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Solid−liquid equilibria (SLE) for the four binary systems of 1-methoxy-2-propanol and 2-butoxy ethanol with benzene and cyclohexane have been measured by a visual method. For correlating the experimental SLE data, the enthalpy of fusion for 1-methoxy-2-propanol has been measured additionally using a Tian-Calvet batch calorimeter. For the description of the SLE data, the Wilson equation has been used with good results. The SLE data were also compared with predicted data using modified UNIFAC (Dortmund).

Objective: It has earlier been demonstrated that capsaicin-induced desensitization improves insulin sensitivity in normal rats. However, whether increased capsaicin-sensitive nerve activity precedes the onset of insulin resistance in diet-induced obesity – and therefore might be involved in the pathophysiology – is not known. Further, it is of relevance to investigate whether capsaicin desensitization improves glycaemic control even in obese individuals and we therefore chose the obese Zucker rats to test this.Design and methods: Plasma levels of calcitonin gene-related peptide (CGRP; a marker of sensory nerve activity) was assessed in 8-week-old Zucker rats. To investigate whether capsaicin desensitization (100 mg/kg at 9 weeks of age) would also ameliorate glycaemia in this non-diabetic model, we assessed oral glucose tolerance at 7 weeks after capsaicin.Results: It was found that plasma CGRP levels were elevated in obese Zucker rats prior to the onset of obesity (16.1±3.4 pmol/l in pre-obese Zucker rats vs 6.9±1.1 pmol/l in lean littermates; P= 0.015) despite similar body weights. Furthermore, capsaicin desensitization reduced both fasting blood glucose (4.3±0.2 mmol/l vs 5.1±0.2 mmol/l in controls; P= 0.050) as well as the mean blood glucose level during an oral glucose tolerance test (OGTT) (6.8±0.3 mmol/l vs 8.6±0.5 mmol/l in control obese rats; P= 0.024) whereas the plasma insulin levels during the OGTT were unchanged. However this did not lead to an improvement in insulin resistance or to a reduction of tissue triglyceride accumulation in muscle or liver.Conclusion: We concluded that capsaicin-induced sensory nerve desensitization improves glucose tolerance in Zucker rats. Since, in this study, plasma CGRP levels, a marker of sensory nerve activity, were increased in the pre-obese rats, our data support the hypothesis that increased activity of sensory nerves precedes the development of obesity and insulin resistance in Zucker rats.

High-fat diet and obesity are known to be of major importance for development of type 2 diabetes in humans. High-fat feeding can induce syndromes of glucose intolerance andor insulin resistance in several species, and the Göttingen minipig might be a useful model for studying the effect of dietary high-fat intake and obesity on glucose homeostasis and the susceptibility to diabetes. The present study was designed as a pilot study to investigate the effects of obesity caused by high-fat high-energy feeding on oral and intravenous glucose tolerance. Male Göttingen minipigs were fed a control diet (CD) or a high-fat high-energy diet (HFD) for 3 months. Body weight (32.6 ± 2.4 kg vs. 24.9 ± 0.5 kg, p< 0.001 ) and total (13.2 ± 3.2 vs. 6.1 ± 0.5, p 0.002 ) and truncal (11.0 ± 3.9 vs. 1.8 ± 1.1, p 0.001 ) fat percent were increased significantly, whereas relative lean body mass was decreased (84.8 ± 3.3 vs. 91.9 ± 0.5, p 0.002 ) in the HFD group compared to CD. Fasting plasma glucose (4.3 ± 0.4 mM vs. 3.6 ± 0.3 mM, p 0.023 ) and insulin (80 ± 23 pM vs. 23 ± 21 pM, p 0.012 ) were increased in the HFD group compared to CD, but oral glucose tolerance was not significantly changed. Insulin responses to intravenous glucose were increased (6741 ± 2538 vs. 3938 ± 771 pM 3 min, p 0.050 ), while glucose clearance was not changed by HFD vs. CD, thus indicating insulin resistance. In conclusion, changes in body weight and composition, resulting in minor abnormalities in glucose tolerance and insulin sensitivity, characterized by slight hyperglycemia and compensatory hyperinsulinemia, can be induced in the male Göttingen minipig by high-fat high-energy feeding for 3 months. This approach seems to be an interesting and promising method for establishment of a nonrodent model of insulin resistance or type 2 diabetes.

ABSTRACTPhoenix 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 emission levels. To determine a method to comply with the new dioxin/furan regulations, Phoenix Services performed trials with powdered activated carbon (PAC). Although the results with carbon were acceptable, Phoenix Services decided to replace their woven fiberglass filter bags with catalytic filters that simultaneously destroy dioxins and furans and collect particulate matter (PM). The catalytic filter system offered several advantages to Phoenix Services, including destruction of dioxins and furans instead of adsorption on carbon. The catalytic filters also offered a passive solution that did not require new carbon injection equipment. In January 2000, a campaign to measure dioxins/furans and PM was undertaken.

