| 61. |
- Ahlström, Lars-Henric, et al.
(författare)
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Optimization of an analytical procedure for the determination of banned azo dyes in leather
- 2005
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Ingår i: Analytical and Bioanalytical Chemistry. - : Springer Science and Business Media LLC. - 1618-2642 .- 1618-2650. ; 382:5, s. 1320-1327
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Tidskriftsartikel (refereegranskat)abstract
- The possibility of improving an existing method, based on supercritical-fluid extraction (SFE) and microwave-assisted extraction (MAE), for the determination of banned azo dyes in leather has been studied. Thus, optimization of experimental conditions in different steps (degreasing, reduction, and extraction) of the analytical procedure was performed. The influence of different variables (reaction time, temperature, and concentration of reducing agent) on the reduction process was evaluated by use of a factorial design. It was found that the concentration of the reducing agent and the interaction between time and temperature were the most influential variables. Consequently, by applying a higher temperature, the reaction time could be halved. The use of acidified water as extraction solvent in MAE was also investigated. Usually 1 mol L-1 HCl was superior to methanol and buffer in terms of extraction efficiency. In conclusion, the present method gave significantly higher recoveries in comparison with the original method. All dyes were determined indirectly by measuring their corresponding harmful amines, formed after reduction by use of sodium dithionite.
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| 62. |
- Ahlström, Lars-Henric, et al.
(författare)
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Standard addition - A way of improving quantification of banned azo dyes in leather
- 2005
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Ingår i: Journal of Separation Science. - : Wiley. - 1615-9314 .- 1615-9306. ; 28:17, s. 2407-2412
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Tidskriftsartikel (refereegranskat)abstract
- An analytical procedure based on supercritical-fluid extraction and microwave-assisted extraction was applied on six different real leather samples for the determination of banned azo dyes. Determination of the dyes was performed indirectly by measuring their corresponding harmful aromatic amines, formed after reduction. A comparative study between external standard calibration and standard addition using both the dyes as well as the corresponding amines showed that the latter quantification method provided the highest accuracy.
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| 63. |
- Ahmed, R K S, et al.
(författare)
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Antigen-specific beta-chemokine production and CD8(+) T-cell noncytotoxic antiviral activity in HIV-2-infected individuals
- 2005
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Ingår i: Scandinavian Journal of Immunology. - : Wiley. - 1365-3083 .- 0300-9475. ; 61:1, s. 63-71
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Tidskriftsartikel (refereegranskat)abstract
- Human immunodeficiency virus-2 (HIV-2) is less pathogenic than HIV-1, and the disease progression in HIV-2-infected individuals seems to be similar to that seen in HIV-1-infected long-term nonprogressors. Cell-mediated immune responses and the production of noncytotoxic CD8(+) T-cell antiviral factors (CAF) and beta-chemokines have been correlated to protection against HIV-1 and associated with asymptomatic infection and slower disease progression. We investigated the antigen-induced beta-chemokine production in HIV-2-infected patients living in Sweden and in Guinea-Bissau. We also compared in vitro CD8(+) T-cell-mediated noncytotoxic antiviral activity against beta-chemokine-sensitive R5 virus (HIV-1(Bal)) and beta-chemokine-insensitive X4 virus (HIV-1(IIIB)) in HIV-2-infected patients with that in HIV-1-infected patients. HIV-2-specific beta-chemokine production was demonstrated in a majority of the HIV-2-infected subjects. CD8(+) T cells of both HIV-1 and HIV-2-infected individuals suppressed R5 virus replication in vitro in a similar manner, while the inhibition of X4 virus replication seemed to be more frequent and of a higher magnitude among HIV-2-infected patients compared to HIV-1-infected subjects. Taken together, our results indicate that the production of CD8(+) T-cell noncytotoxic antiviral factors may contribute to the low transmission of the virus and slower disease progression in HIV-2-infected patients.
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| 64. |
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| 65. |
- Ahnesjö, Anders, et al.
(författare)
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Beam modeling and verification of a photon beam multisource model.
- 2005
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Ingår i: Medical Physics. - : Wiley. - 0094-2405. ; 32:6, s. 1722-37
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Tidskriftsartikel (refereegranskat)abstract
- Dose calculations for treatment planning of photon beam radiotherapy require a model of the beam to drive the dose calculation models. The beam shaping process involves scattering and filtering that yield radiation components which vary with collimator settings. The necessity to model these components has motivated the development of multisource beam models. We describe and evaluate clinical photon beam modeling based on multisource models, including lateral beam quality variations. The evaluation is based on user data for a pencil kernel algorithm and a point kernel algorithm (collapsed cone) used in the clinical treatment planning systems Helax-TMS and Nucletron-Oncentra. The pencil kernel implementations treat the beam spectrum as lateral invariant while the collapsed cone involves off axis softening of the spectrum. Both algorithms include modeling of head scatter components. The parameters of the beam model are derived from measured beam data in a semiautomatic process called RDH (radiation data handling) that, in sequential steps, minimizes the deviations in calculated dose versus the measured data. The RDH procedure is reviewed and the results of processing data from a large number of treatment units are analyzed for the two dose calculation algorithms. The results for both algorithms are similar, with slightly better results for the collapsed cone implementations. For open beams, 87% of the machines have maximum errors less than 2.5%. For wedged beams the errors were found to increase with increasing wedge angle. Internal, motorized wedges did yield slightly larger errors than external wedges. These results reflect the increased complexity, both experimentally and computationally, when wedges are used compared to open beams.
