Evaluation of a Direct Fed Microbial an an Enzymatically Hydrolyzed Yeast Product Fed Alone or in Combination to Beef Steers Administered Ractopamine Hydrochloride 28 Days Prior to Harvest During Summer Months in the Northern Plains

Study Description: Single-sourced, newly weaned steers (n=256; initial BW=542 ± 3.7lb; n=64 steers/treatment; 8 steers/pen) were blocked by location in a 2×2 factorial arrangement of DFM (Certillus CP B1801 Dry; Bacillus subtilis, Lactobacillus plantarum; 28 g/steer·d-1) and YCW (Celmanax; 18 g/steer·d-1). Temperature-humidity index (THI) was calculated as: THI=0.81×ambient temperature+[relative humidity×(ambient temperature-14.40)]+46.40. On d-1 and 2 and d-21 and 22 on RH, respiration rate (RR) and panting scores (PS) were determined before and after AM and PM feedings (0700h, 1100h, 1400h, 1700h). RR (n=3 steers/pen) was calculated from: 600/seconds required for 10 flank movements. PS utilized this scoring system: 0 (not distressed) to 4.5 (severely distressed)

Evaluation of a Direct Fed Microbial and/or an Enzymatically Hydrolyzed Yeast Product in Diets Containing Monensin Sodium on Feedlot Phase Growth Performance, Efficiency of Dietary Net Energy Utilization, and Carcass Characteristics in Newly Weaned Beef Steers Fed in Confinement for 258 Days

Study Description: Single-sourced, newly weaned steers (n = 256; initial body weight (BW) = 542 ± 3.7 lb) were allotted to 32 pens (n = 8 pens/treatment with 8 steers/pen). Steers were blocked by location in a 2x2 factorial treatment arrangement of DFM (Certillus CP B1801 Dry; Bacillus subtilis, Lactobacillus plantarum; 28 g/steer·d-1) and YCW (Celmanax; 18 g/steer·d-1). Steers were vaccinated and poured at processing and individually weighed on d 1, 14, 42 (end of receiving phase; implanted), 77, 105 (end of growing phase), 133, 161 (implanted), 182, 230 (start ractopamine HCl) and 258. Growth performance and carcass measurements were recorded

The object sculpture

Wilson co-curated an international survey exhibition of 30 sculptures past and present, each work by a different artist. Works were installed throughout the Henry Moore Institute, from the front steps to the library, the final work being the catalogue, designed as a piece of work by artist Pae White. An exhibition arising out of a unique set of curatorial conditions – the entire budget and apparatuses of the museum were handed over to three artists seen, through their exhibited work, to have manifested a particular interest in the condition of sculpture today. Together, they were set the task of answering the question ‘What is Sculpture?’ Over the following 18 months, through extensive meetings and correspondences, an exhibition was made which took the full extent of the Institute as its frame, from the library to the front steps. The artists employed an independent researcher to gather information surrounding each chosen work, and offered all this archival material to the sculptor Pae White who was asked to produce a catalogue as the final artwork for exhibition. The collection of works and texts on display articulated the shared international and historical context in which the artists agreed they now work. But the exhibition also announced its own particular modus operandi – each discrete artwork was carefully installed according to its own needs, as well as being there as representative of its class of sculpture. Visitors were invited to encounter discrete works in the first instance, divorced from their contexts, and this prioritising of direct experience was reflected in the invitation cards, where the list of works took precedence over the list of artists. The catalogue, as well as being an artwork in its own right, provided factual material surrounding each exhibited piece with a minimum of interpretation, offering the first step in helping visitors piece together a more contextual reading. Wilson took full equal part in the curatorial process up to final installation of the works. The exhibition was widely reviewed and has an international reputation - it helped set the terms for discussing contemporary sculptural practice

Cloning and characterization of murine p16(INK4a) and p15(INK4b) genes

Progression through the G1 phase of the cell cycle is regulated in part by the D-type cyclin-dependent kinases, cdk4 and cdk6. Genes encoding two specific inhibitors of these kinases, human p16((INK4a/MTS1)) and p15((INK4b/MTS2)) map to a region of common cytogenetic abnormalities on chromosome 9p21. The murine cognates of these genes were isolated and identified as mouse p16(INK4a) and p15(INK4b) based on their homology to their human counterparts and their selective transcriptional induction by SV40T-antigen and TGF-β, respectively. Both genes map to position C3-C6 on mouse chromosome 4, in a region syntenic with human chromosome 9p. Amplification of polyadenylated mRNA by polymerase chain reactions revealed no expression of mouse p16(INK4a) in, many normal tissues, whereas p15(INK4b) was expressed ubiquitously. Like human p16(INK4a), mouse p16(INK4a) binds specifically to cdk4 and cdk6 in vitro and inhibits the phosporylation of the retinoblastoma protein, pRb, by each of these cyclin D-dependent kinases. In mouse MEL erythroleukemia cells, p16(INK4a) associates preferentially with cdk6 under conditions where cdk4 and cdk6 are coexpressed at equivalent levels. Expression vectors encoding human or mouse p16(INK4a) caused G1 phase arrest in NIH3T3 fibroblasts, and cyclin D1- and cdk4-dependent pRb kinase activities were inhibited in the p16(INK4a)-arrested cells