The purpose of this study is to describe a subset of atypical hepatic hemangiomas that enhance rapidly and diffusely and to determine whether heavily T2-weighted images could distinguish between atypically enhancing liver hemangiomas and hypervascular malignancies. A retrospective search of MR records identified seven patients with liver hemangiomas that demonstrated diffuse early enhancement and 23 patients with biopsy-proven malignant liver lesions that were hypervascular on dynamic gadolinium-enhanced MR images. Quantitative analysis of signal intensity measurements was performed on the T2-weighted images, heavily T2-weighted (TE > 140), and dynamic gadolinium-enhanced images. Blinded reader comparison of the T2-weighted images and gadolinium-enhanced images was performed. Hypervascular hemangiomas enhanced to a greater degree than hypervascular malignant liver lesions on the early phase gadolinium-enhanced images. Perilesional parenchymal enhancement was demonstrated in five cases of rapidly enhancing hemangiomas. Signal intensity and contrast-to-noise ratios on the heavily T2-weighted images of the hemangiomas were significantly greater than that of the hypervascular malignant lesions (P < .05). Hemangiomas were differentiated from the hypervascular malignant liver lesions with high accuracy (97-100%) by three blinded readers based on the T2-weighted images. A subset of hemangiomas have atypical rapid diffuse enhancement on dynamic gadolinium-enhanced images. These atypical hemangiomas can be distinguished from hypervascular malignant liver lesions on T2-weighted MR images.

Adult↗

PubMedDate not supplied

Models for assessing scar tissue inhibitors.

The main purpose of animal models for proliferative vitreoretinopathy (PVR) is to develop pharmacologic therapies for this common cause of blindness. A very large number of pharmacologic agents appear to have potential use in this application by preventing cell proliferation and/or contraction. In practice, however, it has been found that prohibitively extensive numbers of animals and laboratory services are required to establish drug efficacy, safety, and dosage regimes. To lessen this work load and to accelerate drug screening programs, the authors have developed an in vitro model for PVR based on chorioretinal fibroblast growth in three-dimensional collagen lattices. This model yields precise data on the effect of drugs on cell proliferation and contractility. Trifluoperazine, colchicine, 5-fluorouracil, dexamethasone, and penicillamine were screened in this model. The first three agents were found to be inhibitory; on the basis of the pharmacokinetic data, obtained dosage regimes for animal testing were developed. The results obtained are discussed in terms of the in vitro model and the biochemical action of these drugs on the cellular events in PVR. In vitro screening of drugs prior to animal testing offers a significant advance in the quest for a pharmacologic prevention of blindness due to PVR.

Animals↗

PubMedDate not supplied

Models for assessing scar tissue inhibitors.

The main purpose of animal models for proliferative vitreoretinopathy (PVR) is to develop pharmacologic therapies for this common cause of blindness. A very large number of pharmacologic agents appear to have potential use in this application by preventing cell proliferation and/or contraction. In practice, however, it has been found that prohibitively extensive numbers of animals and laboratory services are required to establish drug efficacy, safety, and dosage regimes. To lessen this work load and to accelerate drug screening programs, the authors have developed an in vitro model for PVR based on chorioretinal fibroblast growth in three-dimensional collagen lattices. This model yields precise data on the effect of drugs on cell proliferation and contractility. Trifluoperazine, colchicine, 5-fluorouracil, dexamethasone, and penicillamine were screened in this model. The first three agents were found to be inhibitory; on the basis of the pharmaco kinetic data, obtained dosage regimes for animal testing were developed. The results obtained are discussed in terms of the in vitro model and the biochemical action of these drugs on the cellular events in PVR. In vitro screening of drugs prior to animal testing offers a significant advance in the quest for a pharmacologic prevention of blindness due to PVR.

Animals↗

PubMedDate not supplied

An analysis checklist for audiovisuals when used as educational resources.

Explore the source record for details and available documents.

Audiovisual Aids↗

PubMedDate not supplied

Corticosteroids and progesterone in amniotic fluid and maternal plasma of the rat and their relation to parturition.

The concentration of total and free corticosteroids, total progesterone and corticosteroid binding activity were determined in the amniotic fluid of rats on each of the 5 days before birth. The levels of total and free corticosteroids were low 4 days before birth but increased to peak levels (15.8 +/- 2.9 micrograms/100 ml and 6.4 +/- 1.1 micrograms/100 ml, respectively) 1 day prior to birth. These increases in the concentration of corticosteroids in amniotic fluid coincided with changes in the level of free corticosteroids but not total corticosteroids in foetal plasma. The level of corticosteroid binding activity increased from 0.9 +/- 0.15 micrograms corticosterone bound/100 ml 4 days before birth to peak at 13.3 +/- 0.8 micrograms corticosterone bound/100 ml 2 days prior to birth. Preliminary investigations suggest that the binding activity is due to a corticosteroid binding globulin-like protein. The concentration of progesterone in amniotic fluid was low compared to that found in maternal plasma and they were not significantly correlated. The concentration of total and free corticosteroids in maternal plasma did not change significantly (P > 0.05) during the 4 days preceding birth and did not correlate with levels of total and free corticosteroids in amniotic fluid. However, there was a significant negative correlation (P < 0.01) between the declining level of progesterone in maternal plasma and increasing levels of total and free corticosteroids in amniotic fluid.

Adrenal Cortex Hormones↗