| 1. |
- Johansson, Sveneric, et al.
(författare)
-
New forbidden and fluorescence Fe III lines identified in HST spectra of eta Carinae
- 2001
-
Ingår i: Astronomy and Astrophysics. - 1432-0746. ; 361, s. 977-977
-
Tidskriftsartikel (refereegranskat)abstract
- We discuss the origin of eight emission lines in the spectra of gas blobs close to the central star of eta Carinae. The spectra have been obtained with the Goddard High Resolution Spectrograph (GHRS) and the Space Telescope Imaging Spectrograph (STIS) onboard the Hubble Space Telescope. Between 2400 and 2500 Å five narrow lines are identified as new forbidden lines of doubly ionized iron, [Fe III]. We present gA-value data for the corresponding transitions, which combine two different metastable configurations of Fe III. An anomalous intensity of the narrow Fe III line (UV 34) at 1914 Å is explained as fluorescence due to HLyalpha pumping. A level mixing of about 1% increases the f-value of the pumped excitation channel by more than two orders of magnitude, which makes the pumping efficient and the fluorescence significant. We introduce a new designation for fluorescence lines photoexcited by an accidental resonance, eg. < Fe III> in the case of doubly ionized iron. Based on observations with the NASA/ESA Hubble Space Telescope, and supported by grant numbers GO-6501 and GO-7302 from the Space Telescope Science Institute. The STScI is operated by the Association of Universities for Research in Astronomy, Inc., under NASA contract NAS5-26555.
|
|
| 2. |
|
|
| 3. |
|
|
| 4. |
|
|
| 5. |
- Blomqvist, G, et al.
(författare)
-
Effect of acute hyperketonemia on the cerebral uptake of ketone bodies in nondiabetic subjects and IDDM patients
- 2002
-
Ingår i: American journal of physiology. Endocrinology and metabolism. - : American Physiological Society. - 0193-1849 .- 1522-1555. ; 283:1, s. E20-E28
-
Tidskriftsartikel (refereegranskat)abstract
- Using R-β-[1-11C]hydroxybutyrate and positron emission tomography, we studied the effect of acute hyperketonemia (range 0.7–1.7 μmol/ml) on cerebral ketone body utilization in six nondiabetic subjects and six insulin-dependent diabetes mellitus (IDDM) patients with average metabolic control (HbA1c = 8.1 ± 1.7%). An infusion of unlabeled R-β-hydroxybutyrate was started 1 h before the bolus injection of R-β-[1-11C]hydroxybutyrate. The time course of the radioactivity in the brain was measured during 10 min. For both groups, the utilization rate of ketone bodies was found to increase nearly proportionally with the plasma concentration of ketone bodies (1.0 ± 0.3 μmol/ml for nondiabetic subjects and 1.3 ± 0.3 μmol/ml for IDDM patients). No transport of ketone bodies from the brain could be detected. This result, together with a recent study of the tissue concentration of R-β-hydroxybutyrate in the brain by magnetic resonance spectroscopy, indicate that, also at acute hyperketonemia, the rate-limiting step for ketone body utilization is the transport into the brain. No significant difference in transport and utilization of ketone bodies could be detected between the nondiabetic subjects and the IDDM patients.
|
|
| 6. |
|
|
| 7. |
|
|
| 8. |
|
|
| 9. |
|
|
| 10. |
- Cotter, MA, et al.
(författare)
-
Effects of proinsulin C-peptide in experimental diabetic neuropathy: vascular actions and modulation by nitric oxide synthase inhibition
- 2003
-
Ingår i: Diabetes. - : American Diabetes Association. - 0012-1797 .- 1939-327X. ; 52:7, s. 1812-1817
-
Tidskriftsartikel (refereegranskat)abstract
- Proinsulin C-peptide treatment can partially prevent nerve dysfunction in type 1 diabetic rats and patients. This could be due to a direct action on nerve fibers or via vascular mechanisms as C-peptide stimulates the nitric oxide (NO) system and NO-mediated vasodilation could potentially account for any beneficial C-peptide effects. To assess this further, we examined neurovascular function in streptozotocin-induced diabetic rats. After 6 weeks of diabetes, rats were treated for 2 weeks with C-peptide to restore circulating levels to those of nondiabetic controls. Additional diabetic groups were given C-peptide with NO synthase inhibitor NG-nitro-l-arginine (l-NNA) co-treatment or scrambled C-peptide. Diabetes caused 20 and 16% reductions in sciatic motor and saphenous sensory nerve conduction velocity, which were 62 and 78% corrected, respectively, by C-peptide. l-NNA abolished C-peptide effects on nerve conduction. Sciatic blood flow and vascular conductance were 52 and 41%, respectively, reduced by diabetes (P < 0.001). C-peptide partially (57–66%) corrected these defects, an effect markedly attenuated by l-NNA co-treatment. Scrambled C-peptide was without effect on nerve conduction or perfusion. Thus, C-peptide replacement improves nerve function in experimental diabetes, and the data are compatible with the notion that this is mediated by a NO-sensitive vascular mechanism.
|
|
