Planning ahead in Missouri's dairy industry

Text of caption on page 6 is cut off due to tight binding."Dairying originated as a way men could turn supplies of forage into profitable human food by applying their skill and labor to the management of herds of milking animals. This objective still applies-but how the means have changed! Methods of getting milk out of a cow, to and through the market, and into the kitchens of consumers have gone from hand style to "untouched by human hand" marvels of mechanization. Even the cow, the factory that does the conversion, has been modified into a manufacturing machine that grows more efficient and productive each year. Average production per cow has climbed from 4,218 to 8,513 pounds per year in the past 40 years. Missouri cows haven't produced as well, but have climbed from 3,300 to 7,400 pounds in the same period. That's one of the problems we need to correct in the next few years to stay in competition. Progress has been slow in increasing forage yields but that's coming in for attention now. This publication reviews where Missouri's dairy industry stands now, where we're headed if present trends continue., and what needs to be done to improve the position of dairying. Ten and 20 years from now we want to be in the forefront."--Page 1.Prepared by O.E. Allen, Edward J. Constien, J.E. Edmondson, Alfred Lane, W.J. Murphy, Leroy Peters, Alva L. Preston, Jr., Edward R. Wiggins, Fred H. Meinershagen (Chairman

Shedding light on the elusive role of endothelial cells in cytomegalovirus dissemination.

Cytomegalovirus (CMV) is frequently transmitted by solid organ transplantation and is associated with graft failure. By forming the boundary between circulation and organ parenchyma, endothelial cells (EC) are suited for bidirectional virus spread from and to the transplant. We applied Cre/loxP-mediated green-fluorescence-tagging of EC-derived murine CMV (MCMV) to quantify the role of infected EC in transplantation-associated CMV dissemination in the mouse model. Both EC- and non-EC-derived virus originating from infected Tie2-cre(+) heart and kidney transplants were readily transmitted to MCMV-naïve recipients by primary viremia. In contrast, when a Tie2-cre(+) transplant was infected by primary viremia in an infected recipient, the recombined EC-derived virus poorly spread to recipient tissues. Similarly, in reverse direction, EC-derived virus from infected Tie2-cre(+) recipient tissues poorly spread to the transplant. These data contradict any privileged role of EC in CMV dissemination and challenge an indiscriminate applicability of the primary and secondary viremia concept of virus dissemination

RAGE and Modulation of Ischemic Injury in the Diabetic Myocardium

OBJECTIVE—Subjects with diabetes experience an increased risk of myocardial infarction and cardiac failure compared with nondiabetic age-matched individuals. The receptor for advanced glycation end products (RAGE) is upregulated in diabetic tissues. In this study, we tested the hypothesis that RAGE affected ischemia/reperfusion (I/R) injury in the diabetic myocardium. In diabetic rat hearts, expression of RAGE and its ligands was enhanced and localized particularly to both endothelial cells and mononuclear phagocytes

Lack of the Receptor for Advanced Glycation End-Products Attenuates E. coli Pneumonia in Mice

Background: The receptor for advanced glycation end-products (RAGE) has been suggested to modulate lung injury in models of acute pulmonary inflammation. To study this further, model systems utilizing wild type and RAGE knockout (KO) mice were used to determine the role of RAGE signaling in lipopolysaccharide (LPS) and E. coli induced acute pulmonary inflammation. The effect of intraperitoneal (i.p.) and intratracheal (i.t.) administration of mouse soluble RAGE on E. coli injury was also investigated. Methodology/Principal Findings: C57BL/6 wild type and RAGE KO mice received an i.t. instillation of LPS, E. coli, or vehicle control. Some groups also received i.p. or i.t. administration of mouse soluble RAGE. After 24 hours, the role of RAGE expression on inflammation was assessed by comparing responses in wild type and RAGE KO. RAGE protein levels decreased in wild type lung homogenates after treatment with either LPS or bacteria. In addition, soluble RAGE and HMGB1 increased in the BALF after E. coli instillation. RAGE KO mice challenged with LPS had the same degree of inflammation as wild type mice. However, when challenged with E. coli, RAGE KO mice had significantly less inflammation when compared to wild type mice. Most cytokine levels were lower in the BALF of RAGE KO mice compared to wild type mice after E. coli injury, while only monocyte chemotactic protein-1, MCP-1, was lower after LPS challenge. Neither i.p. nor i.t. administration of mouse soluble RAGE attenuated the severity of E. coli injury in wild type mice. Conclusions/Significance: Lack of RAGE in the lung does not protect against LPS induced acute pulmonary inflammation, but attenuates injury following live E. coli challenge. These findings suggest that RAGE mediates responses to E. coli-associated pathogen-associated molecular pattern molecules other than LPS or other bacterial specific signaling responses. Soluble RAGE treatment had no effect on inflammation. © 2011 Ramsgaard et al

Role of the receptor for advanced glycation endproducts (RAGE) in retinal vasodegenerative pathology during diabetes in mice

Aims/hypothesis: The receptor for AGEs (RAGE) is linked to proinflammatory pathology in a range of tissues. The objective of this study was to assess the potential modulatory role of RAGE in diabetic retinopathy. Methods: Diabetes was induced in wild-type (WT) and Rage mice (also known as Ager mice) using streptozotocin while non-diabetic control mice received saline. For all groups, blood glucose, HbA and retinal levels of methylglyoxal (MG) were evaluated up to 24\ua0weeks post diabetes induction. After mice were killed, retinal glia and microglial activation, vasopermeability, leucostasis and degenerative microvasculature changes were determined. Results: Retinal expression of RAGE in WT diabetic mice was increased after 12\ua0weeks (p < 0.01) but not after 24\ua0weeks. Rage mice showed comparable diabetes but accumulated less MG and this corresponded to enhanced activity of the MG-detoxifying enzyme glyoxalase I in their retina when compared with WT mice. Diabetic Rage mice showed significantly less vasopermeability, leucostasis and microglial activation (p < 0.05–0.001). Rage mice were also protected against diabetes-related retinal acellular capillary formation (p < 0.001) but not against pericyte loss. Conclusions/interpretation: Rage in diabetic mice is protective against many retinopathic lesions, especially those related to innate immune responses. Inhibition of RAGE could be a therapeutic option to prevent diabetic retinopathy

RAGE Regulates Immune Cell Infiltration and Angiogenesis in Choroidal Neovascularization

Purpose: RAGE regulates pro-inflammatory responses in diverse cells and tissues. This study has investigated if RAGE plays a role in immune cell mobilization and choroidal neovascular pathology that is associated with the neovascular form of agerelated macular degeneration (nvAMD). Methods: RAGE null (RAGE-/-) mice and age-matched wild type (WT) control mice underwent laser photocoagulation to generate choroidal neovascularization (CNV) lesions which were then analyzed for morphology, S100B immunoreactivity and inflammatory cell infiltration. The chemotactic ability of bone marrow derived macrophages (BMDMs) towards S100B was investigated. Results: RAGE expression was significantly increased in the retina during CNV of WT mice (