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BACKGROUND Sepsis is a major cause of morbidity and mortality worldwide. Early recognition and treatment of sepsis is associated with improved outcome. Emergency departments (EDs) are the main department where patients with sepsis are presented. But recognition in the ED remains difficult. Different alert and triage systems, screening scores and intervention strategies have been developed to assist clinicians in early recognition of sepsis and to optimize management. OBJECTIVES this narrative review describes currently applied interventions or interventions we can start using today such as screening scores, (automated) triage systems, sepsis teams, and clinical pathways in sepsis care, and summarizes evidence for the effect of implementation of these interventions in the ED on patient management and outcomes. SOURCES A systematic literature search was conducted in PubMed resulting in 32 eligible studies. CONTENT The main sepsis interventions in the ED are (automated) triage systems, sepsis teams and clinical sential, preferably as part of a clinical pathway. BACKGROUND Thyroid hormone promotes remyelination in multiple sclerosis (MS) animal models through a variety of mechanisms. Liothyronine (L-T3) is a short-acting thyroid hormone with demonstrated safety and tolerability for short-term and chronic use in euthyroid adults with other health conditions, but has not been studied in people with MS. The objectives of this single-center, phase I, placebo-controlled, clinical trial were to determine the safety, tolerability, and optimal dosing of L-T3 in people with MS in preparation for a phase 2 remyelination clinical trial. Secondary goals included exploration of the reliability of functional and clinical measurements of myelination in the anterior visual pathway over one week. METHODS Groups of six clinically stable people with MS were randomized in a 42 ratio to receive L-T3 or placebo. The first group received 50 mcg total daily dose (TDD) of L-T3, with escalating doses of L-T3 in subsequent groups, up to potentially 150 mcg TDD in the final group. Prior to enronts were poor sleep and loose stools. No treatment effect of L-T3 was observed over one week. Therefore, data from patients on L-T3 and placebo were pooled to explore VEP and LCLA reliability. The intraclass correlations of VEP 17', VEP 34' and LCLA were 0.836, 0.860, and 0.932, respectively. The mean differences in values between visits 1 and 2 for VEP 17' and 34' and LCLA were 1.9 ms/eye (SD 6.5), 0.4 ms/eye (6.3), and 0.8/eye (3.6), respectively. CONCLUSIONS This study confirms the short-term safety and tolerability of L-T3 in people with MS, with 75 mcg TDD as the MTD. Our results also support that, despite small variations over one week, VEP with various check sizes and Sloan LCLA are reliable functional and clinical outcome measures that could be used in remyelination clinical trials in MS. A future phase 2 clinical trial to investigate the efficacy of L-T3 as a remyelination therapy may be warranted. This trial was registered on clinicaltrials.gov (NCT02760056). Published by Elsevier B.V.Teriflunomide is an oral first-line disease modifying treatment (DMT) for patients with relapsing-remitting multiple sclerosis (RRMS). It can take up to two years to achieve systemic clearance of teriflunomide to an acceptable level, but this washout period may be accelerated by administration of cholestyramine. Relapse of multiple sclerosis (MS) during washout of teriflunomide or other first-line DMT is not as common. We report two patients with RRMS who experienced a relapse after the accelerated elimination period (AEP) of teriflunomide and confirmation of negative plasmatic levels ( less then 0.02 µg/ml). In cases of risk of MS activity, we should not wait for teriflunomide negative plasmatic levels confirmation before starting the next DMT to reduce the risk of relapse. Pancreatic ductal adenocarcinoma (PDAC) is one of the most invasive solid tumours and has the highest cancer-related mortality rate. Despite intense investigation, the molecular mechanisms underlying the invasiveness and aetiology of PDAC remain elusive. MicroRNAs (miRNAs) are key regulators of tumour cell plasticity, but their roles in PDAC metastasis have not been characterized. Our early studies showed that dysbindin protein levels are elevated in PDAC patients compared with control individuals and that dysbindin upregulation elicits PDAC cell proliferation via the PI3K pathway. Here, we show that dysbindin promoted PDAC metastasis via the NF-κB/MDM2 signalling axis. Increased dysbindin levels correlated with aggressive features in PDAC, and the overexpression of dysbindin significantly promoted PDAC metastasis and invasion in vitro and in vivo. Surprisingly, dysbindin was identified as a direct target of miR-342-3p, which promotes NF-κB activation and PDAC metastasis. Thus, dysbindin-mediated NF-κB activation via miR-342-3p represents a context-dependent switch that enables PDAC cell proliferation and metastasis. Our data suggest that dysbindin and miR-342-3p are potential leads for the development of targeted therapy for PDAC. Human papillomavirus (HPV) is an etiological risk factor for a subset of head and neck squamous cell carcinoma (HNSCC). HPV + HNSCC is more radiosensitive than HPV- HNSCC, however, the mechanism underlying this observation remains unknown. Tumor microenvironment can regulate tumor response to radiation therapy. Secretory exosomes are emerging as crosstalk mediators between tumor cells and the tumor microenvironment. Zilurgisertib fumarate In this study, we attempted to determine the role of HPV + HNSCC exosomes in increased radiation sensitivity. We found that HPV + HNSCC exosomes were able to transform macrophages into the M1 phenotype, which subsequently increased the radiosensitivity of HNSCC. miR-9 was found enriched in HPV + HNSCC exosomes and it could be transported into macrophages, inducing M1 macrophage polarization via downregulation of PPARδ. After incubating with M1 macrophages or macrophages treated with miR-9 mimics, HNSCC had strikingly increased radiosensitivity. The clinical significance of miR-9 in HNSCC was confirmed by using profiling data from The Cancer Genome Atlas.
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