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Robert, N., Walzer, C., Ruegg, S. R., Kaczensky, P., Ganbaatar, O., & Stauffer, C. (2005). Pathologic findings in reintroduced Przewalski's horses (Equus caballus przewalskii) in southwestern Mongolia. J Zoo Wildl Med, 36(2), 273–285.
Abstract: The Przewalski's horse (Equus caballus przewalskii) was extinct in the wild by the mid 1960s. The species has survived because of captive breeding only. The Takhin Tal reintroduction project is run by the International Takhi Group; it is one of two projects reintroducing horses to the wild in Mongolia. In 1997 the first harem group was released. The first foals were successfully raised in the wild in 1999. Currently, 63 Przewalski's horses live in Takhin Tal. Little information exists on causes of mortality before the implementation of a disease-monitoring program in 1998. Since 1999, all dead horses recovered (n = 28) have been examined and samples collected and submitted for further investigation. Equine piroplasmosis, a tick-transmitted disease caused by Babesia caballi or Theileria equi, is endemic in Takhin Tal and was identified as the cause of death of four stallions and one stillborn foal. In December 2000, wolf predation was implicated in the loss of several Przewalski's horses. However, thorough clinical, pathologic, and bacteriologic investigations performed on dead and surviving horses of this group revealed lesions compatible with strangles. The extreme Mongolian winter of 2000-2001 is thought to have most probably weakened the horses, making them more susceptible to opportunistic infection and subsequent wolf predation. Other occasional causes of death since 1999 were trauma, exhaustion, wasting, urolithiasis, pneumonia, abortion, and stillbirth. The pathologic examination of the Przewalski's horses did not result in a definitive diagnosis in each case. Several disease factors were found to be important in the initial phase of the reintroduction, which could potentially jeopardize the establishment of a self-sustaining population.
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Nicol, C. J., Yoon, M., Ward, J. M., Yamashita, M., Fukamachi, K., Peters, J. M., et al. (2004). PPARgamma influences susceptibility to DMBA-induced mammary, ovarian and skin carcinogenesis. Carcinogenesis, 25(9), 1747–1755.
Abstract: Peroxisome proliferator-activated receptor gamma (PPARgamma), a member of the nuclear receptor superfamily, plays a role in adipocyte differentiation, type II diabetes, macrophage response to inflammation and is suggested to influence carcinogen-induced colon cancer. Studies done in vitro and in vivo also revealed that PPARgamma ligands might promote differentiation and/or regression of mammary tumors. To directly evaluate the role of PPARgamma in mammary carcinogenesis, PPARgamma wild-type (+/+) or heterozygous (+/-) mice were administered 1 mg 7,12-dimethylbenz[a]anthracene (DMBA) by gavage once a week for 6 weeks and followed for a total of 25 weeks. Compared with congenic PPARgamma(+/+) littermate controls, PPARgamma(+/-) mice had early evidence for increased susceptibility to DMBA-mediated carcinogenesis based on a 1.6-fold increase in the percentage of mice with skin papillomas, as well as a 1.7-fold increase in the numbers of skin papillomas per mouse (P < 0.05). Similarly, PPARgamma(+/-) mice also had a 1.5-fold decreased survival rate (P = 0.059), and a 1.7-fold increased incidence of total tumors per mouse (P < 0.01). Moreover, PPARgamma(+/-) mice had an almost 3-fold increase in mammary adenocarcinomas (P < 0.05), an over 3-fold increase in ovarian granulosa cell carcinomas (P < 0.05), an over 3-fold increase in malignant tumors (P < 0.02) and a 4.6-fold increase in metastatic incidence. These results are the first to demonstrate an increased susceptibility in vivo of PPARgamma haploinsufficiency to DMBA-mediated carcinogenesis and suggest that PPARgamma may act as a tumor modifier of skin, ovarian and breast cancers. The data also support evidence suggesting a beneficial role for PPARgamma-specific ligands in the chemoprevention of mammary, ovarian and skin carcinogenesis.
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Munoz-Sanz, A. (2006). [Christopher Columbus flu. A hypothesis for an ecological catastrophe]. Enferm Infecc Microbiol Clin, 24(5), 326–334.
Abstract: When Christopher Columbus and his men embarked on the second Colombian expedition to the New World (1493), the crew suffered from fever, respiratory symptoms and malaise. It is generally accepted that the disease was influenza. Pigs, horses and hens acquired in Gomera (Canary Islands) traveled in the same ship. The pigs may well have been the origin of the flu and the intermediary hosts for genetic recombination of other viral subtypes. The Caribbean archipelago had a large population of birds, the natural reservoir of the avian influenza virus. In this ecological scenario there was a concurrence of several biological elements that had never before coexisted in the New World: pigs, horses, the influenza virus and humans. We propose that birds are likely to have played an important role in the epidemiology of the flu occurring on the second Colombian trip, which caused a fatal demographic catastrophe, with an estimated mortality of 90% among the natives.
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