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| 66. |
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| 67. |
- Ahrén, Bo, et al.
(författare)
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Improved meal-related beta-cell function and insulin sensitivity by the dipeptidyl peptidase-IV inhibitor vildagliptin in metformin-treated patients with type 2 diabetes over 1 year.
- 2005
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Ingår i: Diabetes Care. - : American Diabetes Association. - 1935-5548 .- 0149-5992. ; 28:8, s. 1936-1940
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE—To examine the effects of dipeptidyl peptidase-IV (DPP-4) inhibition on meal-related β-cell function and insulin sensitivity over 52 weeks in type 2 diabetes. RESEARCH DESIGN AND METHODS—In a 12-week core study, placebo (n = 51) or vildagliptin (n = 56; 50 mg OD) was added to metformin treatment (1.5–3.0 mg/day). A 40-week extension followed in 71 patients. Meal tests were performed at 0, 12, 24, and 52 weeks; glucose, insulin, and C-peptide were evaluated. RESULTS—In subjects completing 52 weeks with participation in all meal tests (n = 57), HbA1c (A1C) decreased in the vildagliptin/metformin group (VM group, n = 31) but increased in the placebo/metformin group (PM group, n = 26; between-group difference −1.0 ± 0.2%; P < 0.001; baseline of all subjects combined 7.7 ± 0.1%). Also, fasting glucose decreased in the VM group but increased in the PM group (difference −0.9 ± 0.3 mmol/l, P = 0.016; baseline 9.8 ± 0.3 mmol/l). Insulin secretion (postmeal suprabasal area under the 0- to 30-min C-peptide curve divided by the 30-min increase in glucose) was increased in the VM group but was reduced in the PM group (difference +0.011 ± 0.03 pmol/l 30 min/mmol/l, P = 0.018; baseline 0.036 ± 0.02). Insulin sensitivity during meal ingestion (oral glucose insulin sensitivity) increased in the VM group but was not altered in the PM group (difference +27 ± 4 ml · min−1 · m−2, P = 0.036; baseline 246 ± 6). Insulin secretion related to insulin sensitivity (adaptation index) increased in the VM group but decreased in the PM group (difference +3.2 ± 1.0, P = 0.040; baseline 9.1 ± 0.5). The change in adaptation index correlated to the change in A1C (r = −0.39, P = 0.004). CONCLUSIONS—This study presents evidence that DPP-4 inhibition by vildagliptin when added to metformin in type 2 diabetes over 52 weeks improves β-cell function along with improved postmeal insulin sensitivity.
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| 68. |
- Ahrén, Bo, et al.
(författare)
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Inhibition of dipeptidyl peptidase-4 augments insulin secretion in response to exogenously administered glucagon-like peptide-1, glucose-dependent insulinotropic polypeptide, pituitary adenylate cyclase-activating polypeptide, and gastrin-releasing peptide in mice
- 2005
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Ingår i: Endocrinology. - : The Endocrine Society. - 0013-7227 .- 1945-7170. ; 146:4, s. 2055-2059
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Tidskriftsartikel (refereegranskat)abstract
- Inhibition of dipeptidyl peptidase- 4 ( DPP- 4) is currently being explored as a new approach to the treatment of type 2 diabetes. This concept has emerged from the powerful and rapid action of the enzyme to inactivate glucagon- like peptide-1 ( GLP- 1). However, other bioactive peptides with potential influence of islet function are also substrates of DPP- 4. Whether this inactivation may add to the beneficial effects of DPP- 4 inhibition is not known. In this study, we explored whether DPP- 4 inhibition by valine- pyrrolidide ( val- pyr; 100 mu mol/ kg administered through gastric gavage at t = -30 min) affects the insulin and glucose responses to iv glucose ( 1 g/ kg) together with GLP- 1 ( 10 nmol/ kg), glucose- dependent insulinotropic polypeptide ( GIP; 10 nmol/ kg), pituitary adenylate cyclase- activating polypeptide 38 ( PACAP38; 1.3 nmol/ kg), or gastrin- releasing peptide ( GRP; 20 nmol/ kg) given at t = 0 in anesthetized C57BL/ 6J mice. It was found that the acute ( 1 - 5 min) insulin response to GLP- 1 was augmented by val- pyr by 80% ( 4.2 +/- 0.4 vs. 7.6 +/- 0.8 nmol/ liter), that to GIP by 40% ( 2.7 +/- 0.3 vs. 3.8 +/- 0.4 nmol/ liter), that to PACAP38 by 75% ( 4.6 +/- 0.5 vs. 8.1 +/- 0.6 nmol/ liter), and that to GRP by 25% ( 1.8 +/- 0.2 vs. 2.3 +/- 0.3 nmol/ liter; all P < 0.05 or less). This was associated with enhanced glucose elimination rate after GLP- 1 [ glucose elimination constant ( K-G) 2.1 +/- 0.2 vs. 3.1 +/- 0.3%/ min] and PACAP38 ( 2.1 +/- 0.3 vs. 3.2 +/- 0.3%/ min; both P < 0.01), but not after GIP or GRP. The augmented insulin response to GRP by val- pyr was prevented by the GLP- 1 receptor antagonist, exendin(3) ( 9- 39), raising the possibility that GRP effects may occur secondary to stimulation of GLP- 1 secretion. We conclude that DPP- 4 inhibition augments the insulin response not only to GLP- 1 but also to GIP, PACAP38, and GRP.
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| 69. |
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| 70. |
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