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Our aim was to determine the degree of bias in CT scanogram measurements. We obtained standard lateral and anteroposterior (AP) pelvimetry scanograms of a phantom pelvis after placing ball bearings or aluminium rods to mark bony landmarks. Computed tomography pelvimetry was carried out at the manufacturer‐recommended table height on two commercial CT scanners and at 10‐mm increments up to 50 mm above and below this height. The AP inlet, AP outlet, interspinous distance and transverse diameters were each measured three times for each scanogram. The true measurements were obtained directly from the disassembled phantom. Bias was defined as the difference between the CT measurement and the true measurement. Observer error was negligible. The transverse diameter was overestimated at high table positions and underestimated at low table positions on both scanners (+6 to ?10 mm). After correcting for geometric distortion, up to 6 mm bias was still present. The point at which no bias occurred was different for each scanner and did not correspond to the manufacturers’ recommended table height. The outlet was overestimated on both scanners by up to 5 mm. The true inlet measurement was overestimated by 1.2 mm. The interspinous distance was minimally underestimated on both scanners. The measurements on CT scanogram were underestimated or overestimated in an inconsistent and unpredictable fashion, varying from one type of measurement to another and from CT scanner to CT scanner. This has implications for the accuracy and clinical utility of measurements obtained from a CT scanogram.  相似文献   
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Nuclear magnetic resonance proton imaging was used to obtain images of goat fetuses in utero. The long T1 relaxation time of amniotic fluid makes it appear black on proton density images when examined using the Aberdeen imager, and so allows very good discrimination of the position and structure of the fetus. Some fetal internal tissues can be seen on T1 images. These findings suggest that NMR imaging has great potential in pregnancy studies.  相似文献   
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Summary Two patients with liver failure secondary to isoniazid hepatotoxicity were successfully treated with orthotopic liver transplantation. A 49-year-old man received isoniazid prophylaxis for a positive tuberculin test, and a 60-year-old woman was treated for active pulmonary tuberculosis with isoniazid, rifampin, and pyrazinamide. Both patients developed hepatic failure 4 and 1.5 months after initiation of antituberculous drug therapy, respectively. Liver transplantation was performed for progressive hepatic failure and was successful in both patients. The patient with active pulmonary tuberculosis was successfully treated with a modified antituberculous drug regimen while taking standard doses of immunosuppressive drugs after transplantation. In conclusion, liver transplantation is feasible and effective therapy for patients with isoniazid-induced hepatic failure, and active pulmonary tuberculosis may represent a relative rather than absolute contraindication to transplantation.  相似文献   
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The AraC-resistant rat leukemic cell line RO/1-A has been shown to have a typical deoxycytidine kinase (DCK)-deficient phenotype and cannot metabolize the antileukemic drugs cytarabine (AraC) and decitabine (DAC). To investigate the relative contribution of mutations in the dck gene to the development of in vitro-induced AraC-resistance, a neomycin selectable plasmid construct harboring the wild-type dck coding region was transfected into RO/1-A. Polymerase chain reaction analysis confirmed the presence of vector DNA in the target cells (RO/1-ADCK) that were stably transfected and monitored over a period of 14 weeks. Northern and Western blot analysis showed restoration of dck mRNA and protein expression. Initial rate measurements of DCK activity showed that Km values for dck were only slightly altered as a result of transfection, whereas strongly increased Vmax values were observed, resulting in a 12-fold increased phosphorylation efficiency for both dC and AraC, compared with the AraC-sensitive parental cell line RO/1 from which the RO/1-A was originally derived. In vitro sensitivity to AraC- and DAC-mediated cytotoxicity was fully restored in RO/1-ADCK. The data pinpoint acquired DCK deficiency caused by mutations of the dck gene as the major cause of AraC resistance in this model.  相似文献   
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