essaging within the EMR could enable "closed loop" communication that helps ensure safe transitions of care for high-risk patients.Eosinophils play a pivotal role in the inflammatory pathology of asthma and have been the target of new biologic treatments for patients with eosinophilic asthma. Given the central role of interleukin (IL)-5 in the eosinophil lifecycle, several therapies directed against the IL-5 pathway have been developed, including the anti-IL-5 antibodies mepolizumab and reslizumab and the IL-5 receptor α (IL-5Rα)-directed cytolytic antibody benralizumab. Eosinophil-depleting therapies represent a relatively new class of asthma treatment, and it is important to understand their long-term efficacy and safety. Eosinophils have been associated with host protection and tumor growth, raising potential concerns about the consequences of long-term therapies that deplete eosinophils. However, evidence for these associations in humans is conflicting and largely indirect or based on mouse models. Substantial prospective clinical trial and postmarketing data have accrued, providing insight into the potential risks associated with eosinophil depletion. In this review, we explore the current safety profile of eosinophil-reducing therapies, with particular attention to the potential risks of malignancies and severe infections and a focus on benralizumab. Benralizumab is an IL-5Rα-directed cytolytic monoclonal antibody that targets and efficiently depletes blood and tissue eosinophils through antibody-dependent cell-mediated cytotoxicity. Benralizumab is intended to treat patients with severe, uncontrolled asthma with eosinophilic inflammation. The integrated analyses of benralizumab safety data from the phase III SIROCCO and CALIMA trials and subsequent BORA extension trial for patients with asthma, and the phase III GALATHEA and TERRANOVA trials for patients with chronic obstructive pulmonary disease, form the principal basis for this review.Neuropilin-1 (NRP-1) is known to be related to various types of cancer and is considered a novel tumor marker or therapeutic target. The aim of this study was to identify the clinical implications of NRP-1 expression in terms of prognosis in patients with gastric cancer. A total of 265 patients who underwent radical gastrectomy for the treatment of gastric cancer from 2008 to 2011 were included in this retrospective study. NRP-1 expression of tumors was determined by immunohistochemistry. The patients' clinicopathological characteristics, operative details, and long-term outcomes were retrospectively analyzed. A total of 181 (68.3%) patients demonstrated expression of NRP-1. No survival difference was observed according to NRP-1 expression in any patient. The patients were divided into the gland formation (GF) and the no gland formation (nGF) types, according to histology. NRP-1 expression rates were 65.6% (84/128) and 70.8% (97/137), respectively. NRP-1 expression was not an independent prognostic factor in the GF group, although patients who expressed NRP-1 had better survival outcomes. In contrast, patients who expressed NRP-1 in the nGF group had worse 5-year survival rates (p = 0.027), and NRP-1 was an independent prognostic factor in a multivariate analysis (hazard ratio, 1.923; 95% confidence interval, 1.041-3.551). NRP-1 expression in patients with nGF type gastric cancer is predictive of a poor prognosis.The patient was a 67-year-old man with advanced hepatocellular carcinoma (HCC) due to chronic hepatitis B. selleck inhibitor Due to refractoriness to radiofrequency ablation and transcatheter arterial chemoembolization, lenvatinib, a new oral mutikinase inhibitor, was started with a daily dose of 12 mg. However, on day 6 the patient developed acute-onset, right upper quadrant pain associated with fever; laboratory tests revealed leukocytosis and liver dysfunction. CT scan showed the swollen gallbladder with wall thickening with no evidence of gallstones, and the diagnosis of acute acalculous cholecystitis was made. After the resolution of cholecystitis by antibiotics and endoscopic nasogallbladder drainage placement, lenvatinib was resumed at a reduced daily dose of 4 mg. However, acute acalculous cholecystitis recurred, supporting lenvatinib as a cause of acute acalculous cholecystitis. Using the Naranjo adverse drug reaction probability scale, a score of 6 was derived, which indicates that this adverse event was probably caused by lenvatinib. In summary, we present a patient with advanced HCC who underwent repeated episodes of acute acalculous cholecystitis as a rare adverse event associated with lenvatinib.PURPOSE OF REVIEW The aim of the review is to conduct a literature search on cost-effectiveness or cost savings of osteoporosis fracture liaison services. RECENT FINDINGS We identified four types of FLS. A total of 11 cost-effectiveness studies examining 15 models of secondary fracture prevention models were identified. Nine models were found to be cost-saving, and five were found to be cost-effective. It is possible to adopt a cost-effective model for fracture liaison services and expand across geographical regions. Adopting registries can have the added benefit of monitoring quality improvement practices and treatment outcomes. Challenges exist in implementing registries where centralized data collections across different chronic conditions are politically driving agendas. In order to align political and organizational strategic plans, a core set of outcome evaluations that are both focused on patient and provider experience in addition to treatment outcomes can be a step toward achieving better health and services.BACKGROUND In liver cirrhosis, a marked splanchnic vasodilation causes an increase in portal blood flow, contributing to the development of portal hypertension. AIM To evaluate if, in experimental cirrhosis, a different vascular reactivity exists between splenic and mesenteric components of the splanchnic circulation. METHODS Liver cirrhosis was induced in Sprague Dawley rats by common bile duct ligation. In sections of splenic and superior mesenteric arteries, cumulative dose-response curves were obtained. mRNA expression of endothelial nitric oxide synthase (eNOS), inducible NOS (iNOS), and prostaglandin I2 synthase (PTGIS) was evaluated. RESULTS In cirrhotic rats, mesenteric but not splenic arteries showed a significant increase in endothelium-dependent relaxation to acetylcholine. In control and cirrhotic rats, COX inhibition alone did not significantly change the response of mesenteric arteries to acetylcholine; after inhibiting also NOS, the relaxation was completely abolished in control but only partially decreased in cirrhotic rats.