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Jordan, J. (1970). [Modern views on the structure and function of the vomeronasal (Jacobson's) organ in mammals]. Otolaryngol Pol, 24(4), 457–462.
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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.
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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.
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Nicol, C. J., Adachi, M., Akiyama, T. E., & Gonzalez, F. J. (2005). PPARgamma in endothelial cells influences high fat diet-induced hypertension. Am J Hypertens, 18(4 Pt 1), 549–556.
Abstract: BACKGROUND: Peroxisome proliferator-activated receptor gamma (PPARgamma) ligands improve human hypertension. However, the mechanism and site of this effect remains unknown, confounded by PPARgamma expression in many cell types, including endothelial cells (ECs). METHODS: To evaluate the vascular role of PPARgamma we used a conditional null mouse model. Specific disruption of PPARgamma in ECs was created by crossing Tie2-Cre+ transgenic (T2T+) and PPARgamma-floxed (fl/fl) mice to generate PPARgamma (fl/fl)T2T+ (PPARgamma E-null) mice. Conscious 8- to 12-week-old congenic PPARgamma (fl/fl)Cre- (wild type) and PPARgamma E-null mice were examined for changes in systolic blood pressure (BP) and heart rate (HR), untreated, after 2 months of salt-loading (drinking water), and after treatment for 3 months with high fat (HF) diet alone or supplemented during the last 2 weeks with rosiglitazone (3 mg/kg/d). RESULTS: Untreated PPARgamma E-nulls were phenotypically indistinguishable from wild-type littermates. However, compared to similarly treated wild types, HF-treated PPARgamma E-nulls had significantly elevated systolic BP not seen after normal diet or salt-loading. Despite sex-dependent baseline differences, salt-loaded and HF-treated PPARgamma E-nulls of either sex had significantly elevated HR versus wild types. Interestingly, rosiglitazone improved serum insulin levels, but not HF diet-induced hypertension, in PPARgamma E-null mice. CONCLUSIONS: These results suggest that PPARgamma in ECs not only is an important regulator of hypertension and HR under stressed conditions mimicking those arising in type 2 diabetics, but also mediates the antihypertensive effects of rosiglitazone. These data add evidence supporting a beneficial role for PPARgamma-specific ligands in the treatment of hypertension, and suggest therapeutic strategies targeting ECs may prove useful.
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McClearn, G. E. (1971). Behavioral genetics. Behav Sci, 16(1), 64–81.
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Yamada, T., Rojanasuphot, S., Takagi, M., Wungkobkiat, S., & Hirota, T. (1971). Studies on an epidemic of Japanese encephalitis in the northern region of Thailand in 1969 and 1970. Biken J, 14(3), 267–296.
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Nelson, W. A., Keirans, J. E., Bell, J. F., & Clifford, C. M. (1975). Host-ectoparasite relationships. J Med Entomol, 12(2), 143–166.
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Harman, F. S., Nicol, C. J., Marin, H. E., Ward, J. M., Gonzalez, F. J., & Peters, J. M. (2004). Peroxisome proliferator-activated receptor-delta attenuates colon carcinogenesis. Nat Med, 10(5), 481–483.
Abstract: Peroxisome proliferator-activated receptor-delta (PPAR-delta; also known as PPAR-beta) is expressed at high levels in colon tumors, but its contribution to colon cancer is unclear. We examined the role of PPAR-delta in colon carcinogenesis using PPAR-delta-deficient (Ppard(-/-)) mice. In both the Min mutant and chemically induced mouse models, colon polyp formation was significantly greater in mice nullizygous for PPAR-delta. In contrast to previous reports suggesting that activation of PPAR-delta potentiates colon polyp formation, here we show that PPAR-delta attenuates colon carcinogenesis.
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Rumiantsev, S. N. (1973). [Biological function of Clostridium tetani toxin (ecological and evolutionary aspects)]. Zh Evol Biokhim Fiziol, 9(5), 474–480.
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Tempelis, C. H., & Nelson, R. L. (1971). Blood-feeding patterns of midges of the Culicoides variipennis complex in Kern County, California. J Med Entomol, 8(5), 532–534.
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