The first electrochemical dehydrogenative C-S bond formation leading to thienoacene derivatives is described. Several thienoacene derivatives were synthesized via dehydrogenative C-H/S-H coupling. The addition of nBu4 NBr, which catalytically promoted the reaction as a halogen mediator, was essential. © 2020 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.When faced with changing contingencies, animals can use memory to flexibly guide actions, engaging both frontal and temporal lobe brain structures. Damage to the hippocampus (HPC) impairs episodic memory, and damage to the prefrontal cortex (PFC) impairs cognitive flexibility, but the circuit mechanisms by which these areas support flexible memory processing remain unclear. The present study investigated these mechanisms by temporarily inactivating the medial PFC (mPFC), the dorsal HPC (dHPC), and the ventral HPC (vHPC), individually and in combination, as rats learned spatial discriminations and reversals in a plus maze. Bilateral inactivation of either the dHPC or vHPC profoundly impaired spatial learning and memory, whereas bilateral mPFC inactivation primarily impaired reversal versus discrimination learning. Inactivation of unilateral mPFC together with the contralateral dHPC or vHPC impaired spatial discrimination and reversal learning, whereas ipsilateral inactivation did not. Flexible spatial learning thus depends on both the dHPC and vHPC and their functional interactions with the mPFC. © 2020 Wiley Periodicals, Inc.BACKGROUND A fundamental challenge for Emergency Department (ED) clinicians is to relieve severe, acute pain while simultaneously avoiding adverse events associated with opioid analgesics. Because there is evidence that intravenous (IV) acetaminophen is an effective adjuvant analgesic in post-operative settings, we examined whether it also has a role in the ED. METHODS This was a two-arm, double-blind randomized clinical trial. All patients received 1mg IV hydromorphone. Patients were then randomized to receive 1g IV acetaminophen or placebo. The primary outcome was the between-group difference in change in pain from baseline (before treatment), to 60 minutes after administration of study drugs, measured on an 11-point numerical rating scale (NRS). RESULTS Of 828 patients screened, 162 were enrolled and 159 had the primary outcome. Patients allocated to acetaminophen + hydromorphone had a mean decline in pain from baseline to 60 minutes of 6.2 NRS units; those receiving placebo + hydromorphone had a mean decline of 5.4, a difference of 0.8 NRS units (95% confidence interval (CI) -0.01, 1.8). Two patients in each group received additional analgesics in the first 60 minutes of the study. At 120 minutes the NRS pain difference was 0.6 (95% CI -0.4, 1.6). 26.9% of patients who received acetaminophen wanted more analgesia, versus 37.7% of those given placebo (difference -10.8%, 95% CI -24.3%, 4.4%). Incidence of adverse effects was similar in both groups. CONCLUSION The addition of 1g of IV acetaminophen to 1mg of IV hydromorphone provided neither clinically meaningful nor statistically superior analgesia than hydromorphone alone. This article is protected by copyright. All rights reserved.Incidence of Burkitt's lymphoma post-transplant lymphoproliferative disorder (BL-PTLD) in solid organ transplant (SOT) recipients in 1.4%-1.6% with unknown cure rate. We report a case of Epstein-Barr virus (EBV) positive, late-onset BL-PTLD in a 24-year-old EBV donor positive/recipient negative female. This is the first reported case of advanced BL-PTLD post-heart transplant in an adult. This is also the first reported case of treatment of advanced BL-PTLD in a heart transplant recipient with a combined chemotherapy regimen without anthracyclines to avoid cardiotoxicity. The patient received 6 cycles of R-COEP (rituximab with cyclophosphamide, vincristine, etoposide, prednisone) over 6 months and subsequently 3 cycles of high-dose methotrexate (MTX) over 3 months for CNS prophylaxis. She remains without evidence of disease at 19 months post-treatment. This case demonstrates that an anthracycline-free regimen can be the therapy option for patients with BL-PTLD after heart transplantation. © 2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.BACKGROUND AND AIMS Heat shock factor (HSF4) plays a vital role in carcinogenesis and tumour progression. However, its clinical significance implications in hepatocellular carcinoma (HCC) remained elusive. METHODS RT-PCR and western blot were used to detect the HSF4 expression levels in HCC cells and tissues. Immunohistochemistry staining was performed on a tissue microarray containing 104 HCC patients received radical resection. In vitro effects of HSF4 on proliferation, migration and invasion were determined by colony formation and transwell assays in HCCLM3, Huh7, MHCC97L and SMMC7721 cells. Epithelial-mesenchymal transition (EMT) was identified by RT-PCR, WB and immunofluorescence in HCCLM3 and MHCC97L cells. AKT pathway activation was detected by WB and dual luciferase report system in HCCLM3 and MHCC97L cells. RESULTS HSF4 expression was higher in primary HCC tissues derived from recurrent patients, and positively correlated with invasiveness potentials of cell lines. Clinically, patients with high HSF4 expression had significant poorer prognosis.  https://www.selleckchem.com/products/actinomycin-d.html  In vitro experiments showed HSF4 silencing inhibited HCC cell proliferation, migration and invasion, whereas HSF4 overexpression had inverse effects. Moreover, silence of HSF4 induced an epithelial-like phenotype, whereas the overexpression of HSF4 resulted in a mesenchymal-like phenotype in HCC by activating AKT pathway. Further experiments showed that HSF4 could activate AKT pathway in a hypoxia-inducible factor-1α (HIF-1α) dependent, but transforming growth factor-β (TGF-β) independent manner. CONCLUSIONS HSF4 is upregulated in HCC, resulting in greater proliferation, migration and invasion capacities. Moreover, high HSF4 expression is a promising predictive indicator of poor outcome after radical resection. HSF4 may promote aggressive tumour behaviour by enhancing EMT through activating AKT pathway in a HIF1α-dependent manner. © 2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.