Transgenic mice are often used to study the physiologic role of a known gene. The design of experiments with transgenic mice usually does not take into account strain and sex differences, at least in isolated vessels. Therefore, we have compared the contractile response of isolated aortae and isolated pulmonary arteries of male and female mice of different strains (CD1, BL6, and DBA). Contractile stimulation was achieved by depolarization due to KCl, α1-adrenoceptor stimulation by phenylephrine and inhibition of protein phosphatase activity by cantharidin. In isolated aorta, strain-specific differences in contractility and sex-specific differences could be observed. The concentration of phenylephrine (PE) inducing half maximal contraction (EC50) was different between aortae from DBA male mice and the other strains tested. Phasic contractions of isolated aortic rings due to PE were seen in all mice except DBA male. In isolated pulmonary arteries, strain-specific differences and sex-specific differences could be observed. The EC50-values of PE were not different between all groups. Phasic contractions due to PE were only seen in pulmonary arteries from CD1 male and BL6 female. In conclusion, strain- and sex-specific differences should be considered in selecting mice used for transgenesis or gene targeting experiments.
Many opportunities exist to reduce enteric methane (CH4) and other greenhouse gas (GHG) emissions per unit of product from ruminant livestock. Research over the past century in genetics, animal health, microbiology, nutrition, and physiology has led to improvements in dairy production where intensively managed farms have GHG emissions as low as 1 kg of CO2 equivalents (CO2e)/kg of energy-corrected milk (ECM), compared with >7 kg of CO2e/kg of ECM in extensive systems. The objectives of this review are to evaluate options that have been demonstrated to mitigate enteric CH4 emissions per unit of ECM (CH4/ECM) from dairy cattle on a quantitative basis and in a sustained manner and to integrate approaches in genetics, feeding and nutrition, physiology, and health to emphasize why herd productivity, not individual animal productivity, is important to environmental sustainability. A nutrition model based on carbohydrate digestion was used to evaluate the effect of feeding and nutrition strategies on CH4/ECM, and a meta-analysis was conducted to quantify the effects of lipid supplementation on CH4/ECM. A second model combining herd structure dynamics and production level was used to estimate the effect of genetic and management strategies that increase milk yield and reduce culling on CH4/ECM. Some of these approaches discussed require further research, but many could be implemented now. Past efforts in CH4 mitigation have largely focused on identifying and evaluating CH4 mitigation approaches based on nutrition, feeding, and modifications of rumen function. Nutrition and feeding approaches may be able to reduce CH4/ECM by 2.5 to 15%, whereas rumen modifiers have had very little success in terms of sustained CH4 reductions without compromising milk production. More significant reductions of 15 to 30% CH4/ECM can be achieved by combinations of genetic and management approaches, including improvements in heat abatement, disease and fertility management, performance-enhancing technologies, and facility design to increase feed efficiency and life-time productivity of individual animals and herds. Many of the approaches discussed are only partially additive, and all approaches to reducing enteric CH4 emissions should consider the economic impacts on farm profitability and the relationships between enteric CH4 and other GHG.
Skeletal muscles of transgenic mice expressing altered bovine growth hormones (bGH) have been compared with those of nontransgenic mice to determine whether muscle fiber type-specific responses or histopathologies are associated with the altered gene. The slow soleus and predominantly fast gastrocnemius muscles were prepared for myofibrillar ATPase activity (to determine muscle fiber type) and histological examination from mice that were either giant (M4 line), larger than normal (M11 line), dwarf (G119K line), or nontransgenic (NTC). No histopathology was observed in any of the muscles. Although body weights were significantly different between all four lines of mice, only the giant M4 mice had significantly larger muscle fibers than the other lines of mice, while neither the G119K nor M11 lines were significantly different from the NTC for either muscle. No fiber type-specific differences were noted. These results suggest that the different muscles are the product of differences in numbers of muscle fibers expressed in the G119K and M11 lines of mice; the increase in body mass matched the fiber size growth only in the giant M4 line. Therefore, the altered bGH genes may be acting on fetal liver and myoblast/myotube GH receptors to change the GH and IGF-I regulated pattern of muscle development, and eventually, to determine the adult muscle fiber numbers.