Oxygen solubility in methanol, n-propanol, dibutyl ether, toluene, and octane, and nitrogen solubility in ethanol, n-propanol and 2-methyltetrahydrofuran was measured at pressures up to 10 MPa in the temperature range between 298 K and 398 K using the static synthetic method. The experimental results were used to extend the range of applicability of the Soave–Redlich–Kwong (PSRK) model for the prediction of air solubility in organic solvents and solvent mixtures by fitting the missing gas–solvent group interaction parameters. The required pressure range of gas solubility data for fitting the PSRK group interaction parameters was defined by analysing the significance of the data for the optimized parameters. The applied experimental method was analysed in detail since its use at higher pressures requires the consideration of the partial molar volumes of the dissolved gases when solving the mass and volume balance equations during the data treatment.

The present study compared estimates of body composition derived from dual-emission X-ray absorptiometry (DEXA) and from chemical analyses. The primary aim was to compare the two methods because growth hormone (GH) may cause fluid retention, and DEXA does not distinguish water from lean mass. Hypophysectomized rats were fed ad libitumand were treated with continuous infusions of rat GH in doses of 0, 10, 30, and 100 μg/day for 14 days. By chemical analysis, a decrease in percentage fat from 12.9% in the control group to 11.3%, 11.0%, and 10.2% in the low, medium, and high dose groups was observed (P < 0.0001). The fat percentages were about 3–4% higher by DEXA, but showed the same decline (P < 0.03). Lean mass increased from 74.4% in the control group to 75.8%, 78.0%, and 78.6% in the treatment groups (P < 0.001). A significant increase in the wet weight of the quadriceps muscle, but no difference in dry weight was observed in all four treatment groups, indicating that the increase in muscle weight was exclusively caused by water. This accumulation of water was reflected in the total water content of the carcasses, which increased from 62.0% in the control group to 64.9%, 66.1%, and 66.8% in the GH groups (P < 0.0001). The protein content decreased from 19.8% in the control group to 19.4%, 19.1%, and 18.9% in the GH groups (P < 0.001). Regardless of the decrease in protein, the GH treated groups contained more water in relation to protein as the g water/g protein ratio was increased by 13% from 3.14 in the control group to 3.55 in the group treated with the highest GH dose (P < 0.0001). Also, a close relationship between feed intake and body weight were found, together with increases in epiphyseal growth plate width, insulin-like growth factor I (IGF-I), and insulin-like growth factor binding protein 3 (IGFBP-3). In conclusion, the study shows that estimation of lean mass by DEXA should be carefully evaluated when used in connection with treatment of drugs that cause water retention.

Ipamorelin is a new and potent synthetic pentapeptide which has distinct and specific growth hormone (GH)-releasing properties. With the objective of investigating the effects on longitudinal bone growth rate (LGR), body weight (BW), and GH release, ipamorelin in different doses (0, 18, 90 and 450 μg/day) was injected s.c. three times daily for 15 days to adult female rats. After intravital tetracycline labelling on days 0, 6, and 13, LGR was determined by measuring the distance between the respective fluorescent bands in the proximal tibia metaphysis. Ipamorelin dose-dependently increased LGR from 42 μm/day in the vehicle group to 44, 50, and 52 μm/day in the treatment groups (P<0.0001). There was also a pronounced and dose-dependent effect on BW gain. The treatment did not affect total IGF-I levels, IGFBPs, or serum markers of bone formation and resorption. The number of tartrate-resistant acid phosphatase-positive multinuclear cells in the metaphysis of the tibia did not change significantly with treatment. The responsiveness of the pituitary to a provocative i.v. dose of ipamorelin or GHRH showed that the plasma GH response was marginally reduced (P<0.03) after ipamorelin, but unchanged after GHRH. The pituitary GH content was unchanged by ipamorelin treatment. Whether ipamorelin or other GH secretagogues may have a place in the treatment of children with growth retardation requires demonstration in future clinical studies.

Improvements in immunologic techniques have resulted in increased accuracy and precision in the diagnosis of leukemia and lymphoma. Provisional recommendations for routine application of these techniques in leukemia and lymphoma are presented, although this area continues to undergo clarification as new data become available.

The incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are important in blood glucose regulation.However, both incretin hormones are rapidly degraded by the enzyme dipeptidyl peptidase IV (DPPIV). The concept of DPPIV inhibition as a treatment for type 2 diabetes was evaluated in a new large animal model of insulin-deficient diabetes and reduced β-cell mass, the nicotinamide (NIA) (67 mg/kg) and streptozotocin (STZ) (125 mg/kg)–treated minipig, using the DPPIV inhibitor, valine pyrrolidide (VP) (50 mg/kg).VP did not significantly affect levels of intact GLP-1 but increased levels of intact GIP (from 4543 ± 1880 to 9208 ± 3267 pM × min; P<.01), thus improving glucose tolerance (area under the curve [AUC] for glucose reduced from 1904 ± 480 to 1582 ± 353 mM × min;P = .05).VP did not increase insulin levels during the oral glucose tolerance test (OGTT) but increased the insulinogenic index in normal animals (from 83 ± 42 to 192 ± 108; P < .05), but not after NIA + STZ, possibly because of less residual insulin secretory capacity in these animals. GIP seems to contribute to the antihyperglycemic effect of VP in this model; however, additional mechanisms for the effect of DPPIV inhibition cannot be excluded. The authors conclude that DPPIV inhibitors may be useful to treat type 2 diabetes, even when this is due to reduced β-cell mass.