Localization of preangiotensinogen messenger RNA sequences in the rat brain.

Angiotensinogen (renin substrate) and its messenger RNA are known to accumulate in the rat brain. We have cloned rat preangiotensinogen cDNAs and used them as probes to measure the accumulation of preangiotensinogen messenger RNA sequences in eight regions of rat brain, as well as in liver and kidney. The brain regions examined were the cerebral cortex, hippocampus, striatum, cerebellum, diencephalon (including basal forebrain structures), midbrain, brainstem, and pituitary. On a tissue weight basis, the accumulation of preangiotensinogen RNA sequences was greatest in the liver, midbrain, and brainstem. The relative concentrations of messenger RNA were ranked as follows: liver, brainstem, midbrain greater than cerebellum, diencephalon greater than hippocampus greater than cortex, striatum, kidney greater than pituitary. Relative RNA concentrations from liver to kidney varied over a 16-fold range. Liver and brain preangiotensinogen RNA sequences were indistinguishable in size as measured by gel electrophoresis; however, the kidney sequences appeared some 100 nucleotides larger. Our data agree with previous measurements of angiotensinogen in the rat brain as assayed by renin-catalyzed angiotensin I release.

Multiple sclerosis presenting as transverse myelopathy: clinical and MRI features.

We described specific MRI features of MS presenting with acute partial transverse myelopathy. We reviewed the clinical histories and MRI studies of brain and spinal cord of 24 patients, using axial and sagittal images of the spinal cord to define patterns of signal abnormality in the context of clinical presentation, course, and vertebral column structural pathology. The heterogeneity of spinal cord tract involvement was greater than previously reported, with signal abnormality identified within the central cord, crossing the gray-white junction, and involving all four major funiculi. Correlation between spinal cord MRI findings and neurologic deficits was strong (100% by axial images; 96% by sagittal images). Serial spinal cord MRI demonstrated the dynamic nature of the signal abnormalities over time and in response to high-dose steroid treatment. No cranial MRI abnormality initially was seen in 36% of cases with evidence of demyelinating disease on concurrent spinal MRI.

Genetics of protein I of Neisseria gonorrhoeae: construction of hybrid porins.

Protein I (PI), the major outer membrane protein of Neisseria gonorrhoeae, is a porin and occurs in two major immunochemical classes, A and B. By using shuttle mutagenesis to insert a selectable marker close to the PI structural gene, evidence was obtained from transformation experiments to demonstrate that the PI structural gene is equivalent to the defined locus nmp and that the genes for PI class A and PI class B are alleles of the same locus. The PI class B gene of strain MS11 was cloned and sequenced, and comparison of this sequence with the gene sequence of PI class A of FA19 revealed a number of regions of significant divergence. By selection for the closely linked marker in transformations between the two strains, a series of strains with a hybrid PI was obtained. Analysis of these strains with monoclonal antibodies and oligonucleotides specific to PI class A or PI class B elucidated the nature and location of some of the surface-exposed epitopes, a thorough characterization of which is a prerequisite for understanding the role of PI in gonococcal pathogenesis and its possible use as a component of a vaccine.