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Within the energy transition and decarbonization of the industrial sector, one of the main challenges is identifying competitive solutions to capture CO2 from chemical and energy plants to reduce emissions. The reduction of the carbon footprint as well as the valorization of CO2‐rich gases are of increasing interest for many industries and methanol is a perfect fit for energy storage, for producing clean fuels, and as building block for producing high value chemicals. In this article, an update of recent developments by Air Liquide Engineering & Construction regarding methanol technology is provided, focusing on CO2 reduction of large‐scale plants and on new solutions for CO2 utilization. For large‐scale methanol plants, drop‐in solutions using carbon capture technologies can be proposed to dramatically decrease the CO2 emissions. [ABSTRACT FROM AUTHOR]

BACKGROUND: Exposure reconstructions and risk assessments for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and other dioxins rely on estimates of elimination rates. Limited data are available on elimination rates for congeners other than TCDD. [...]

At present, the best available estimators of [beta]-cell mass in humans are those based on measurement of insulin levels or appearance rates in the circulation. In several animal models, these estimators have been validated against [beta]-cell mass in lean animals. However, as many diabetic humans are obese, a correlation between in vivo tests and [beta]-cell mass must be evaluated over a range of body weights to include different levels of insulin sensitivity. For this purpose, obese (n = 10) and lean (n = 25) Gottingen minipigs were studied. [beta]-Cell mass had been reduced (n = 16 lean, n = 5 obese) with a combination of nicotinamide (67 mg/kg) and streptozotocin (125 mg/kg), acute insulin response (AIR) to intravenous glucose and/or arginine was tested, pulsatile insulin secretion was evaluated by deconvolution (n = 30), and [beta]-cell mass was determined histologically. AIR to 0.3 ([r.sup.2] = 0.4502, P < 0.0001) or 0.6 g/kg glucose ([r.sup.2] = 0.6806, P < 0.0001), 67 mg/kg arginine ([r.sup.2] = 0.5730, P < 0.001), and maximum insulin concentration ([r.sup.2] = 0.7726, P < 0.0001) were all correlated to [beta]-cell mass when evaluated across study groups, and regression lines were not different between lean and obese groups except for AIR to 0.3 g/kg glucose. Baseline pulse mass was not significantly correlated to [beta]-cell mass across the study groups ([r.sup.2] = 0.1036, NS), whereas entrained pulse mass did show a correlation across groups ([r.sup.2] = 0.4049, P < 0.001). This study supports the use of in vivo tests of insulin responses to evaluate [beta]-cell mass over a range of body weights in the minipig. Extensive stimulation of insulin secretion by a combination of glucose and arginine seems to give the best correlation to [beta]-cell mass. animal model; streptozotocin; arginine; pulsatile insulin secretion

Recent studies have suggested that sensory nerves may influence insulin secretion and action. The present study investigated the effects of resiniferatoxin (RTX) inactivation of sensory nerves (desensitization) on oral glucose tolerance, insulin secretion and whole body insulin sensitivity in the glucose intolerant, hyperinsulinemic, and insulin-resistant obese Zucker rat. After RTX treatment (0.05 mg/kg RTX sc given at ages 8, 10, and 12 wk), fasting plasma insulin was reduced (P < 0.0005), and oral glucose tolerance was improved (P < 0.005). Pancreas perfusion showed that baseline insulin secretion (7 mM glucose) was lower in RTX-treated rats (P = 0.01). Insulin secretory responsiveness to 20 mM glucose was enhanced in the perfused pancreas of RTX-treated rats (P < 0.005) but unaffected in stimulated, isolated pancreatic islets. At the peak of spontaneous insulin resistance in the obese Zucker rat, insulin sensitivity was substantially improved after RTX treatment, as evidenced by higher glucose infusion rates (GIR) required to maintain euglycemia during a hyperinsulinemic euglycemic (5 mU * [kg.sup.-1] * [min.sup.-1]) clamp (GI[R.sub.60-120 min] 5.97 [+ or -] 0.62 vs. 11.65 [ + or -] 0.83 mg * [kg.sup.-l] * [min.sup.-1] in RTX-treated rats, P = 0.003). In conclusion, RTX treatment and, hence, sensory nerve desensitization of adult male obese Zucker rats improved oral glucose tolerance by enhancing insulin secretion, and, in particular, by improving insulin sensitivity. capsaicin; hyperinsulinemic englycemic clamp; obesity

NN2211 is a long-acting, metabolically stable glucagon-like peptide-1 (GLP-1) derivative designed for once daily administration in humans. NN2211 dose dependently reduced the glycemic levels in ob/ob mice, with antihyperglycemic activity still evident 24 h postdose. Apart from an initial reduction in food intake, there were no significant differences between NN2211 and vehicle treatment, and body weight was not affected. Histological examination revealed that [beta]-cell proliferation and mass were not increased significantly in ob/ob mice with NN2211, although there was a strong tendency for increased proliferation. In db/db mice, exendin-4 and NN2211 decreased blood glucose compared with vehicle, but NN2211 had a longer duration of action. Food intake was lowered only on day 1 with both compounds, and body weight was unaffected. [beta]-Cell proliferation rate and mass were significantly increased with NN2211, but with exendin-4, only the [beta]-cell proliferation rate was significantly increased. In conclusion, NN2211 reduced blood glucose after acute and chronic treatment in ob/ob and db/db mice and was associated with increased [beta]-cell mass and proliferation in db/db mice. NN2211 is currently in phase 2 clinical development. incretin hormones; diabetes; animal models; glucagon-like peptide-1

ABSTRACT Phoenix Services, Inc., owns and operates the Baltimore Regional Medical Waste Incinerator in Baltimore, MD. New regulations for dioxins and furans imposed a limit that was considerably below historical [...]

Nonrodent models of diabetes are needed for practical and physiological reasons. Induction of mild insulin-deficient diabetes was investigated in male Gottingen minipigs by use of streptozotocin (STZ) alone (75, 100, and 125 mg/kg) or 125 mg/kg combined with pretreatment with nicotinamide (NIA; 0, 20, 67, 100, 150, and 230 mg/kg). Use of NIA resulted in a less steep slope of the regression line between fasting plasma glucose and changing doses compared with STZ [-7.0 [+ or -] 1.4 vs. 29.7 [+ or -] 7.0 mM * [mg.sup.-1] [kg.sup.-1], P < 0.0001]. Intermediate NIA doses induced moderate changes of glucose tolerance [glucose area under the curve increased from 940 [+ or -] 175 to 1,598 [+ or -] 462 mM * min, P < 0.001 (100 mg/kg) and from 890 [+ or -] 109 to 1,669 [+ or -] 691 mM * min, P = 0.003 (67 mg/kg)] with reduced insulin secretion [1,248 [+ or -] 602 pM * min after 16 days and 1,566 [+ or -] 190 pM * min after 60 days vs. 3,251 [+ or -] 804 pM * min in normal animals (P < 0.001)] and [beta]-cell mass [5.5 [+ or -] 1.4 mg/kg after 27 days and 7.9 [+ or -] 4.1 mg/kg after 60 days vs. 17.7 [+ or -] 4.7 mg/kg in normal animals (P = 0.009)]. The combination of NIA and STZ provided a model characterized by fasting and especially postprandial hyperglycemia and reduced, but maintained, insulin secretion and [beta]-cell mass. This model holds promise as an important tool for studying the pathophysiology of diabetes and development of new pharmacological agents for treatment of the disease. in vivo pharmacology; large-animal model; glucose tolerance; [beta]-cell reduction; glucose-stimulated insulin secretion.