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| 2. |
- Lynch, S.A., et al.
(författare)
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Toward silicon-based lasers for terahertz sources
- 2006
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Ingår i: IEEE Journal of Selected Topics in Quantum Electronics. - 1077-260X .- 1558-4542. ; 12:6, s. 1570-1577
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Tidskriftsartikel (refereegranskat)abstract
- Producing an electrically pumped silicon-based laser at terahertz frequencies is gaining increased attention these days. This paper reviews the recent advances in the search for a silicon-based terahertz laser. Topics covered include resonant tunneling in p-type Si/SiGe, terahertz intersubband electroluminescence from quantum cascade structures, intersubband lifetime measurements in Si/SiGe quantum wells, enhanced optical guiding using buried suicide layers, and the potential for exploiting common impurity dopants in silicon such as boron and phosphorus to realize a terahertz laser. © 2006 IEEE.
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| 3. |
- Zhao, Ming, et al.
(författare)
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Strain-symmetrized Si/SiGe multi-quantum well structures grown by molecular beam epitaxy for intersubband engineering
- 2006
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Ingår i: Journal of luminescence. - : Elsevier BV. - 0022-2313. ; 121:2, s. 403-408
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Tidskriftsartikel (refereegranskat)abstract
- Three strain-symmetrized Si/SiGe multi-quantum well structures, designed for probing the carrier lifetime of intrawell intersubband transitions between heavy hole 1 (HH1) and light hole 1 (LH1) states with transition energies below the optical phonon energy, were grown by molecular beam epitaxy at low temperature on fully relaxed SiGe virtual substrates. The grown structures were characterized by using various experimental techniques, showing a high crystalline quality and very precise growth control. The lifetime of the LH1 excited state was determined directly with pump-probe spectroscopy. The measurements indicated an increase of the lifetime by a factor of 2 due to the increasingly unconfined LH1 state, which agreed very well with the design. It also showed a very long lifetime of several hundred picoseconds for the holes excited out of the well to transit back to the well through a diagonal process.
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| 4. |
- Elmståhl, Barbara, et al.
(författare)
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Histomorphological Changes after Renal X-Ray Arteriography Using Iodine and Gadolinium Contrast Media in an Ischemic Porcine Model.
- 2007
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Ingår i: Acta Radiologica. - : SAGE Publications. - 1600-0455 .- 0284-1851. ; 48:10, s. 1109-1119
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Tidskriftsartikel (refereegranskat)abstract
- Background: Gadolinium contrast media (Gd-CM) are regarded as non-nephrotoxic or considerably less nephrotoxic than iodine contrast media (I-CM), and have therefore come to be used as a substitute for I-CM in patients with renal insufficiency in a variety of radiographic examinations. Purpose: To investigate renal histomorphological changes caused by Gd-CM in comparison with I-CM after renal X-ray arteriography in an ischemic porcine model, and to evaluate these changes in relation to the nephrotoxicity of the CM used. Material and Methods: Test solutions: gadopentetate, gadodiamide, iohexol, gadobutrol, iopromide, iodixanol, mannitol, and saline. The experiments were performed on 152 animals. Each pig was randomized to receive one test solution injected into the balloon-occluded (10 min) right renal artery. The kidneys were evaluated histomorphologically. The severity of histomorphological changes was graded subjectively: 1 = minimal, 2 = mild, 3 = moderate, and 4 = marked. Results: The main histological changes were 1) proximal tubular and glomerular necrosis, 2) hemorrhage/congestion of the cortex, medulla, and glomeruli, 3) proximal tubular vacuolation, and 4) protein-filled tubules in the cortex and medulla. Necrosis and hemorrhage/congestion were more frequent after injections with gadopentetate, mannitol solution iso-osmotic to gadopentetate, and gadobutrol compared to all other groups (P<0.001). The degree of necrosis and hemorrhage/congestion was related to the degree of impairment of renal function, but inversely related to vacuolation and tubular protein filling. Conclusion: In ischemic porcine kidneys, the histomorphological changes caused by Gd-CM are similar to those caused by I-CM. Vacuolation appears to be independent of the osmolality and viscosity of the CM, and does not seem to be an indicator of renal impairment. “High-osmolal” Gd-CM are more nephrotoxic than “low- and iso-osmolal” I-CM when compared in equal volumes of concentrations, resulting in equal X-ray attenuation.
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| 5. |
- Graslund, S, et al.
