Linkage map on chromosome 21q and the association of a DNA haplotype with a propensity to nondisjunction and trisomy 21.
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Chromosomes, Human, 21-22 and Y↗
Biomedical subjects
A C Warren
Publications and source records attributed to A C Warren.
Tax policy and equipment leasing after TEFRA.
The Tax Equity and Fiscal Responsibility Act of 1982 substantially modified the "safe harbor" leasing provisions enacted by the Economic Recovery Tax Act of 1981. In this Comment, Professors Warren and Auerbach argue that the modifications did not remedy the defects they identified in an earlier Article and that a new category of "finance leases" may prove to be nearly as valuable for some taxpayers as were safe harbor leases before the 1982 changes.
Equipment and Supplies↗
Supercoiling of DNA and nuclear conformation during the cell-cycle.
When cells are lysed in solutions containing high concentrations of salt and a non-ionic detergent, structures are released which retain many of the morphological features of nuclei. These nucleoids contain superhelical DNA but are depleted of nuclear protein. We have analysed DNA conformation in nucleoids derived from HeLa cells synchronized at different stages in the cell cycle. The gross differences in nuclear morphology seen during the cell cycle are reflected in the morphology of the nucleoids; for example, the individual chromosomes of mitotic cells remain identifiable and aggregated within the mitotic nucleoid. The sedimentation rate of nucleoids in sucrose gradients reflects the gross nuclear morphology; the small S-phase nucleoids sediment 9 times faster than the large mitotic nucleoids. Despite these large differences at the gross level of organization, both the degree of supercoiling and the size of the units in which supercoiling is maintained are roughly similar in the nucleoids derived from cells in the different phases. The protein content of the various nucleoids is also very similar. Like the nucleoids made from randomly growing cultures of cells, mitotic nucleoids are excellent templates for the RNA polymerase of Escherichia coli.
Cell Cycle↗
A molecular genetic approach to amyotrophic lateral sclerosis.
Disorders of the motor neurons may affect both the upper and lower neurons, primarily the lower motor neurons as in the spinal muscular atrophies are primarily the upper motor neurons as in the familial spastic paraplegias. Amyotrophic lateral sclerosis is a degenerative disorder of the motor neuron that results in paralysis and wasting of voluntary muscles. Large motor neurons in the cerebral cortex, brain stem and spinal cord degenerate or are lost. Hyaline inclusions may be seen in the cytoplasm of surviving motor neurons. Acute axonal degeneration of peripheral motor fibers occurs at all levels, including the distal axon. Subclinical involvement of the spinecerebellar tracts, posterior column and Clarke's column as well as loss of large neurons in the dorsal root ganglia and neurons of oculomotor nuclei has been reported. The average duration of life onset of symptoms of amyotrophic lateral sclerosis is three years and ninety per cent of patients died within 5 years. The basic mechanism of disease in amyotrophic lateral sclerosis remains unknown. There is no known treatment that will prevent, reverse or otherwise alter the course of the disease. Autosomal dominant and autosomal recessive forms of amyotrophic lateral sclerosis are genetic models of amyotrophic lateral sclerosis which may provide insight into the disease mechanism of sporadic amyotrophic lateral sclerosis, five to ten percent of adult cases of amyotrophic lateral sclerosis with early onset of symptoms and a more benign course. It is conceivable that both genetic and sporadic forms of amyotrophic lateral sclerosis result from failure of the same or similar neuronal mechanism triggered by defective genes and by an environment agent in sporadic amyotrophic lateral sclerosis.
Amyotrophic Lateral Sclerosis↗
Brain atrophy in 18 patients with Down syndrome: a CT study.
Individuals with Down syndrome develop neuropathologic and in some cases clinical evidence of Alzheimer disease after age 40. We compared CT scans of 18 Down syndrome subjects, 26-70 years old (seven of whom satisfied criteria for dementia), with 175 screened normal volunteer control subjects for evidence of cortical and subcortical atrophy. CT scans were analyzed as a function of age and cognitive status. The suprasellar cistern ratio, presumed to measure mesial temporal-lobe atrophy (or hypoplasia), was correlated with severity of cognitive impairment, even when age effects were removed. The suprasellar cistern ratio predicted dementia status with an accuracy of greater than 75%. Brain measurements on CT scans showed a distinct pattern of increased abnormality with age in patients with Down syndrome; this differed clearly from that seen in controls.
Adult↗