Compilation of results of the ICPPR non-Apis working group with a special focus on the bumblebee acute oral and contact toxicity ring test 2014 ICPPR Non-Apis Working Group

Although honeybee risk assessment for chemicals has been rigorously revised recently, methods and techniques available for non-apis pollinators are scarce. An ICPPR working group “non-apis” was established in 2013 to address these knowledge gaps. Acute contact tests were designed and performed with solitary bees Osmia sp. but still require further optimization. Ring tests on acute oral and contact toxicity for the bumblebee Bombus sp. were developed and performed in 2014. Thirteen European laboratories participated in the trials and in most cases control mortality was < 10% after 96h, indicating that the developed methodologies were feasible in a variety of laboratories. The oral exposure and the group contact exposure tests were each found to generate more variable LD50 estimates, whereas the endpoints obtained in the single contact tests were more consistent among laboratories. The difference in the two different contact test designs indicates the presence of a ‘housing’ effect, which makes the group housing less favorable. In addition, the use of Tween80 as a wetting agent was found to be unsuccessful

Reanimation cardio-pulmonaire en Suisse: le temps d'agir! [Cardiopulmonary resuscitation in Switzerland: time to act!]

Cardiovascular related deaths still represent about 50% of all demises despite their decreasing incidence in the United States and in Switzerland. About two thirds of these deaths are due to ischemic heart disease in which half of the patients die outside hospital, the majority of them two hours after the first symptoms. Moreover, sudden death is the first symptom of coronary artery disease in 25% of cases. In this country few of these persons receive adequate basic life support (BLS) at the scene because a coordinated plan to teach BLS to the citizen does not yet exist in Switzerland. With the aid of specialized medical societies, the Swiss Red Cross and affiliated organizations, it is proposed to elaborate a plan to teach BLS to the general public in Switzerland on the basis of the future European guidelines for BLS

Glucose-Induced Glucagon-Like Peptide 1 Secretion Is Deficient in Patients with Non-Alcoholic Fatty Liver Disease

BACKGROUND & AIMS: The incretins glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are gastrointestinal peptide hormones regulating postprandial insulin release from pancreatic β-cells. GLP-1 agonism is a treatment strategy in Type 2 diabetes and is evaluated in Non-alcoholic fatty liver disease (NAFLD). However, the role of incretins in its pathophysiology is insufficiently understood. Studies in mice suggest improvement of hepatic steatosis by GLP-1 agonism. We determined the secretion of incretins after oral glucose administration in non-diabetic NAFLD patients. METHODS: N=52 patients (n=16 NAFLD and n=36 Non-alcoholic steatohepatitis (NASH) patients) and n=50 matched healthy controls were included. Standardized oral glucose tolerance test was performed. Glucose, insulin, glucagon, GLP-1 and GIP plasma levels were measured sequentially for 120 minutes after glucose administration. RESULTS: Glucose induced GLP-1 secretion was significantly decreased in patients compared to controls (p<0.001). In contrast, GIP secretion was unchanged. There was no difference in GLP-1 and GIP secretion between NAFLD and NASH subgroups. All patients were insulin resistant, however HOMA2-IR was highest in the NASH subgroup. Fasting and glucose-induced insulin secretion was higher in NAFLD and NASH compared to controls, while the glucose lowering effect was diminished. Concomitantly, fasting glucagon secretion was significantly elevated in NAFLD and NASH. CONCLUSIONS: Glucose-induced GLP-1 secretion is deficient in patients with NAFLD and NASH. GIP secretion is contrarily preserved. Insulin resistance, with hyperinsulinemia and hyperglucagonemia, is present in all patients, and is more severe in NASH compared to NAFLD. These pathophysiologic findings endorse the current evaluation of GLP-1 agonism for the treatment of NAFLD.status: publishe

Glucose-Induced Glucagon-Like Peptide 1 Secretion Is Deficient in Patients with Non-Alcoholic Fatty Liver Disease

<div><p>Background & Aims</p><p>The incretins glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are gastrointestinal peptide hormones regulating postprandial insulin release from pancreatic β-cells. GLP-1 agonism is a treatment strategy in Type 2 diabetes and is evaluated in Non-alcoholic fatty liver disease (NAFLD). However, the role of incretins in its pathophysiology is insufficiently understood. Studies in mice suggest improvement of hepatic steatosis by GLP-1 agonism. We determined the secretion of incretins after oral glucose administration in non-diabetic NAFLD patients.</p><p>Methods</p><p>N = 52 patients (n = 16 NAFLD and n = 36 Non-alcoholic steatohepatitis (NASH) patients) and n = 50 matched healthy controls were included. Standardized oral glucose tolerance test was performed. Glucose, insulin, glucagon, GLP-1 and GIP plasma levels were measured sequentially for 120 minutes after glucose administration.</p><p>Results</p><p>Glucose induced GLP-1 secretion was significantly decreased in patients compared to controls (p<0.001). In contrast, GIP secretion was unchanged. There was no difference in GLP-1 and GIP secretion between NAFLD and NASH subgroups. All patients were insulin resistant, however HOMA2-IR was highest in the NASH subgroup. Fasting and glucose-induced insulin secretion was higher in NAFLD and NASH compared to controls, while the glucose lowering effect was diminished. Concomitantly, fasting glucagon secretion was significantly elevated in NAFLD and NASH.</p><p>Conclusions</p><p>Glucose-induced GLP-1 secretion is deficient in patients with NAFLD and NASH. GIP secretion is contrarily preserved. Insulin resistance, with hyperinsulinemia and hyperglucagonemia, is present in all patients, and is more severe in NASH compared to NAFLD. These pathophysiologic findings endorse the current evaluation of GLP-1 agonism for the treatment of NAFLD.</p></div