(författare)
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Protein production and purification
- 2008
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Ingår i: Nature methods. - : Springer Science and Business Media LLC. - 1548-7105 .- 1548-7091. ; 5:2, s. 135-146
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Tidskriftsartikel (refereegranskat)
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| 6. |
- Harrington, Robert A., et al.
(författare)
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The Thrombin Receptor Antagonist for Clinical Event Reduction in Acute Coronary Syndrome (TRA.CER) trial : study design and rationale
- 2009
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Ingår i: American Heart Journal. - : Elsevier BV. - 0002-8703 .- 1097-6744. ; 158:3, s. 327-334
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Tidskriftsartikel (refereegranskat)abstract
- Background The protease-activated receptor 1 (PAR-1), the main platelet receptor for thrombin, represents a novel target for treatment of arterial thrombosis, and SCH 530348 is an orally active, selective, competitive PAR-1 antagonist. We designed TRA.CER to evaluate the efficacy and safety of SCH 530348 compared with placebo in addition to standard of care in patients with non-ST-segment elevation (NSTE) acute coronary syndromes (ACS) and high-risk features. Trial design TRA.CER is a prospective, randomized, double-blind, multicenter, phase III trial with an original estimated sample size of 10,000 subjects. Our primary objective is to demonstrate that SCH 530348 in addition to standard of care will reduce the incidence of the composite of cardiovascular death, myocardial infarction (MI), stroke, recurrent ischemia with rehospitalization, and urgent coronary revascularization compared with standard of care alone. Our key secondary objective is to determine whether SCH 530348 will reduce the composite of cardiovascular death, MI, or stroke compared with standard of care alone. Secondary objectives related to safety are the composite of moderate and severe GUSTO bleeding and clinically significant TIMI bleeding. The trial will continue until a predetermined minimum number of centrally adjudicated primary and key secondary end point events have occurred and all subjects have participated in the study for at least I year. The TRA.CER trial is part of the large phase III SCH 530348 development program that includes a concomitant evaluation in secondary prevention. Conclusion TRA.CER will define efficacy and safety of the novel platelet PAR-1 inhibitor SCH 530348 in the treatment of high-risk patients with NSTE ACS in the setting of current treatment strategies.
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| 7. |
- Klionsky, Daniel J., et al.
(författare)
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Guidelines for the use and interpretation of assays for monitoring autophagy in higher eukaryotes
- 2008
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Ingår i: Autophagy. - : Landes Bioscience. - 1554-8627 .- 1554-8635. ; 4:2, s. 151-175
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Forskningsöversikt (refereegranskat)abstract
- Research in autophagy continues to accelerate,1 and as a result many new scientists are entering the field. Accordingly, it is important to establish a standard set of criteria for monitoring macroautophagy in different organisms. Recent reviews have described the range of assays that have been used for this purpose.2,3 There are many useful and convenient methods that can be used to monitor macroautophagy in yeast, but relatively few in other model systems, and there is much confusion regarding acceptable methods to measure macroautophagy in higher eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers of autophagosomes versus those that measure flux through the autophagy pathway; thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from fully functional autophagy that includes delivery to, and degradation within, lysosomes (in most higher eukaryotes) or the vacuole (in plants and fungi). Here, we present a set of guidelines for the selection and interpretation of the methods that can be used by investigators who are attempting to examine macroautophagy and related processes, as well as by reviewers who need to provide realistic and reasonable critiques of papers that investigate these processes. This set of guidelines is not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to verify an autophagic response.
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| 8. |
- Kragic, Danica, et al.
(författare)
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RETRACTED: Human-Machine Collaborative Systems for Microsurgical Applications
- 2005
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Ingår i: Robotics Research. - Berlin, Heidelberg : Springer Berlin/Heidelberg. - 3540232141 ; , s. 162-171
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Konferensbidrag (refereegranskat)abstract
- We describe our current progress in developing Human-Machine Collaborative Systems (HMCSs) for microsurgical applications such as vitreo-retinal eye surgery. Three specific problems considered here are (1) developing of systems tools for describing and implementing an HMCS, (2) segmentation of complex tasks into logical components given sensor traces of a human performing the task, and (3) measuring HMCS performance. Our goal is to integrate these into a full microsurgical workstation with the ability to automatically 11 parse" traces of user execution into a task model which is then loaded into the execution environment, providing the user with assistance using online recognition of task state. The major contributions of our work to date include an XML task graph modeling framework and execution engine, an algorithm for real-time segmentation of user actions using continuous Hidden Markov Models, and validation techniques for analyzing the performance of HMCSs.
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| 9. |
- Li, Jing, et al.
