|
|
Nelson, W. A., Keirans, J. E., Bell, J. F., & Clifford, C. M. (1975). Host-ectoparasite relationships. J Med Entomol, 12(2), 143–166.
|
|
|
|
Valova, G. P., & Mefod'ev, V. V. (1972). [Specific features of an epidemic process in leptospiroses in northern conditions in Western Siberia]. Zh Mikrobiol Epidemiol Immunobiol, 49(11), 138–145.
|
|
|
|
Menges, R. W., Furcolow, M. L., Selby, L. A., Habermann, R. T., & Smith, C. D. (1967). Ecologic studies of histoplasmosis. Am J Epidemiol, 85(1), 108–119.
|
|
|
|
Arakawa, H., Arakawa, K., Blanchard, D. C., & Blanchard, R. J. (2008). A new test paradigm for social recognition evidenced by urinary scent marking behavior in C57BL/6J mice. Behav. Brain. Res., 190(1), 97–104.
Abstract: Olfaction is a major sensory element in intraspecies recognition and communication in mice. The present study investigated scent marking behaviors of males of the highly inbred C57BL/6J (C57) strain in order to evaluate the ability of these behaviors to provide clear and consistent measures of social familiarity and response to social signals. C57 males engage in scent marking when placed in a chamber with a wire mesh partition separating them from a conspecific. Male mice (C57 or outbred CD-1 mice) showed rapid habituation of scent marking (decreased marking over trials) with repeated exposure at 24-h intervals, to a stimulus animal of the C57 or CD-1 strains, or to an empty chamber. Subsequent exposure to a genetically different novel mouse (CD-1 after CD-1 exposure, or CD-1 after C57 exposure) or to a novel context (different shaped chamber) produced recovery of marking, while responses to a novel but genetically identical mouse (C57 after C57 exposure) or to the empty chamber did not. This finding demonstrated that male mice differentiate familiar and novel conspecifics as expressed by habituation and recovery of scent marking, but neither C57 or CD-1 mice can differentiate new vs. familiar C57 males; likely due to similarities in their odor patterns. The data also indicate that scent marking can differentiate novel from familiar contexts.
|
|
|
|
Boray, J. C. (1969). Experimental fascioliasis in Australia. Adv Parasitol, 7, 95–210.
|
|
|
|
Nosek, J. (1972). The ecology and public health importance of Dermacentor marginatus and D. reticulatus ticks in Central Europe. Folia Parasitol (Praha), 19(1), 93–102.
|
|
|
|
Scherer, W. F., & Dickerman, R. W. (1972). Ecologic studies of Venezuelan encephalitis virus in southeastern Mexico. 8. Correlations and conclusions. Am J Trop Med Hyg, 21(2), 86–89.
|
|
|
|
Houpt, K. A. (1976). Animal behavior as a subject for veterinary students. Cornell Vet, 66(1), 73–81.
Abstract: Knowledge of animal behavior is an important asset for the veterinarian; therefore a course in veterinary animal behavior is offered at the New York State College of Veterinary Medicine as an elective. The course emphasizes the behavior of those species of most interest to the practicing veterinarian: cats, dogs, horses, cows, pigs and sheep. Dominance heirarchies, animal communication, aggressive behavior, sexual behavior and maternal behavior are discussed. Play, learning, diurnal cycles of activity and sleep, and controls of ingestive behavior are also considered. Exotic and zoo animal behaviors are also presented by experts in these fields. The critical periods of canine development are related to the optimum management of puppies. The behavior of feral dogs and horses is described. The role of the veterinarian in preventing cruelty to animals and recognition of pain in animals is emphasized. Whenever possible behavior is observed in the laboratory or on film.
|
|
|
|
Crosby, M. B., Svenson, J. L., Zhang, J., Nicol, C. J., Gonzalez, F. J., & Gilkeson, G. S. (2005). Peroxisome proliferation-activated receptor (PPAR)gamma is not necessary for synthetic PPARgamma agonist inhibition of inducible nitric-oxide synthase and nitric oxide. J Pharmacol Exp Ther, 312(1), 69–76.
Abstract: Peroxisome proliferation-activated receptor (PPAR)gamma agonists inhibit inducible nitric-oxide synthase (iNOS), tumor necrosis factor-alpha, and interleukin-6. Because of these effects, synthetic PPARgamma agonists, including thiazolidinediones, are being studied for their impact on inflammatory disease. The anti-inflammatory concentrations of synthetic PPARgamma agonists range from 10 to 50 microM, whereas their binding affinity for PPARgamma is in the nanomolar range. The specificity of synthetic PPARgamma agonists for PPARgamma at the concentrations necessary for anti-inflammatory effects is thus in question. We report that PPARgamma is not necessary for the inhibition of iNOS by synthetic PPARgamma agonists. RAW 264.7 macrophages possess little PPARgamma, yet lipopolysaccharide (LPS)/interferon (IFN)gamma-induced iNOS was inhibited by synthetic PPARgamma agonists at 20 microM. Endogenous PPARgamma was inhibited by the transfection of a dominant-negative PPARgamma construct into murine mesangial cells. In the transfected cells, synthetic PPARgamma agonists inhibited iNOS production at 10 microM, similar to nontransfected cells. Using cells from PPARgamma Cre/lox conditional knockout mice, baseline and LPS/IFNgamma-induced nitric oxide levels were higher in macrophages lacking PPARgamma versus controls. However, synthetic PPARgamma agonists inhibited iNOS at 10 microM in the PPARgamma-deficient cells, similar to macrophages from wild-type mice. These results indicate that PPARgamma is not necessary for inhibition of iNOS expression by synthetic PPARgamma agonists at concentrations over 10 microM. Intrinsic PPARgamma function, in the absence of synthetic agonists, however, may play a role in inflammatory modulation.
|
|
|
|
McClearn, G. E. (1971). Behavioral genetics. Behav Sci, 16(1), 64–81.
|
|
