The tax viral protein of the HTLV-I transformed T-cell can activate the VEGF gene and other pro-angiogenic factors that facilitate the adhesion process between endothelial cells and HTLV-I infected lymphocytes (13). Likewise, it is known NVP-LDE225 cell line that HTLV1-transformed lymphocytes have higher endothelial adhesive capacity than nontransformed lymphocytes and develop communicating junctions with endothelial cells (6). Nevertheless, it is unknown whether the same characteristic is present in HTLV-I-infected lymphocytes with no malignant transformation. This effect was described

in other viral infections such as in cytomegalovirus (CMV) infection. CMV promotes vascular injury and modulates VEGF gene expression and, consequently, stimulates VEGF secretion in acute infection (14). As in ATLL, we have both infected cells and tumor cells and in HTLV-I carriers we have only infected cells. Analyses of these patients are important to add knowledge concerning angiogenesis find more in ATLL. According to our results, we may argue whether increase of angiogenesis in ATLL is associated with the neoplastic cell or is a consequence of the viral action. Our study has some limitations. We did not measure VEGF plasma levels in HTLV-I carriers, but our results allow us to hypothesize that HTLV-I carriers may have high levels of angiogenic factors. However, this hypothesis remains as an open

question and needs to be proven in studies with a larger number of patients. Indeed, Olopatadine to clarify whether angiogenesis increase in ATLL is caused by leukemic

cell or by the virus or both, studies to investigate VEGF and EPC levels in ATLL in comparison to HTLV-I carriers need to be performed. Finally, if angiogenesis in ATLL is secondary to neoplastic cell stimuli, EPC levels should be studied in the future as a new predictive marker for disease progression. In conclusion we showed higher levels of EPCs in HTLV-I carriers in comparison to healthy subjects. However, our results should be confirmed and validated by other authors. “
“In Table 1 of the article by Zhang H-Q et al. (Arch Med Res 2010;49(1):46-49), there was an error in the presentation of the third genotype listed under the heading Genotypes. It should read ff and not Ff. Also, the ARCMED manuscript number was printed incorrectly. The correct number is ARCMED-09-00457. We apologize for any confusion or inconvenience this may have caused. “
“The authors would like to revise the authorship for their article in Archives of Medical Research 42 (2011) 613-619. The revised authorship should be Gang Cheng,a,∗ Hui Wang,b,∗ Huacong Deng,a Changquan Huang,b and Qingxiu Liub aDepartment of Nuclear Medicine and Endocrinology, The First Affiliated Hospital, Chongqing Medical University, Chongqing, China bDepartment of Geriatrics, The Third Hospital of Mianyang, Mianyang, China _________________________________ Both authors are considered first author.