© 2018, Springer Science+Business Media, LLC, part of Springer Nature. Children with specific learning disorders (SLDs) face a unique set of socio-emotional challenges as a result of their academic difficulties. Although a higher prevalence of anxiety in children with SLD is often reported, there is currently no research on cognitive mechanisms underlying this anxiety. One way to elucidate these mechanisms is to investigate attentional bias to threatening stimuli using a dot-probe paradigm. Our study compared children ages 9–16 with SLD (n = 48) to typically-developing (TD) controls (n = 33) on their attentional biases to stimuli related to general threats, reading, and stereotypes of SLD. We found a significant threat bias away from reading-related stimuli in the SLD, but not TD group. This attentional bias was not observed with the general threat and stereotype stimuli. Further, children with SLD reported greater anxiety compared to TD children. These results suggest that children with SLD experience greater anxiety, which may partially stem from reading specifically. The finding of avoidance rather than vigilance to reading stimuli indicates the use of more top-down attentional control. This work has important implications for therapeutic approaches to anxiety in children with SLD and highlights the need for attention to socio-emotional difficulties in this population. Future research is needed to further investigate the cognitive aspects of socio-emotional difficulties in children with SLD, as well as how this may impact academic outcomes.

The UDP-glucuronosyltransferase (UGT) family of enzymes plays a vital role in the detoxification of carcinogens as well as clearance of anti-cancer drugs. In humans, 19 UGT family members have been identified and are expressed in a tissue specific manner throughout the body. However, the UGTs have not been previously characterized in melanocytes or melanoma. In the present study, UGT2B7, UGT2B10, and UGT2B15 were identified as being normally expressed in human melanocytes. The same three UGT family members were also expressed in the primary melanoma cell line WM115. No UGT expression was detected in another primary melanoma cell line, WM3211, or in any metastatic melanoma cell line examined. These results suggest that UGT expression is lost during melanoma progression. Treatment of WM3211 or metastatic melanoma cell lines with anti-cancer agents (including vemurafenib) induced expression of UGT2B7, UGT2B10 and UGT2B15 demonstrating that melanoma cells retain the ability to re-express these same three UGTs. The corresponding increase in glucuronidation activity in melanoma cells following anti-cancer treatment was also observed. Furthermore, knockdown of UGT2B7 in WM115 cells sensitized these cells to treatment by adriamycin and epirubicin indicating that UGT2B7 is involved in resistance to these drugs. However, knockdown of UGT2B7 had no effect on temozolomide toxicity. Taken together, these results clearly demonstrate a role for UGTs in melanoma etiology. Since the UGTs are drug metabolism enzymes, we propose that re-expression of the UGTs constitutes a previously unsuspected mechanism for intratumoral drug resistance in melanoma. © 2012 Dellinger et al.