| 51. |
|
|
| 52. |
- Lindgren, David, et al.
(författare)
-
Optical characterization of InAs quantum wells and dots grown radially on wurtzite InP nanowires.
- 2013
-
Ingår i: Nanotechnology. - : IOP Publishing. - 0957-4484 .- 1361-6528. ; 24:22
-
Tidskriftsartikel (refereegranskat)abstract
- Correlated micro-photoluminescence (μPL) and cathodoluminescence (CL) measurements are reported for single core-shell InP-InAs wurtzite nanowires grown using metal-organic vapor phase epitaxy. Samples covering a radial InAs shell thickness of 1-12 ML were investigated. The effective masses for the wurtzite material were determined from the transition energy dependence of the InAs shell thickness, using a model based on linear deformation potential theory. InP cores with segments of mixed zincblende and wurtzite, on which quantum dots nucleated selectively, were also investigated. Narrow peaks were observed by μPL and the spatial origin of the emission was identified with CL imaging.
|
|
| 53. |
|
|
| 54. |
- Lindgren, David, et al.
(författare)
-
Study of carrier concentration in single InP nanowires by luminescence and Hall measurements
- 2015
-
Ingår i: Nanotechnology. - : IOP Publishing. - 0957-4484 .- 1361-6528. ; 26:4
-
Tidskriftsartikel (refereegranskat)abstract
- The free electron carrier concentrations in single InP core-shell nanowires are determined by micro-photoluminescence, cathodoluminescence (CL) and Hall effect measurements. The results from luminescence measurements were obtained by solving the Fermi-Dirac integral, as well as by analyzing the peak full width at half maximum (FWHM). Furthermore, the platform used for Hall effect measurements, combined with spot mode CL spectroscopy, is used to determine the carrier concentrations at specific positions along single nanowires. The results obtained via luminescence measurements provide an accurate and rapid feedback technique for the epitaxial development of doping incorporation in nanowires. The technique has been employed on several series of samples in which growth parameters, such as V/III-ratio, temperature and dopant flows, were investigated in an optimization procedure. The correlation between the Hall effect and luminescence measurements for extracting the carrier concentration of different samples were in excellent agreement.
|
|
| 55. |
|
|
| 56. |
- Lindkvist, Björn, et al.
(författare)
-
A Prospective Cohort Study of Smoking in Acute Pancreatitis.
- 2008
-
Ingår i: Pancreatology. - : Elsevier BV. - 1424-3903. ; 8:1, s. 63-70
-
Tidskriftsartikel (refereegranskat)abstract
- Background/Aims: Little is known about risk factors for acute pancreatitis other than gallstones and alcohol consumption. The aim of this study was to investigate if smoking or body mass index (BMI) are associated with acute pancreatitis and to determine relative risks (RR) for acute pancreatitis related to smoking, BMI, and alcohol consumption. Methods: From 1974 to 1992, selected birth-year cohorts of residents in Malmo, Sweden (born 1921-1949) were invited to a health-screening investigation including physical examination, blood sampling and a questionnaire. In total, 33,346 individuals participated. Cases of acute pancreatitis were identified from diagnosis registries (n = 179). Incidence rates were calculated in different risk factor categories. A Cox's analysis revealed RR. Results: Current versus never smoking at baseline was associated with acute pancreatitis (RR 2.14, 95% confidence interval (CI) 1.48-3.09) after adjustment for age, sex, BMI and alcohol consumption. This association was stronger in heavy smokers (20-30 cigarettes/day) (RR 3.19, 95% CI 2.03-5.00). Smoking was associated with a RR of 3.57 (95% CI 0.98-13.0) for acute pancreatitis in subjects who reported no alcohol consumption. An increased risk for acute pancreatitis was also found for high versus low risk, self-reported alcohol consumption (RR 2.55, 95% CI 1.59-4.08) and for gamma-GT levels in the highest versus the lowest quartile (RR 2.14, 95% CI 1.32-3.49). There was also a weak correlation between BMI and acute pancreatitis. Conclusions: Smoking is associated with the incidence of acute pancreatitis in a dose-response manner. Copyright (c) 2008 S. Karger AG, Basel and IAP.
|
|
| 57. |
|
|
| 58. |
- Lindkvist, Björn, et al.
(författare)
-
Cathepsin B activates human trypsinogen 1 but not proelastase 2 or procarboxypeptidase B
- 2006
-
Ingår i: Pancreatology. - : Elsevier BV. - 1424-3903. ; 6:3, s. 224-231
-
Tidskriftsartikel (refereegranskat)abstract
- Background/Aims: Activation of trypsinogen to trypsin is a crucial step in the development of acute pancreatitis. The cause of this activation is not known although suggested explanations include autoactivation, cathepsin B-mediated activation and activation by mast cell tryptase. The aim of this study was to investigate cathepsin B and tryptase activation of pancreatic zymogens. Methods: Trypsinogen-1, proelastase, and procarboxypeptidase B were purified from human pancreatic juice. Human cathepsin B and beta I- tryptase are commercial products. Activation and degradation of zymogens were measured by activity towards specific substrates for trypsin and pancreatic elastase, ELISAs for procarboxypeptidase B and its activation peptide, and a radioimmunoassay for the trypsinogen activation peptide. Results: Cathepsin B caused activation of trypsinogen-1 with a trypsin yield of about 30% of that produced by enterokinase. Proelastase and procarboxypeptidase B was not activated by cathepsin B. None of the zymogens were inactivated by cathepsin B. Neither monomeric nor tetrameric tryptase could activate any of the examined zymogens. Conclusion: Cathepsin B is a competent activator of trypsinogen-1, although not as efficient as enterokinase. If cathepsin B is to play a role in protease activation in acute pancreatitis, this most probably occurs by activation of trypsinogen.
|
|
| 59. |
- Lindkvist, Björn, et al.
(författare)
-
Long-term nicotine exposure causes increased concentrations of trypsinogens and amylase in pancreatic extracts in the rat.
- 2008
-
Ingår i: Pancreas. - 0885-3177. ; 37:3, s. 288-294
-
Tidskriftsartikel (refereegranskat)abstract
- To develop radioimmunoassays (RIAs) for rat trypsinogens 1 and 2 and to investigate the effect of nicotine exposure on concentration and production of pancreatic zymogens in the rat. METHODS: Male Sprague-Dawley rats were supplied with either normal or nicotine-containing (0.77 mM) water for 28 days and were then killed. Rabbit antibodies for the activation peptides of trypsinogens 1 and 2 were obtained for use in the RIAs. Concentrations of the both trypsinogens in pancreatic extracts were measured by the RIAs after activation by enterokinase. DNA and amylase were measured using commercial kits. mRNA for trypsinogens 1 and 2, procolipase, and cholecystokinin receptor was measured by in situ hybridization. RESULTS: The specificity of the RIA for the trypsinogen 1 activation peptide was satisfactory. The RIA for the trypsinogen 2 activation peptide showed a limited cross-reaction toward the synthetic trypsinogen 1 activation peptide, but the importance of this cross-reaction was moderate when investigated in samples of activated trypsinogens. Weight gain was reduced in nicotine-treated animals. Concentrations of amylase, trypsinogen 1, trypsinogen 2, and the ratio of trypsinogen 2 to 1 were all increased in pancreatic extracts of nicotine-fed animals. Total DNA and mRNA for the trypsinogens, procolipase, and cholecystokinin receptor were not affected by nicotine exposure. CONCLUSIONS: The combination of increased proenzyme concentrations and unaffected mRNA levels suggests that nicotine impairs secretion rather than production of pancreatic zymogens.
|
|
| 60. |
|
|
