No role is played by the P2X receptors in the caudal aspect of MR. Further investigations are needed to improve the current view of this system and the mechanisms involved in its physiological function. There is no conflict of interest. We would like to thank Rubens F.
de Melo for the excellent technical assistance in the histological procedures. We also would like to thank Catherine Dunford who kindly suggested English corrections to the manuscript. This work was supported by Fundação de Amparo à Pesquisa do Estado ATM Kinase Inhibitor order de São Paulo (FAPESP: #07/51581-2 and #06/60696-5) and Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq). “
“It has been 10 years since the outbreak of severe acute respiratory syndrome (SARS) caused by a novel coronavirus which was ABT-888 nmr subsequently named SARS coronavirus (SARS-CoV) (Peiris et al., 2003b). SARS-CoV is phylogenetically diverged from other known coronaviruses associated with human infections including human coronavirus (HCoV)-OC43, HCoV-229E, HCoV-NL63 and Middle East respiratory syndrome coronavirus (MERS-CoV), but closely related to the civet and the bat SARS-CoVs, a group of lineage B betacoronaviruses found in civets, raccoon dogs, ferret badgers and Chinese horseshoe bats (Rhinolophus sinicus) in Guangdong Province of South China ( Chan et al., 2013c) The Chinese horseshoe
bat appears to be the natural reservoir of the ancestral SARS-CoV, because the Ka/Ks ratios (rate of nonsynonymous mutation/rate of synonymous mutation) of Fossariinae the S, orf3a, and nsp3 genes were low, while those of the civet strains in both the 2003 and the minor 2004 outbreaks were high, suggesting a rapidly evolving process of gene adaptation in the animals ( Lau et al., 2005b and Li et al., 2005a). SARS emerged as an outbreak of atypical acute, community-acquired pneumonia in late 2002. The initial cases were animal handlers in Guangzhou Province
having regular contact with wild game food animals, suggesting that civets could serve as an intermediate amplification host, and later the patients’ close household and hospital contacts. The human SARS-CoV subsequently evolved and was capable of person-to-person transmission. The epidemic was rapidly and globally disseminated when a medical professor from a teaching hospital in Guangzhou, who was considered as a “super-spreader” of SARS, came to Hong Kong on 21 February 2003. During his stay in hotel M, he transmitted the infection to other residents, and the secondary cases spread the disease to hospitals in Hong Kong, and to other countries including Vietnam, Singapore, and Canada. Eventually, a total of 8096 patients were infected in over 30 countries among 5 continents and 774 (9.5%) of them died (Cheng et al., 2007a).