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    • It is now well established that

    2018-11-13

    It is now well established that long MWCNTs (Poland et al., 2008), as well as large CNT-aggregates of short CNTs (Kolosnjaj-Tabi et al., 2010), can induce granuloma formation in animal models. At this stage, the sizes of CNTs we observed are not large enough to induce such granuloma formation. However, it is also well established that CNTs due to their large specific surface and chemical characteristics can adsorb a large variety of substances from gases and metals to large and small molecules (Ren et al., 2011). Thus, they may act as efficient vectors for air pollutants. In addition, we wish to emphasize that in contrast to previous studies (Kulkarni et al., 2006) the main objective of this work was to characterize the PM found in the lungs of Parisian children and not to establish any link between the presence of PM in the BALF samples and the asthma condition of the examinees. Due to low concentrations of PM inside the cells it is impossible, at this time, to accurately quantify the carbon content of the lung cells. Alveolar macrophages phagocytosis may be impaired in asthmatic patients (Brugha et al., 2014) (i.e. the loading of CNTs seen in this population may be less than for normal children), and asthmatic persons may have an altered deposition pattern. Besides, children deposition pattern may significantly differ from the adult ones. Thus, if CNTs are present in all examined BALFs from asthmatic children they should be present in healthy persons who have less difficulty in breathing. Thus, it is reasonable to conclude that modern humans are being routinely exposed to airborne CNT materials derived from anthropogenic sources.
    Conclusions The scarcity of the observed PMs inside the cells is in line with recent reports showing that long-term exposure to fine particulate air pollution was associated with adverse health effects, even within very low concentration ranges (Beelen et al., 2014). Although the toxicity of carbon nanotubes is still a matter of debate, it is well established that long carbon nanotubes (Poland et al., 2008) and large Tenovin-6 cost of short ones (Kolosnjaj-Tabi et al., 2010) can induce a granulomatous reaction. Based on asbestos-like pathogenicity, it is believed that bio-persistent fiber-shaped nanomaterials that deposit in the lungs can cause oxidative stress and inflammation and could translocate to the pleura, ultimately leading to fibroplasia and neoplasia in the lungs and the pleura (Guarnieri and Balmes, 2014). Current research suggests that fibrous shape of carbon nanotubes could elicit effects similar to asbestos (Guarnieri and Balmes, 2014). Although the size of the observed carbon nanotubes inside lung cells at this time is not large enough to induce granuloma formation, their presence urgently requires more information on their fate and toxicity.
    Authors\' Contributions
    Declaration of Interests
    Role of Funding Source and Ethics Committee Approval
    Funding
    Acknowledgment LJW wishes to thank the Welch Foundation (Grant C-0627) for partial support of this work.
    Introduction Mimecan, also known as an osteoinductive factor or osteoglycin, is a 12kDa secreted protein corresponding to the 105 C-terminal amino acids (residues 176–280) of the preproprotein encoded by the osteoinductive factor gene (Oif), first identified in the organic matrix of bovine bone by chromatography (Bentz et al., 1989). Furthermore, a 25kDa keratin sulfate proteoglycan in bovine cornea was shown to be encoded by the cDNA of this gene, representing the 223 C-terminal amino acids of the encoded protein (residues 58–280) (Funderburgh et al., 1997). The full-length mimecan cDNA was identified from the human pituitary, and was submitted to GenBank (accession no. AF100758) in our previous study (Hu et al., 2000). The genomic structure of mimecan is highly conserved among different species. The human mimecan precursor (298 amino acids) exhibits 92% homology with bovine mimecan (299 amino acids), suggesting a functional importance (Madisen et al., 1990). However, the physiological functions of mimecan remain elusive. Several studies suggest mimecan may be an essential component of normal vascular extracellular matrix, and it is involved in atherosclerosis (Kampmann et al., 2009). Mimecan is considered a major putative regulator of the left ventricular mass (Petretto et al., 2008), and the absence of mimecan has been observed in the development of colorectal cancer (Wang et al., 2007). In our previous study, mimecan was coexpressed with adrenocorticotropic hormone (ACTH) in corticotroph cells of the pituitary, and was up-regulated by glucocorticoids (Ma et al., 2010). Moreover, mimecan regulates ACTH secretion in corticotroph cells, and may play roles in the coordination of the hypothalamus–pituitary–adrenal axis (Ma et al., 2011). These previous results suggest that mimecan is an important factor involved in the physiological and biological functions. In the current study, we report that mimecan is highly expressed in adipose tissue, and it acts as a satiety factor inhibiting food intake by inducing interleukin (IL)-1β and IL-6 expression in the hypothalamus.