(författare)
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CYP3A phenotyping approach to predict systemic exposure to EGFR tyrosine kinase inhibitors
- 2006
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Ingår i: Journal of the National Cancer Institute. - : Oxford University Press (OUP). - 0027-8874 .- 1460-2105. ; 98:23, s. 1714-1723
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Tidskriftsartikel (refereegranskat)abstract
- Background: Gefitinib is an orally active inhibitor of epidermal growth factor receptor (EGFR) tyrosine kinase (TK) with activity in non-small-cell lung cancer. The response to gefitinib is variable, possibly because of interindividual variation in the activity of cytochrome P450 3A (CYP3A), the principal enzyme that metabolizes gefitinib. We prospectively assessed the influence of CYP3A activity on gefitinib disposition and toxicity. Methods: Twenty-seven patients with advanced cancer were treated with daily oral gefitinib at 250 mg (n = 13) or 500 mg (n = 14) for 28 days. Concentration-time profiles of midazolam and geftinib were constructed based on measurement of their concentration in serial blood samples using high-performance liquid chromatography and mass spectroscopy. CYP3A activity was determined at baseline by assessment of midazolam apparent oral clearance. Pharmacokinetic studies were performed for a period of 28 days, and population modeling was performed using NONMEM software. A structural pharmacokinetic model was developed to describe the concentration-time profiles of unbound and total gefitinib plasma concentrations, and patient-specific covariates were added to the model to account for unexplained interindividual variability in pharmacokinetic parameters. Statistical tests were two-sided. Results: Gefitinib pharmacokinetics exhibited wide interindividual variability (interindividual variability on total and unbound gefitinib apparent oral clearance was 79% and 74%, respectively). Midazolam clearance (mean = 40 L/h, range = 10-111) was highly correlated with that of total and unbound gefitinib (R2 = .60 and R2 = .68, respectively) and with steady-state plasma through concentrations of gefitinib (R2 = .58 and R2 = .60, respectively), and it accounted for approximately 40% of interindividual variability in gefitinib clearance in the pharmacokinetic model. Both total and unbound gefitinib steady-state plasma trough concentrations were associated with the development of diarrhea (P <.05), but not skin rash. At a dose of 250 mg gefitinib, 11 of 13 patients achieved steady-state plasma trough concentrations above the IC 50 for inhibition of mutant EGFR in vitro (0.015 μM), but only one achieved a steady-state plasma trough concentration above the IC 50 for inhibition of wild-type EGFR (0.1 μM). Conclusions: As an in vivo phenotypic probe of CYP3A, midazolam oral clearance may have utility for prediction of gefitinib exposure and dose selection. A pharmacokinetic model incorporating this indicator of CYP3A activity has potential for optimization of treatment with gefitinib and other TK inhibitors that are metabolized in a similar manner.
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| 10. |
- Li, Wei, 1962-, et al.
(författare)
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Foam cell death induced by 7β-hydroxycholesterol is mediated by labile iron-driven oxidative injury : Mechanisms underlying induction of ferritin in human atheroma
- 2005
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Ingår i: Free Radical Biology & Medicine. - : Elsevier BV. - 0891-5849 .- 1873-4596. ; 39:7, s. 864-875
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Tidskriftsartikel (refereegranskat)abstract
- Human atherosclerotic lesions typically contain large amounts of ferritin associated with apoptotic macrophages and foam cells, although the reasons are unknown. In the present investigation, we studied the relationship between ferritin induction and occurrence of apoptosis in 7β-hydroxycholesterol (7β-OH)-treated monocytic cells and macrophages. We found that 7β-OH enlarges the intracellular labile iron pool, increases formation of reactive oxygen species (ROS), and induces ferritin and cytosolic accumulation of lipid droplets, lysosomal destabilization, and apoptototic macrophage death. Since ferritin is a phase II-type protective protein, our findings suggest that ferritin upregulation here worked as an inefficient defense mechanism. Addition to the culture medium of both a membrane-permeable iron chelator 10-phenanthroline and the non-membrane-permeable iron chelators apoferritin and desferrioxamine afforded significant protection against the 7β-OH-induced effects. Consequently, endocytosed iron compounds dramatically augmented 7β-OH-induced cytotoxicity. We conclude that oxidized lipid 7β-OH causes not only foam cell formation but also oxidative damage with abnormal metabolism of cellular iron. The findings suggest that modulation of iron metabolism in human atheroma may be a potential therapeutic strategy against atherosclerosis. © 2005 Elsevier Inc. All rights reserved.
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