On September 5, 1867 20 carloads of Texas Longhorn cattle left Abilene, Kansas to journey to the stockyards of Chicago. This was the first shipment of cattle by rail in the United States and a historic moment for the beef cattle industry. Historical accounts of the cattle industry indicate a range of concerns about cattle transport. In 1872 George T. Angell's book "Cattle Transport in the United States" unleashed public outcry. The next year Congress passed the twenty-eight hour law to protect livestock in transit. Concerns expressed by early "reformers" included time in transit, mortality, use of whips and prods, and overcrowding.
The majority of beef cattle raised in the United States will undergo transport at least once. Ninety-five percent are hauled by truck. Transportation is generally regarded as stressful to cattle and includes physical and psychological stimuli that can be averse. Behavior, pathology and physiology have been used to identify and characterize cattle response to transport. Physiological measures indicate that transport can result in immune supression which can lead to disease and increased pathogen shedding. Empirical evidence shows that neutrophil to lymphocyte ratio is markedly increased during transport and handling. Loading, loss of balance and falling are distressful to cattle. For example, mean heart rates are lower for cattle transported over smooth roads than on rough roads with frequent intersections. Crowding and motion of the truck tend to reduce agonistic behaviors. Age is an important consideration. Young cattle (<4 wk) do not tolerate transport as well and their physiological response is different from older cattle. Strategies to reduce transportation stress include preconditioning, administration of vitamins, feeding high-energy diets and electrolyte therapy. Research is needed to evaluate cattle behavior during transport as related to space allowance/configuration, vehicle movement, social grouping, in addition to measuring physiological changes and disease processes.
The development, function and regression of the primate corpus luteum during the luteal phase of the menstrual cycle is accompanied by, and presumably dependent upon, formation, maintenance and degeneration of the luteal microvasculature. Recent studies established that microvascular endothelial cells comprise >95% of proliferating cells in luteal tissue; steroidogenic cells were not proliferating. Endothelial cell proliferation varied during the luteal lifespan, with the percent dividing (Ki67-positive) cells highest during luteal development, declining by midluteal phase, and reaching low levels after luteolysis (40, 28, and <5%, respectively). The factors controlling microvascular events in the corpus luteum, including endothelial cell proliferation, are poorly understood. Studies were designed to determine if concepts arising from embryologic models apply to the corpus luteum during the menstrual cycle, i.e., that a balance between vascular endothelial growth factor (VEGF) and the angiopoietins (Ang-1 and its endogenous antagonist, Ang-2) influences the growth, maturation, and destruction of vessels. The results support a novel role of the midcycle gonadotropin surge to stimulate VEGF (protein) and Ang-1 (mRNA) expression in luteinizing granulosa cells of the periovulatory follicle. Moreover, Ang-1 but not VEGF expression may be promoted, at least in part, by LH-induced progesterone production. Following luteal development, levels of VEGF mRNA and protein in luteal cells peak by midluteal phase and decline at luteal regression. In contrast, Ang-2 expression peaks abruptly in the regressing corpus luteum near the end of the cycle. Preliminary data indicate that macaque endothelial cells from the corpus luteum contain VEGF receptors (Flt-1 and KDR) and respond to VEGF in vitro with increased proliferation. Luteal cell-endothelial cell interaction, via the VEGF-/Ang-receptor pathways, may control the microvasculature, and hence development and function of the corpus luteum during the ovarian cycle.