[Gamma-globulin level in the cerebrospinal fluid in relation to the clinical picture and the course of disseminated sclerosis].
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Biomedical subjects
Publications and source records attributed to J Vymazal.
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T1 and T2 of paramagnetic ions in free and chelated form were measured over the range of clinical magnetic resonance imaging field strengths (0.02-1.5 T). T1 values agreed with published data; however, to our knowledge, the field dependence of T2 has not been systematically studied before Mn2+, Cr3+, and Fe3+ all showed T2 reduction at high field strengths, although reduction due to Fe3+ was minimal. This is believed to be due to "contact" interactions, which have been previously noted for manganese. No such T2 reduction was seen in the chelates, except that dysprosium chelate (but not free ion) showed an anomalous decrease in T2 at high field strengths, which may possibly be explained by a dephasing effect caused by the large magnetic moment of Dy3+.
The frequency dependence of T1 and T2 was measured for homogeneous suspensions of magnetite and iron oxyhydroxide particles in water with various concentrations of gelatin. The transverse relaxivity showed two types of behavior: (a) For magnetic particles, there was a rapid increase in T2 relaxivity with frequency, followed by a saturation plateau, which accorded with the Langevin magnetization function. From these curves, the magnetic moment of the particle domains was estimated to range from 0.8 to 6.3 x 10(4) Bohr magnetons. (b) For iron oxyhydroxide (ferritin, ferrihydrite, and akaganéite) particles, T2 relaxivity increased linearly with frequency, the slope of the increase characteristic for each particle. T2 relaxivity generally increased with increasing gelatin concentration, corresponding to the measured decrease in the water diffusion coefficient. For iron oxides, homogeneously distributed either as iatrogenic agents or endogenous biominerals, these findings may aid in the interpretation of in vivo relaxivity and the effect on MR imaging.
A protein-encaged superparamagnetic iron oxide has been developed and characterized by using horse spleen apoferritin as a novel bioreactive environment. The roughly spherical magnetoferritin molecules, 120 A in diameter, are composed of a monocrystalline maghemite or magnetite core 73 A +/- 14 in diameter. Except for the additional presence of iron-rich molecules of higher molecular weight, the appearance and molecular weight (450 kd) of magnetoferritin are identical to that of natural ferritin; the molecules are externally indistinguishable from their precursor, with a pI (isoelectric point) in the range 4.3-4.6. The measured magnetic moment of the superparamagnetic cores is 13,200 Bohr magnetons per molecule, with T1 and T2 relaxivities (r1 and r2) of 8 and 175 L.mmol-1 (Fe).sec-1, respectively, at body temperature and clinical field strengths. The unusually high r2/r1 ratio of 22 is thought to arise from ideal core composition, with no evidence of crystalline paramagnetic inclusions. T2 relaxation enhancement can be well correlated to the field-dependent molecular magnetization, as given by the Langevin magnetization function, raised to a power in the range 1.4-1.6. With its nanodimensional biomimetic protein cage as a rigid, convenient matrix for complexing a plethora of bioactive substances, magnetoferritin may provide a novel template for specific targeting of selected cellular sites.
T2 was measured in samples of human blood and monkey brain over a field range of 0.02-1.5 Tesla, with variable interecho times, and was compared with previous data on ferritin solutions (taken with the same apparatus). 1/T2 in deoxygenated blood increased quadratically with field strength, as noted previously, but in brain gray matter the increase was linear, as also was the case in ferritin solution. In both deoxygenated blood and gray matter, 1/T2 increased with interecho time, but appeared to level off at times around 50 msec, as expected from the theory of diffusion through magnetic gradients. Diffusion times estimated by using the chemical exchange approximation were 3.4 msec for deoxygenated blood and 5.7 msec for the globus pallidus. The quadratic field dependence in blood is consistent with this same theory, but the linear dependence in brain tissue and in ferritin solutions remains unexplained.
A retrospective analysis of 158 T1-weighted and T2-weighted MRI scans of normal brains at 0.5 and 1.5 Tesla was performed. Signal intensities in the frontal cortex, caudate nucleus, putamen, and globus pallidus were divided by those of frontal white matter; and these gray/white ratios were correlated with iron concentration, estimated from the anatomical region and age of the patient. Intraregional plots were also made of gray/white ratio versus age for the 1.5 Tesla scans. The changes in both T1-weighted and T2-weighted ratios were consistent with the hypothesis that 1/T1 and 1/T2 vary linearly with iron concentration, and the corresponding coefficients, determined separately from the interregional and intraregional plots, were generally in agreement. Furthermore, the variability of the MRI ratios at 1.5 Tesla was consistent with expected iron variability except for the cortex, in which partial volume errors due to sulci and white matter caused increased variations. The MRI results agreed well with in vitro data on T1 and T2 in tissue specimens and with other MRI studies. When compared with T1 and T2 in ferritin solution, a significant "tissue relaxation enhancement" was found, attributable to slower diffusion and clustering of ferritin in tissue.
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Computed tomography (CT) was performed on 25 patients with Wilson disease (hepatolenticular degeneration). The diagnosis was confirmed biochemically. CT was normal in seven patients, five of whom presented clinically with the hepatic form of the disease. In 10 patients, CT abnormalities were graded as mild: there were atrophic changes around the basal ganglia and in the cortex and cerebellum. In eight patients, besides areas of atrophy there were low absorption areas subcortically in the frontal lobi and in the cerebellar hemispheres, as well as brainstem atrophy. Hypodense lesions in the lentiform nucleus and the area of the dentate nucleus were also noted, although mathematical analysis in terms of decrease of Hounsfield units failed to demonstrate significant differences from normal values.