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  • 1
    Keywords: CANCER ; tumor ; carcinoma ; Germany ; LUNG ; PERFUSION ; THERAPY ; CT ; DENSITY ; LUNG-CANCER ; NEW-YORK ; TUMORS ; PATIENT ; CONTRAST ; INJECTION ; treatment ; DIFFERENCE ; REGION ; REGIONS ; LOCALIZATION ; PARAMETERS ; tomography ; CARCINOMAS ; COMPUTED-TOMOGRAPHY ; PET ; lung neoplasms ; PULMONARY ; DYNAMIC CT ; X-ray computed
    Abstract: Advanced bronchial carcinomas by means of perfusion and peak enhancement using dynamic contrast-enhanced multislice CT are characterized. Twenty-four patients with advanced bronchial carcinoma were examined. During breathhold, after injection of a contrast-medium (CM), 25 scans were performed (I scan/s) at a fixed table position. Density-time curves were evaluated from regions of interest of the whole tumor and high- and low-enhancing tumor areas. Perfusion and peak enhancement were calculated using the maximum-slope method of Miles and compared with size, localization (central or peripheral) and histology. Perfusion of large tumors (〉50 cm(3)) averaged over both the whole tumor (P=0.001) and the highest enhancing area (P=0.003) was significantly lower than that of smaller ones. Independent of size, central carcinomas had a significantly (P=0.04) lower perfusion (mean 27.9 ml/min/100 g) than peripheral ones (mean 66.5 ml/min/100 9). In contrast, peak enhancement of central and peripheral carcinomas was not significantly different. Between non-small-cell lung cancers and small-cell lung cancers, no significant differences were observed in both parameters. In seven tumors, density increase after CM administration started earlier than in the aorta, indicating considerable blood supply from pulmonary vessels. Tumor perfusion was dependent on tumor size and localization, but not on histology. Furthermore, perfusion CT disclosed blood supply from both pulmonary and/or bronchial vessels in some tumors
    Type of Publication: Journal article published
    PubMed ID: 15029450
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  • 2
    Keywords: Germany ; LUNG ; CT ; EMPHYSEMA ; HIGH-RESOLUTION CT ; QUANTIFICATION ; VOLUME ; PATIENT ; IMPACT ; REDUCTION ; SIMULATION ; PARAMETERS ; COMPUTED-TOMOGRAPHY ; OBSTRUCTIVE PULMONARY-DISEASE ; THIN-SECTION CT ; HELICAL CT ; RE ; multidetector CT ; LUNG-VOLUME ; low dose ; MULTISLICE CT ; 3-dimensional quantitative volumetric analysis ; ALPHA-1-ANTITRYPSIN DEFICIENCY ; dose simulation ; LUNG DENSITY-MEASUREMENTS ; MACROSCOPIC MORPHOMETRY ; multidetector computed tomography ; VOLUME REDUCTION
    Abstract: Purpose: Quantitative evaluation of the lung parenchyma might be impaired or unreliable by use of reduced-dose CT protocols. Aim of the study was to define the threshold where reduced dose has significant impact on quantitative emphysema parameters. Materials and Methods: Thirty patients with severe centrilobular emphysema underwent multidetector computed tomography (120 kV, 150 mAs). Original CT raw data were simulated using 10 mAs settings (10-100 SlMmAs). Quantitative analysis provided lung volume, emphysema volume, emphysema index, mean lung density, and 4 emphysema volume classes. Simulated low-dose results were compared with original acquisition. Results: Emphysema index showed no clinical relevant variation down to 30 SlMmAs. The large emphysema volume class was significantly different below 50 SlMmAs. The intermediate and small classes showed an overproportional variation below 50 SlMmAs. Conclusions: Dose reduction down to 30 SlMmAs is possible for clinical routine. Settings below 50 SlMmAs significantly alter the indetailed 3-dimensional emphysema quantification
    Type of Publication: Journal article published
    PubMed ID: 16778622
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  • 3
    Keywords: tumor ; AGENTS ; BLOOD ; Germany ; IN-VIVO ; MODEL ; PERFUSION ; THERAPY ; VIVO ; imaging ; QUANTIFICATION ; VOLUME ; liver ; TISSUE ; TIME ; BLOOD-FLOW ; INDEX ; CONTRAST ; blood flow ; CONTRAST AGENT ; FLOW ; INJECTION ; BIOLOGY ; metastases ; US ; PARAMETERS ; tomography ; KINETICS ; LIVER METASTASES ; CONTRAST AGENTS ; POWER DOPPLER SONOGRAPHY ; INDUCED DESTRUCTION ; AGENT ; TRANSIT-TIME ; DESTRUCTION ; REAL-TIME ; tissue viability ; OCT ; ENHANCED SONOGRAPHY ; HEPATIC METASTASES ; HEPATIC PERFUSION ; low-MI ultrasound ; MATHEMATICAL-MODEL ; quantification of perfusion ; replenishment kinetics ; TUMOR PERFUSION ; ultrasound contrast agent
