108 research outputs found
The Metal-Insulator Transition in \u3cem\u3eVO\u3csub\u3e2\u3c/sub\u3e\u3c/em\u3e Studied using Terahertz Apertureless Near-Field Microscopy
We have studied the metal-insulator transition in a vanadium dioxide (VO2) thin film using terahertz apertureless near-field optical microscopy. We observe a variation of the terahertz amplitude due to the phase transition induced by an applied voltage across the sample. The change of the terahertz signal is related to the abrupt change of the conductivity of the VO2 film at the metal-insulator transition. The subwavelength spatial resolution of this near-field microscopy makes it possible to detect signatures of micron-scale metallic domains in inhomogeneous VO2 thin films
Evaluation of a structured treatment discontinuation in patients with inoperable alveolar echinococcosis on long-term benzimidazole therapy: A retrospective cohort study.
OBJECTIVES
Alveolar echinococcosis (AE) is an orphan zoonosis of increasing concern in endemic areas, including Europe. It frequently presents in an advanced, inoperable stage, that requires life-long parasitostatic benzimidazole therapy. In some patients, long-term therapy leads to negative anti-Em18 antibody ELISA and PET. It is disputed, whether these patients are truly cured and treatment can be safely discontinued. Our aim was to retrospectively assess long-term outcome of 34 patients with inoperable AE who participated in a previous study to determine feasibility of benzimidazole treatment cessation.
METHODS
Retrospective analysis of medical charts was undertaken in all 34 AE patients who participated in our previous study. Of particular interest were AE recurrence or other reasons for re-treatment in patients who stopped benzimidazole therapy and whether baseline clinical and laboratory parameters help identify of patients that might qualifiy for treatment cessation. Additionally, volumetric measurement of AE lesions on contrast-enhanced cross-sectional imaging was performed at baseline and last follow-up in order to quantify treatment response.
RESULTS
12 of 34 patients stopped benzimidazole therapy for a median of 131 months. 11 of these patients showed stable or regressive AE lesions as determined by volumetric measurement. One patient developed progressive lesions with persistently negative anti-Em18 antibody ELISA but slight FDG-uptake in repeated PET imaging. At baseline, patients who met criteria for treatment cessation demonstrated higher lymphocyte count and lower total IgE.
CONCLUSION
Treatment cessation is feasible in inoperable AE patients, who demonstrate negative anti-Em18 antibody ELISA and PET on follow-up. Close monitoring including sectional imaging is strongly advised
Effect of doping-- and field--induced charge carrier density on the electron transport in nanocrystalline ZnO
Charge transport properties of thin films of sol--gel processed undoped and
Al-doped zinc oxide nanoparticles with variable doping level between 0.8 at%
and 10 at% were investigated. The X-ray diffraction studies revealed a decrease
of the average crystallite sizes in highly doped samples. We provide estimates
of the conductivity and the resulting charge carrier densities with respect to
the doping level. The increase of charge carrier density due to extrinsic
doping were compared to the accumulation of charge carriers in field effect
transistor structures. This allowed to assess the scattering effects due to
extrinsic doping on the electron mobility. The latter decreases from 4.6*10^-3
cm^2/Vs to 4.5*10^-4 cm^2/Vs with increasing doping density. In contrast, the
accumulation leads to an increasing mobility up to 1.5*10^-2 cm^2/Vs. The
potential barrier heights related to grain boundaries between the crystallites
were derived from temperature dependent mobility measurements. The extrinsic
doping initially leads to a grain boundary barrier height lowering, followed by
an increase due to doping-induced structural defects. We conclude that the
conductivity of sol--gel processed nanocrystalline ZnO:Al is governed by an
interplay of the enhanced charge carrier density and the doping-induced charge
carrier scattering effects, achieving a maximum at 0.8 at% in our case.Comment: 8 pages, 7 figure
Assessment of hepatic fibrosis and inflammation with look-locker T1 mapping and magnetic resonance elastography with histopathology as reference standard
Purpose: To compare the diagnostic performance of T1 mapping and MR elastography (MRE) for staging of hepatic fibrosis and grading inflammation with histopathology as standard of reference.
