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Discrete trial instruction (DTI) is a ubiquitous tool used by practitioners in early intervention programs. A common approach to correcting errors during DTI involves providing a single prompt of the target response when a mistake is made (i.e., single-response repetition). Modifications to the single-response repetition approach have been developed to improve acquisition; however, these modifications are often aversive techniques (e.g., increased effort, response cost) and may not be preferred by the children or considered socially acceptable by caregivers. We conducted this study to evaluate the use of a transition from rich to lean reinforcement as a form of error correction. We compared the rich-lean condition to the single-response repetition approach during DTI for 4 boys diagnosed with autism. The rich-lean condition was (a) more efficient in improving accuracy in 6 out of 9 tasks, (b) more preferred by all participants, and (c) socially validated by caregivers. find more © 2020 Society for the Experimental Analysis of Behavior.BACKGROUND AND OBJECTIVES Red blood cell (RBC) transfusions are needed by almost every acute myeloid leukaemia (AML) patient undergoing induction chemotherapy and constitute a cornerstone in supportive measures for cancer patients in general. Randomized controlled trials have shown non-inferiority or even superiority of restrictive transfusion guidelines over liberal transfusion guidelines in specific clinical situations outside of medical oncology. In this study, we analysed whether more restrictive RBC transfusion reduces blood use without affecting hard outcomes. MATERIALS AND METHODS A total of 352 AML patients diagnosed between 2007 and 2018 and undergoing intensive induction chemotherapy were included in this retrospective analysis. In the less restrictive transfusion group, patients received RBC transfusion for haemoglobin levels below 8 g/dl (2007-2014). In the restrictive transfusion group, patients received RBC transfusion for haemoglobin levels below 7 g/dl (2016-2018). Liberal transfusion triggers were never endorsed. RESULTS A total of 268 (76·1%) and 84 (23·9%) AML patients fell into the less restrictive and restrictive transfusion groups, respectively. The less restrictive transfusion group had 1 g/dl higher mean haemoglobin levels, received their first RBC transfusions earlier and needed 1·5 more units of RBC during the hospital stay of induction chemotherapy. Febrile episodes, C-reactive protein levels, admission to the intensive care unit, length of hospital stay as well as response and survival rates did not differ between the two cohorts. CONCLUSION From our retrospective analysis, we conclude that a more restrictive transfusion trigger does not affect important outcomes of AML patients. The opportunity to test possible effects of the more severe anaemia in the restrictive transfusion group on quality of life was missed. © 2020 The Authors. Vox Sanguinis published by John Wiley & Sons Ltd on behalf of International Society of Blood Transfusion.Abdominal aortic aneurysm (AAA) is a potentially lethal disease featured by focal dilatation in the aorta. The transition of vascular smooth muscle cells (SMCs) from a contractile/differentiated to a synthetic/dedifferentiated phenotype is considered to contribute to AAA formation and expansion. Our previous gene microarray data showed that Ventricular Zone Expressed PH Domain Containing 1 (VEPH1) expression increased in angiotensin II (Ang II)-infused aortic tissues. This study was thus performed to further explore the role of VEPH1. Herein, we first demonstrate that VEPH1 increases in the SMCs of Ang II-treated abdominal aortas. As in vivo, Ang II also upregulated VEPH1 expression in cultured hAoSMCs. The dedifferentiation of human aortic SMCs (hAoSMCs) was induced by a 24-hr stimulation of Ang II (1 μM)-the expression of contractile SMC markers, MYH11 and α-smooth muscle actin (α-SMA) decreased and that of synthetic markers, proliferating cell nuclear antigen and Vimentin increased. Inhibition of VEPH1 prevented Ang II-induced pathological dedifferentiation of hAoSMCs as indicated by the restored expression of MYH11 and α-SMA. In contrast, the forced overexpression of VEPH1 aggravated Ang II's effects. Furthermore, we demonstrated that VEPH1 and transforming growth factor-β1 (TGF-β1), a key regulator responsible for vascular SMC differentiation, negatively regulated each other's transcription. In contrast to VEPH1 silencing, its overexpression inhibited recombinant TGF-β1-induced increases in MYH11 and α-SMA and suppressed Smad3 phosphorylation and nuclear accumulation. Collectively, our study demonstrates that VEPH1 elevation promotes the synthetic phenotype switching of AoSMCs and suppressed the TGF-β1/Smad3 signaling pathway. Identification of VEPH1 as a pathogenic molecule for AAA formation provides novel insights into this disease. © 2020 Wiley Periodicals, Inc.Head and neck squamous cell carcinoma (HNSCC) remains a major health problem worldwide. We aimed to identify a robust microRNA (miRNA)-based signature for predicting HNSCC prognosis. The miRNA expression profiles of HNSCC were obtained from The Cancer Genome Atlas (TCGA) database. The TCGA HNSCC cohort was randomly divided into the discovery and validation cohort. A miRNA-based prognostic signature was built up based on TGCA discovery cohort, and then further validated. The downstream targets of prognostic miRNAs were subjected to functional enrichment analyses. The role of miR-1229-3p, a prognosis-related miRNA, in tumorigenesis of HNSCC was further evaluated. A total of 305 significantly differentially expressed miRNAs were found between HNSCC samples and normal tissues. A six-miRNA prognostic signature was constructed, which exhibited a strong association with overall survival (OS) in the TCGA discovery cohort. In addition, these findings were successfully confirmed in TCGA validation cohort and our own independent cohort. The miRNA-based signature was demonstrated as an independent prognostic indicator for HNSCC. A risk signature-based nomogram model was constructed and showed good performance for predicting the OS for HNSCC. The functional analyses revealed that the downstream targets of these prognostic miRNAs were closely linked to cancer progression. Mechanistically, in vitro analysis revealed that miR-1229-3p played a tumor promoting role in HNSCC. In conclusion, our study has developed a robust miRNA-based signature for predicting the prognosis of HNSCC with high accuracy, which will contribute to improve the therapeutic outcome. © 2020 Wiley Periodicals, Inc.

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