Comparative efficacy of two Ivermectin Pour-on anthelmintics in beef steers in a commercial feedyard

Generic products generally have a cost advantage for beef producers over brand-name products. Recently, many beef producers have debated whether to utilize generic anthelmintics in cow/calf herds and feeder cattle. If generics are to be justified, the products must be proven to have efficacy similar to the brand-name product. Previous studies have indicated that generic macrocyclic lactones are less effective in controlling gastrointestinal parasites of cattle than the original brand-name products. The objective of this study was to compare the efficacy of Vetrimec (Norbrook Laboratories Limited, Newry, Co. Down, Northern Ireland) pour-on and Ivomec (Merial Animal Health, Duluth, GA) pour-on by utilizing the fecal egg reduction test in newly arrived feedlot steers

Lensing in the Hercules Supercluster

We report Keck LRIS observations of an arc-like background galaxy near the center of Abell 2152 (z=0.043), one of the three clusters comprising the Hercules supercluster. The background object has a redshift z=0.1423 and is situated 25 arcsec north of the primary component of the A2152 brightest cluster galaxy (BCG). The object is about 15 arcsec in total length and has a reddening-corrected R-band magnitude of $m_R = 18.55\pm0.03$. Its spectrum shows numerous strong emission lines, as well as absorption features. The strength of the H-alpha emission would imply a star formation rate \SFR \approx 3h^{-2} \msun yr$^{-1}$ in the absence of any lensing. However, the curved shaped of this object and its tangential orientation along the major axis of the BCG suggest lensing. We model the A2152 core mass distribution including the two BCG components and the cluster potential. We present velocity and velocity dispersion profile measurements for the two BCG components and use these to help constrain the potential. The lens modeling indicates a likely magnification factor of $\sim1.9$ for the lensed galaxy, making A2152 the nearest cluster in which such significant lensing of a background source has been observed. Finally, we see evidence for a concentration of early-type galaxies at $z=0.13$ near the centroid of the X-ray emission previously attributed to A2152. We suggest that emission from this background concentration is the cause of the offset of the X-ray center from the A2152 BCG. The background concentration and the dispersed mass of the Hercules supercluster could add further to the lensing strength of the A2152 cluster.Comment: Accepted for publication in AJ (January 2001). 9 pages; uses emulateapj.sty. The all-important "Figure 1" is included here in GIF format; for a version which includes Figure 1 as a high-resolution Postscript image, see: http://adcam.pha.jhu.edu/~jpb/a2152.ps.g

Sulforaphane Protects the Liver against CdSe Quantum Dot-Induced Cytotoxicity.

The potential cytotoxicity of cadmium selenide (CdSe) quantum dots (QDs) presents a barrier to their use in biomedical imaging or as diagnostic and therapeutic agents. Sulforaphane (SFN) is a chemoprotective compound derived from cruciferous vegetables which can up-regulate antioxidant enzymes and induce apoptosis and autophagy. This study reports the effects of SFN on CdSe QD-induced cytotoxicity in immortalised human hepatocytes and in the livers of mice. CdSe QDs induced dose-dependent cell death in hepatocytes with an IC50 = 20.4 μM. Pre-treatment with SFN (5 μM) increased cell viability in response to CdSe QDs (20 μM) from 49.5 to 89.3%. SFN induced a pro-oxidant effect characterized by depletion of intracellular reduced glutathione during short term exposure (3-6 h), followed by up-regulation of antioxidant enzymes and glutathione levels at 24 h. SFN also caused Nrf2 translocation into the nucleus, up-regulation of antioxidant enzymes and autophagy. siRNA knockdown of Nrf2 suggests that the Nrf2 pathway plays a role in the protection against CdSe QD-induced cell death. Wortmannin inhibition of SFN-induced autophagy significantly suppressed the protective effect of SFN on CdSe QD-induced cell death. Moreover, the role of autophagy in SFN protection against CdSe QD-induced cell death was confirmed using mouse embryonic fibroblasts lacking ATG5. CdSe QDs caused significant liver damage in mice, and this was decreased by SFN treatment. In conclusion, SFN attenuated the cytotoxicity of CdSe QDs in both human hepatocytes and in the mouse liver, and this protection was associated with the induction of Nrf2 pathway and autophagy

Regulatory network analysis of Paneth cell and goblet cell enriched gut organoids using transcriptomics approaches

The epithelial lining of the small intestine consists of multiple cell types, including Paneth cells and goblet cells, that work in cohort to maintain gut health. 3D in vitro cultures of human primary epithelial cells, called organoids, have become a key model to study the functions of Paneth cells and goblet cells in normal and diseased conditions. Advances in these models include the ability to skew differentiation to particular lineages, providing a useful tool to study cell type specific function/dysfunction in the context of the epithelium. Here, we use comprehensive profiling of mRNA, microRNA and long non-coding RNA expression to confirm that Paneth cell and goblet cell enrichment of murine small intestinal organoids (enteroids) establishes a physiologically accurate model. We employ network analysis to infer the regulatory landscape altered by skewing differentiation, and using knowledge of cell type specific markers, we predict key regulators of cell type specific functions: Cebpa, Jun, Nr1d1 and Rxra specific to Paneth cells, Gfi1b and Myc specific for goblet cells and Ets1, Nr3c1 and Vdr shared between them. Links identified between these regulators and cellular phenotypes of inflammatory bowel disease (IBD) suggest that global regulatory rewiring during or after differentiation of Paneth cells and goblet cells could contribute to IBD aetiology. Future application of cell type enriched enteroids combined with the presented computational workflow can be used to disentangle multifactorial mechanisms of these cell types and propose regulators whose pharmacological targeting could be advantageous in treating IBD patients with Crohn's disease or ulcerative colitis