Methods: 68 patients with various liver diseases undergoing liver biopsy for suspected fibrosis or with an established diagnosis of cirrhosis prospectively underwent look-locker inversion recovery T1 mapping and MRE. T1 relaxation time and liver stiffness (LS) were measured by two readers. Hepatic fibrosis and inflammation were histopathologically staged according to a standardized fibrosis (F0-F4) and inflammation (A0-A2) score. For statistical analysis, independent t test, and Mann-Whitney U test and ROC analysis were performed, the latter to determine the performance of T1 mapping and MRE for fibrosis staging and inflammation grading, as compared to histopathology.
Results: Histopathological analysis diagnosed 9 patients with F0 (13.2%), 21 with F1 (30.9%), 11 with F2 (16.2%), 10 with F3 (14.7%), and 17 with F4 (25.0%). Both T1 mapping and MRE showed significantly higher values for patients with significant fibrosis (F0-1 vs. F2-4; T1 mapping p < 0.0001, MRE p < 0.0001) as well as for patients with severe fibrosis or cirrhosis (F0-2 vs. F3-4; T1 mapping p < 0.0001, MRE p < 0.0001). T1 values and MRE LS were significantly higher in patients with inflammation (A0 vs. A1-2, both p = 0.01). T1 mapping showed a tendency toward lower diagnostic performance without statistical significance for significant fibrosis (F2-4) (AUC 0.79 vs. 0.91, p = 0.06) and with a significant difference compared to MRE for severe fibrosis (F3-4) (AUC 0.79 vs. 0.94, p = 0.03). For both T1 mapping and MRE, diagnostic performance for diagnosing hepatic inflammation (A1-2) was low (AUC 0.72 vs. 0.71, respectively).
Conclusion: T1 mapping is able to diagnose hepatic fibrosis, however, with a tendency toward lower diagnostic performance compared to MRE and thus may be used as an alternative to MRE for diagnosing hepatic fibrosis, whenever MRE is not available or likely to fail due to intrinsic factors of the patient. Both T1 mapping and MRE are probably not sufficient as standalone methods to diagnose hepatic inflammation with relatively low diagnostic accuracy.
Keywords: Biopsy; Fibrosis; Liver; MR elastography; T1 mappin
Assessment of hepatic fibrosis and inflammation with look-locker T1 mapping and magnetic resonance elastography with histopathology as reference standard.
PURPOSE
To compare the diagnostic performance of T1 mapping and MR elastography (MRE) for staging of hepatic fibrosis and grading inflammation with histopathology as standard of reference.
METHODS
68 patients with various liver diseases undergoing liver biopsy for suspected fibrosis or with an established diagnosis of cirrhosis prospectively underwent look-locker inversion recovery T1 mapping and MRE. T1 relaxation time and liver stiffness (LS) were measured by two readers. Hepatic fibrosis and inflammation were histopathologically staged according to a standardized fibrosis (F0-F4) and inflammation (A0-A2) score. For statistical analysis, independent t test, and Mann-Whitney U test and ROC analysis were performed, the latter to determine the performance of T1 mapping and MRE for fibrosis staging and inflammation grading, as compared to histopathology.
RESULTS
Histopathological analysis diagnosed 9 patients with F0 (13.2%), 21 with F1 (30.9%), 11 with F2 (16.2%), 10 with F3 (14.7%), and 17 with F4 (25.0%). Both T1 mapping and MRE showed significantly higher values for patients with significant fibrosis (F0-1 vs. F2-4; T1 mapping p < 0.0001, MRE p < 0.0001) as well as for patients with severe fibrosis or cirrhosis (F0-2 vs. F3-4; T1 mapping p < 0.0001, MRE p < 0.0001). T1 values and MRE LS were significantly higher in patients with inflammation (A0 vs. A1-2, both p = 0.01). T1 mapping showed a tendency toward lower diagnostic performance without statistical significance for significant fibrosis (F2-4) (AUC 0.79 vs. 0.91, p = 0.06) and with a significant difference compared to MRE for severe fibrosis (F3-4) (AUC 0.79 vs. 0.94, p = 0.03). For both T1 mapping and MRE, diagnostic performance for diagnosing hepatic inflammation (A1-2) was low (AUC 0.72 vs. 0.71, respectively).
CONCLUSION
T1 mapping is able to diagnose hepatic fibrosis, however, with a tendency toward lower diagnostic performance compared to MRE and thus may be used as an alternative to MRE for diagnosing hepatic fibrosis, whenever MRE is not available or likely to fail due to intrinsic factors of the patient. Both T1 mapping and MRE are probably not sufficient as standalone methods to diagnose hepatic inflammation with relatively low diagnostic accuracy
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