    Abstract: Low-MI (mechanical index) ultrasound allows real-time observation of replenishment kinetics after destruction ("flash") of ultrasound contrast agents (USCA). We developed an examination protocol and a mathematical model to quantify perfusion of liver tissue and hepatic metastases. Using a modified multivessel model, we attempted a consistent, physiological description of microbubble replenishment in liver tissue. Perfusion parameters were calculated, separately for the arterial and portal venous phase of liver perfusion, using an i.v. bolus injection of 2 x 2.4 mL SonoVue(R). The model was evaluated for 10 examinations of liver metastases using flash/low-MI imaging. In contrast to the established, exponential model, the new model consistently describes the sigmoid replenishment of USCA measured in vivo, using flash/low-MI imaging. Parameters for blood volume, blood velocity and blood flow in liver tissue and metastases can be calculated during the arterial and the portal venous phase after a CA bolus injection. The median arterial perfusion in the examined liver metastases was more than 2.5 times higher than in normal liver tissue, whereas the median perfusion during the portal venous phase was more than five times higher in the liver tissue than that in metastases. Microbubble replenishment measured with flash/low-MI US techniques can be consistently analyzed using the multivessel model, even after a bolus injection of USCA. This allows for the quantification of perfusion of liver tissue and hepatic metastases and provides promising parameters of tissue viability and tumor characterization. (C) 2004 World Federation for Ultrasound in Medicine Biology
    Type of Publication: Journal article published
    PubMed ID: 15582235
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  • 4
    Keywords: brain ; RECEPTOR ; CANCER ; EXPRESSION ; BLOOD ; Germany ; LUNG ; MODEL ; imaging ; lung cancer ; LUNG-CANCER ; POPULATION ; GENE ; GENE-EXPRESSION ; TISSUE ; PATIENT ; CONTRAST ; gene expression ; metastases ; PARAMETERS ; SCINTIGRAPHY ; PET ; SOMATOSTATIN ; QUANTITATIVE ASSESSMENT ; RE ; SOMATOSTATIN ANALOG ; GA-68-DOTATOC ; LOSSES ; uptake ; FDG ; viability ; DOTATOC ; EMISSION-TOMOGRAPHY ; F-18-FDG PET ; kinetic modelling ; kinetic parameters ; non-small cell lung tumours ; TC-99M DEPREOTIDE
    Abstract: Purpose: Dynamic PET studies with Ga-68-DOTATOC were performed in patients with non-small cell lung cancer (NSCLC) to assess the somatostatin receptor 2 (SSTR2) expression. Furthermore, dynamic F-18-fluorodeoxyglucose (FDG) studies were performed in the same patients to compare the SSTR2 expression with the tumour viability. Methods: The study population comprised nine patients, examined with both tracers on two different days within 1 week. Standardised uptake values (SUVs) were calculated and a two-tissue compartment model was applied to the data. Furthermore, a non-compartment model based on the fractal dimension (FD) was applied to the data. Results: The DOTATOC uptake was generally lower than the FDG uptake. Moderately enhanced DOTATOC uptake was noted in seven of the nine tumours. All kinetic parameters exceptk (4) were lower for DOTATOC than for FDG. The mean SUV was 2.018 for DOTATOC, in comparison to 5.683 for FDG. In particular,k (3) was highly variable for DOTATOC and showed an overlap with the normal lung tissue. The fractional blood volumeV (B) was relatively low for both tracers, not exceeding 0.3. The highest significant logarithmic correlation was found for the FD of the two tracers (r=0.764,p=0.017). The logarithmic correlation for SUVs was also significant (r=0.646,p=0.060), as was that forV (B) (r=0.629,p=0.069). In contrast, none of the eight metastases which were positive on FDG PET showed any DOTATOC uptake. Conclusion: The results demonstrated moderate Ga-68-DOTATOC uptake in primary NSCLC but did not provide any evidence for SSTR2 expression in metastases. This may be caused by loss of the gene expression in metastases as compared with the primary tumours
    Type of Publication: Journal article published
    PubMed ID: 16570185
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