Transpiration occurs through stomata. The alteration of stomatal apertures in response to drought stress is an important process associated with water use efficiency (WUE). Trehalose-6-phosphate phosphatase (TPP) family genes have been reported to participate in stomatal aperture adjustment. However, there have been no reports of the trehalose metabolism pathway genes improving WUE, and the upstream signalling pathway modulating these genes is not clear. Here, we demonstrated that a member of the TPP gene family, AtTPPI, confers drought resistance and improves WUE by decreasing stomatal apertures and improving root architecture. The reduced expression of AtTPPI caused a drought-sensitive phenotype, while its overexpression significantly increased drought tolerance. Abscisic acid (ABA)-induced stomatal closure experiments confirmed that AtTPPI mutation increased the stomatal aperture compared to that of wild-type (WT) plants; in contrast, overexpression plants had smaller stomatal apertures than those of WT plants. Moreover, AtTPPI mutation also caused stunted primary root length and compromised auxin transport, while overexpression plants had longer primary root lengths. Yeast one-hybrid assays showed that ABA-responsive element-binding factor1 (ABF1), ABF2 and ABF4 directly regulated AtTPPI expression. In summary, the way AtTPPI responds to drought stress suggests that AtTPPI-mediated stomatal regulation is an important mechanism to cope with drought stress and improve WUE. © The Author(s) 2020. Published by Oxford University Press on behalf of the Society for Experimental Biology.Using one value for an individual's ankle brachial index (ABI) may inadequately quantify the risk for mortality and cardiovascular (CVD) events. Using data from the Multi-Ethnic Study of Atherosclerosis (2000-2015), 6,527 racial/ethnically diverse adults (62±10 years) free of known CVD had ABI assessment of their bilateral dorsalis pedis/posterior tibial arteries (4-vessels total) and followed for total mortality, incident CVD events/mortality.  https://www.selleckchem.com/products/otx015.html  Individuals were classified into 0, 1, 2, 3 or 4 -vessel PAD (ABI ≤0.9). There were 1,202 (18%) deaths, 656 (10%) incident CVD events, and 282 (4.3%) CVD deaths. Of the 6,527 individuals, 5,711 (87.5%) had 0, 460 (7.0%) had 1, 218 (3.3%) had 2, 69 (1.1%) had 3 and 69 (1.1%) had 4 -vessel PAD, respectively. In multivariable Cox models, increasing number of vessels with PAD was associated with higher risk of mortality (p-trend less then 0.001), CVD events (p-trend=0.002) and CVD mortality (p-trend=0.001). Compared to individuals with 0-vessel disease, HRs for mortality were 1.29 (95% CI, 1.06-1.59) for 1-, 1.45 (1.14-1.86) for 2-, 1.58 (1.13-2.21) for 3-, and 2.15 (1.58-2.94) for 4-vessel disease. A similar pattern was seen for CVD events/mortality. These results suggest the importance of accounting for ABI values of all four leg arteries in clinical practice and research. © The Author(s) 2020. Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health. All rights reserved. For permissions, please e-mail journals.permissions@oup.com.OBJECTIVES Although the prevalence of ageism against older people has been well-established, less is known about the characteristics of those experiences or the experiences of young and middle-aged adults. The present study addressed these gaps by examining young, middle-aged, and older adults' self-reports of an ageist action they experienced. METHODS Participants' descriptions were coded for the domain in which the ageist experience occurred, the perpetrator of the ageist experience, and the type of ageist experience. RESULTS Young adults most commonly reported experiencing ageism in the workplace with coworkers as perpetrators. Middle-aged and older adults also reported ageism in the workplace; however, they also frequently reported experiencing ageism while seeking goods and services. Perpetrators of ageism varied more widely for middle-aged and older adults. Regardless of one's age, ageism was commonly experienced in the form of a lack of respect or incorrect assumptions. DISCUSSION . The findings enhance our understanding of ageism across adulthood by considering the domains, perpetrators, and types of ageist expressions that adults of all ages encounter. They also suggest that interventions to reduce age bias will require multifaceted approaches that take into account the different forms that individuals experience across the lifespan. © The Author(s) 2020. Published by Oxford University Press on behalf of The Gerontological Society of America. All rights reserved. For permissions, please e-mail journals.permissions@oup.com.Nemo-like kinase (NLK), an evolutionarily conserved serine/threonine kinase, is highly expressed in the brain, but its function in the adult brain remains not well understood. In this study, we identify NLK as an interactor of huntingtin protein (HTT). We report that NLK levels are significantly decreased in HD human brain and HD models. Importantly, overexpression of NLK in the striatum attenuates brain atrophy, preserves striatal DARPP32 levels, and reduces mutant HTT (mHTT) aggregation in HD mice. In contrast, genetic reduction of NLK exacerbates brain atrophy and loss of DARPP32 in HD mice. Moreover, we demonstrate that NLK lowers mHTT levels in a kinase-activity dependent manner, while having no significant effect on normal HTT protein levels in mouse striatal cells, human cells, and HD mouse models. The NLK-mediated lowering of mHTT is associated with enhanced phosphorylation of mHTT. Phosphorylation defective mutation of Serine at amino acid 120 (S120) abolishes the mHTT-lowering effect of NLK, suggesting that S120 phosphorylation is an important step in the NLK-mediated lowering of mHTT. A further mechanistic study suggests that NLK promotes mHTT ubiquitination and degradation via the proteasome pathway. Taken together, our results indicate a protective role of NLK in HD and reveal a new molecular target to reduce mHTT levels. © The Author(s) 2020. Published by Oxford University Press. All rights reserved. For Permissions, please email journals.permissions@oup.com.