ABSTRACT
Pomalidomide, previously used to treat multiple myeloma, has been reported to cause acute pulmonary toxicity that improves with drug discontinuation. We present a case of delayed pneumonitis with persistent fibrosis associated with pomalidomide. A 61-year-old male treated with pomalidomide and corticosteroids presented with acute on chronic dyspnea, profound hypoxemia, and ground glass opacities on computerized tomographic imaging. Corticosteroid taper and discontinuation of pomalidomide resulted in clinical improvement, but with substantial residual pulmonary fibrosis. Given the temporal improvement, but not resolution, following discontinuation of an agent with an established propensity for lung injury, we attribute this presentation to pomalidomide toxicity.
Subject(s)
Antineoplastic Agents/adverse effects , Lung/drug effects , Multiple Myeloma/drug therapy , Pneumonia/chemically induced , Pulmonary Fibrosis/chemically induced , Thalidomide/analogs & derivatives , Humans , Lung/pathology , Male , Middle Aged , Pneumonia/diagnostic imaging , Pulmonary Fibrosis/diagnostic imaging , Thalidomide/adverse effects , Tomography, X-Ray ComputedABSTRACT
The associational connections within area 7 on the crown of the middle suprasylvian gyrus in adult cats were investigated with extracellular axon tracing techniques. Injections of wheat germ agglutinin conjugated to horseradish peroxidase or of 3H-proline into area 7 revealed the presence of widespread intrinsic connections that extend over the rostral to caudal extent of the middle suprasylvian gyrus (up to 10 mm in one direction from injection sites). The connections have a complex organization with cell bodies and particulate label concentrated in patches. The patches are irregular in shape and do not form any obvious pattern. Although the transported label is concentrated in patches, large numbers of retrogradely labeled cells and significant quantities of anterogradely transported label are found in the spaces between patches. The long associational connections originate from cells in layers 2-6 and project to all cortical layers. Pyramidal cells are the primary source of the projections.
Subject(s)
Cerebral Cortex/anatomy & histology , Animals , Association , Cats , Neural Pathways/anatomy & histologyABSTRACT
Visual cortex damage in newborn kittens produces a 78% loss of retinal X-cells whereas damage in adult cats produces only a 22% loss. Retinal Y- and W-cells are unaffected. The present experiment showed that the critical period for the severe loss of retinal X-cells ends between birth and 2 weeks of age. These results have implications for understanding the neural mechanisms of recovery from early visual cortex damage.
Subject(s)
Retina/pathology , Retinal Ganglion Cells/pathology , Visual Cortex/injuries , Age Factors , Animals , Animals, Newborn , Cats , Retina/growth & development , Retinal Degeneration/etiology , Retinal Degeneration/pathology , Visual Cortex/physiopathology , Visual Pathways/pathology , Visual PerceptionABSTRACT
Recordings were made from single retinal ganglion cell somas in cats whose visual cortical areas 17 and 18 were damaged on the day of birth or in adulthood. Neonatal lesions produced a 78 percent loss of X-cells in the retina, while lesions made in adulthood produced a 22 percent loss. Y-cells and W-cells were unaffected. This retinal abnormality needs to be considered when interpreting studies of behavioral deficits and neural mechanisms of recovery after damage to the visual cortex.
