PROBLEM Systemic maternal inflammation is associated with adverse neonatal sequelae. We tested the hypothesis that IL-1β is a key inflammatory regulator of adverse pregnancy outcomes. METHOD OF STUDY Pregnant mice were treated with intraperitoneal injections of IL-1β (0, 0.1, 0.5, or 1 μg) from embryonic day (E)14 to E17. Placenta and fetal brains were harvested and analyzed for morphologic changes and IL-1β signaling markers.  https://www.selleckchem.com/products/Beta-Sitosterol.html  RESULTS As compared with non-treated dams, maternal injections with IL-1β resulted in increased p-NF-κB and caspase-1 in placentas and fetal brains, but not consistently in spleens, suggesting induction of intrinsic IL-1β production. These findings were confirmed by increased levels of IL-1β in the placentas of the IL-1β-treated dams. Systemic treatment of dams with IL-1β suppressed Stat1 signaling. Maternal inflammation caused by IL-1β treatment reduced fetal viability to 80.6% and 58.9%, in dams treated with either 0.5 or 1 μg of IL-1β, respectively. In the placentas, there was an IL-1β dose-dependent distortion of the labyrinth structure, decreased numbers of mononuclear trophoblast giant cells, and reduced proportions of endothelial cells as compared to placentas from control dams. In fetal brains collected at E17, there was an IL-1β dose-dependent reduction in cortical neuronal morphology. CONCLUSION This work demonstrates that systemic IL-1β injection causes dose-dependent structural and functional changes in the placenta and fetal brain. This article is protected by copyright. All rights reserved.Epstein-Barr virus (EBV) is a tumorigenic virus that can cause various human malignancies such as nasopharyngeal carcinoma (NPC) and gastric cancer (GC). EBV encodes 44 mature micro (mi)RNAs, mostly exhibiting oncogenic properties and promoting cancer progression. However, we have previously found that one EBV-encoded miRNA, namely EBV-miR-BART6-3p, acts as a tumor suppressor by inhibiting metastasis and invasion. Here, we report that EBV-miR-BART6-3p inhibits the proliferation of EBV-associated cancers, NPC, and GC, by targeting and downregulating a long non-coding RNA (lncRNA), LOC553103. Through proteomics analysis, we determined that stathmin (STMN1) is affected by EBV-miR-BART6-3p and LOC553103. Further, via RNA immunoprecipitation and luciferase reporter assay, we confirmed that LOC553103 directly binds and stabilizes the 3'UTR region of STMN1 mRNA. These results indicate that the EBV-miR-BART6-3p/LOC553103/STMN1 axis regulates the expression of cell cycle-associated proteins, which then inhibit EBV-associated tumor cell proliferation. These findings provide potential targets or strategies for novel EBV-related cancer treatments, as well as contributes new insights into the understanding of EBV infection-related carcinogenesis. © 2020 Federation of American Societies for Experimental Biology.Recently, the epidemic of Novel Coronavirus disease 2019 (COVID-19) has become a chief public health challenge for many countries around the world. In Italy, it started in January the 31st with the first 2 cases reported; on Monday the 13th of April, the total confirmed cases were 156.363 with 19.901 total deaths (www.who.int). Turin is the fourth Italian city, with roughly 862.000 inhabitants, and the capital of Piedmont region, one of the most affected by COVID-19. This article is protected by copyright. All rights reserved.INTRODUCTION Ecological studies show association between antimicrobial resistance (AMR), and inappropriate oral antibiotics use. Moderating antibiotic prescribing requires an understanding of all drivers of local prescribing. The aim was to quantify how much is determined by external factors compared with discretionary clinical choices. METHODS Oral antibiotic usage taken from England General Practitioner/Family Doctor practice prescribing data was aggregated using WHO/ATC defined daily doses (DDDs). The average annual antibiotic daily prescribing rate (AAADPR) in each practice was the total DDD of oral antibiotics divided by registered population and 365. The AAADPR of English practices in 2017_18 was linked by regression to factors including demographics, geography, medical comorbidities, clinical performance, patient satisfaction, medical workforce characteristics and prescribing selection. The regression coefficients for modifiable prescribing selection factors were applied to the difference between the mopulation, and prescribing selection are drivers of overall antibiotic prescribing. This analysis provides benchmarks for both non-modifiable and modifiable factors against which practices could evaluate their opportunities to reduce antibiotic prescribing. © 2020 The Authors. International Journal of Clinical Practice published by John Wiley & Sons Ltd.NEW FINDINGS What is the central question of this study? We tested whether intra-nucleus accumbens core (NAcC) amylin receptor (AmyR) activation suppresses feeding, and evaluated whether palatable food intake influences mesocorticolimbic AmyR expression. What is the main finding and its importance? Intra-NAcC AmyR activation reduces food intake in some dietary conditions. We showed that all components of the AmyR are expressed in prefrontal cortex and central nucleus of the amygdala, and demonstrated that fat access impacts AmyR expression in these and other mesocorticolimbic nuclei. These results suggest that palatable food intake may alter amylin signaling in the brain and shed further light onto potential sites of action for amylin. ABSTRACT Amylin is a pancreatic and brain-derived peptide that acts within the central nervous system (CNS) to promote negative energy balance. However, our understanding of the CNS sites of action for amylin remains incomplete. Here, we investigate the effect of amylin recepto2 in the mPFC. Taken together, these results indicate that intra-NAcC AmyR activation can suppress energy intake, and furthermore, suggest that AmyR signaling in a broader range of mesocorticolimbic sites may have a role in mediating the effects of amylin on food intake and body weight. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.