Transmission of the South African asinine strain of equine arteritis virus (EAV) among horses and between donkeys and horses

Lateral and sexual transmission of EAV among horses and lateral transmission between donkeys and horses were attempted by experimental infection with the South African asinine strain. Clinical, immunological and virological responses were evaluated. All intramuscularly inoculated horses developed very mild clinical signs, were viraemic, shed virus from nasopharynx, and seroconverted. Lateral infection was demonstrated in one in-contact mare. Reinfection of two stallions by intranasal instillation was shown by virus recovery from bully-coat cultures. After nasal instillation of virus, one stallion which did not become infected by in-contact exposure, showed slight serous nasal and ocular discharge, contained virus in a blood and nasopharynx and seroconverted. Attempts to transmit the virus from seropositive stallions to seronegative mares by breeding, were not successful; no virus was isolated from semen. All inoculated donkeys and three in-contact horses showed clinical signs consistent with an EAV infection. Although virus was isolated from donkey buffy-coat preparations and the nasopharynx, and they seroconverted, no virus was isolated from the horses, and they failed to seroconvert; it was assumed that their clinical signs were due to factors unrelated to EAV. The South African strain of EAV appears to be poorly transmissible to horses, supporting the findings of other field studies which indicate a widespread distribution and long-standing presence of the virus among South African donkeys, but a very restricted prevalence of seropositive horses.The articles have been scanned in colour with a HP Scanjet 5590; 600dpi. Adobe Acrobat X Pro was used to OCR the text and also for the merging and conversion to the final presentation PDF-format.mn201

Dust in Supernovae and Supernova Remnants I : Formation Scenarios

Supernovae are considered as prime sources of dust in space. Observations of local supernovae over the past couple of decades have detected the presence of dust in supernova ejecta. The reddening of the high redshift quasars also indicate the presence of large masses of dust in early galaxies. Considering the top heavy IMF in the early galaxies, supernovae are assumed to be the major contributor to these large amounts of dust. However, the composition and morphology of dust grains formed in a supernova ejecta is yet to be understood with clarity. Moreover, the dust masses inferred from observations in mid-infrared and submillimeter wavelength regimes differ by two orders of magnitude or more. Therefore, the mechanism responsible for the synthesis of molecules and dust in such environments plays a crucial role in studying the evolution of cosmic dust in galaxies. This review summarises our current knowledge of dust formation in supernova ejecta and tries to quantify the role of supernovae as dust producers in a galaxy.Peer reviewe

History of clinical transplantation

How transplantation came to be a clinical discipline can be pieced together by perusing two volumes of reminiscences collected by Paul I. Terasaki in 1991-1992 from many of the persons who were directly involved. One volume was devoted to the discovery of the major histocompatibility complex (MHC), with particular reference to the human leukocyte antigens (HLAs) that are widely used today for tissue matching.1 The other focused on milestones in the development of clinical transplantation.2 All the contributions described in both volumes can be traced back in one way or other to the demonstration in the mid-1940s by Peter Brian Medawar that the rejection of allografts is an immunological phenomenon.3,4 © 2008 Springer New York

Genome-wide association and Mendelian randomisation analysis provide insights into the pathogenesis of heart failure

Heart failure (HF) is a leading cause of morbidity and mortality worldwide. A small proportion of HF cases are attributable to monogenic cardiomyopathies and existing genome-wide association studies (GWAS) have yielded only limited insights, leaving the observed heritability of HF largely unexplained. We report results from a GWAS meta-analysis of HF comprising 47,309 cases and 930,014 controls. Twelve independent variants at 11 genomic loci are associated with HF, all of which demonstrate one or more associations with coronary artery disease (CAD), atrial fibrillation, or reduced left ventricular function, suggesting shared genetic aetiology. Functional analysis of non-CAD-associated loci implicate genes involved in cardiac development (MYOZ1, SYNPO2L), protein homoeostasis (BAG3), and cellular senescence (CDKN1A). Mendelian randomisation analysis supports causal roles for several HF risk factors, and demonstrates CAD-independent effects for atrial fibrillation, body mass index, and hypertension. These findings extend our knowledge of the pathways underlying HF and may inform new therapeutic strategies