Sward composition and structure influence herbage intake of grazing animals. We conducted a grazing study to examine how forage mixture complexity affected sward structure. Replicated 1‐ha pastures (Hagerstown silt loam soil: fine, mixed, semiactive, mesic, Typic Hapludalf) were planted to either orchardgrass (Dactylis glomerata L.) and white clover (Trifolium repens L.) or a nine‐species mixture [orchardgrass, tall fescue (Festuca arundinacea Schreb.), perennial ryegrass (Lolium perenne L.), Kentucky bluegrass (Poa pratensis L.), red clover (Trifolium pratense L.), birdsfoot trefoil (Lotus corniculatus L.), white clover, alfalfa (Medicago sativa L.), and chicory (Cichorium intybus L.)]. Pastures were stocked rotationally with lactating dairy cows (Bos taurus). Herbage mass, sward height, vertical structure, and nutritive value were measured pre‐ and postgrazing during four periods in each of 2002 and 2003. Pregrazing sward height was similar between the mixtures. Pregrazing herbage mass and sward bulk density were 30% less in the two‐species mixture than the nine‐species mixture in 2002 but similar in 2003. The nine‐species mixture had more herbage dry matter in the upper sward layers than the two‐species mixture. Bulk density of herbage dry matter increased and nutritive value decreased from the top to the bottom of both swards. Cattle grazed deeper into the two‐species sward (18 cm) than the nine‐species mixture (11 cm) in 2003; however, individual botanical components in the upper 25 cm of the canopy were removed similarly between treatments. We conclude that sward structure did not alter the pattern of herbage removal during grazing of simple or complex swards.

ABSTRACT Coxsackievirus B3 (CVB3) is a common factor in human myocarditis. Apoptotic events are present in CVB3-induced disease, but it is unclear how CVB3 is involved in apoptosis and which viral proteins may induce the apoptotic pathway. In this report we demonstrate that the human and murine proapoptotic protein Siva specifically interact with the CVB3 capsid protein VP2. Furthermore, the transcription of Siva is strongly induced in tissue of CVB3-infected mice and is present in the same area which is positively stained for apoptosis, CD27, and CD70. It has been proposed that Siva is involved in the CD27/CD70-transduced apoptosis. Therefore, we suggest a molecular mechanism through which apoptotic events contributes to CVB3-caused pathogenesis.