect, transfection of a FLAG-tagged Tat in 293T cells caused a dramatic shift of P-TEFb out of the large form to a smaller form containing Tat. In vitro, Tat competed with HEXIM1 for binding to 7SK, blocked the formation of the P-TEFb–HEXIM1–7SK complex, and caused the release P-TEFb from a pre-formed P-TEFb–HEXIM1–7SK complex. These findings indicate that Tat can acquire P-TEFb from the large form. In addition, we found that HEXIM1 binds tightly to the HIV 5′ UTR containing TAR and recruits and inhibits P-TEFb activity. This suggests that in the absence of Tat, HEXIM1 may bind to TAR and repress transcription elongation of the HIV LTR

Borderline personality and attention-deficit hyperactivity traits in childhood are associated with hypomanic features in early adulthood

Background There is limited understanding of the symptomatic development of bipolar disorder from childhood to early adulthood. Aims We assessed whether borderline personality disorder traits, ADHD, and emotional, behavioural and social difficulties during childhood were associated with hypomania assessed in young adulthood. Method We used data from the Avon Longitudinal Study of Parents and Children (ALSPAC), to examine associations between measures of childhood psychopathology and lifetime hypomanic features assessed at age 22–23 years using the Hypomania Checklist-32 (HCL-32; n = 3,372). We also conducted a factor analysis of the HCL to identify latent constructs underlying hypomania, and the extent to which childhood psychopathology was associated with these. Results We identified two factors of the HCL corresponding to energy/mood and risk-taking/irritability. There was evidence of association between childhood borderline personality disorder traits and both hypomania factors, with evidence that the association was stronger with the risk-taking/irritability factor. All individual borderline traits, with the exception of fear of abandonment, were associated with hypomania. There was also evidence of association between most other measures of childhood psychopathology (ADHD, hyperactivity, conduct problems, peer relationship problems and reduced prosocial behaviour) and the risk-taking/irritability factor, but much less consistent evidence of association with the energy/mood factor. Limitations The HCL cannot diagnose bipolar disorder and may be subject to reporting bias. Conclusions A broad range of childhood psychopathologies may represent early markers of risk for hypomania. Further studies are required to understand the mechanisms underlying these associations, and to inform earlier detection of bipolar disorder