Universal cytochrome b primers facilitate intraspecific studies in molluscan taxa.

We describe the construction of amplification primers designed to target a portion of the mitochondrial cytochrome b locus in a variety of molluscan taxa. Combinations of two sets of primers successfully amplified cytochrome b from several species of gastropods, bivalves, and cephalopods. Sequence analysis of these amplified products revealed nucleotide diversity in small samples within several of these taxa. We discuss the utility of these primer sets for studies of intraspecific phylogeny in mollusks and potentially other invertebrates.

Neonatal hemochromatosis: a case report.

Hemochromatosis is the excess accumulation of iron in tissue affecting a variety of organ systems leading to hepatic fibrosis and multiorgan system failure. When excess iron accumulation occurs in utero, as with neonatal hemochromatosis, the infant may be stillborn or present with advanced, overwhelming liver disease. Hepatic failure in the newborn encompasses a wide variety of disease entities, and formulation of a differential diagnosis presents a challenge for the clinician. This article reviews one case of neonatal hemochromatosis that was diagnosed and successfully treated. Iron metabolism and overload are discussed, as well as clinical manifestations, current treatment, and the potential for prenatal diagnosis in the future.

Decreased release of D-aspartate in the guinea pig spinal cord after lesions of the red nucleus.

This study attempts to determine if fibers that project from the guinea pig red nucleus to the spinal cord use L-glutamate and/or L-aspartate as transmitters. Unilateral injections of kainic acid were placed stereotaxically in the red nucleus to destroy the cells of origin of the rubrospinal tract. Six days after the injection, Nissl-stained sections through the lesion site showed that the majority of neurons in the red nucleus ipsilateral to the kainic acid injection were destroyed. In addition, the lesioned area included parts of the surrounding midbrain reticular formation. Silver-impregnated, transverse sections of the cervical spinal cord revealed the presence of degenerating fibers contralaterally in laminae IV-VII of the gray matter. Ipsilaterally, very sparse degeneration was evident in laminae VII and VIII of the gray matter. Two to six days after surgery, the electrically evoked, Ca2(+)-dependent release of both D-[3H]aspartate, a marker for glutamatergic/aspartatergic neurons, and gamma-amino[14C]-butyric acid ([14C]GABA) was measured in dissected quadrants of the spinal cervical enlargement. Lesions centered on the red nucleus depressed the release of D-[3H]aspartate by 25-45% in dorsal and ventral quadrants of the cervical enlargement contralaterally. The release of [14C]GABA was depressed by 27% in contralateral ventral quadrants. To assess the contribution of rubro- versus reticulospinal fibers to the deficits in amino acid release, unilateral injections of kainic acid were placed stereotaxically in the midbrain reticular formation lateral to the red nucleus. Nissl-stained sections through the midbrain revealed the presence of extensive neuronal loss in the midbrain and rostral pontine reticular formation, whereas neurons in the red nucleus remained undamaged. In the spinal cord, degenerating axons were present ipsilaterally in laminae VII and VIII of the gray matter. Some fiber degeneration was also evident contralaterally in laminae V and VI of the gray matter. This lesion did not affect the release of either D-[3H]aspartate or [14C]GABA in the spinal cord. The substantial decrements in D-[3H]aspartate release following red nucleus lesions suggests that the synaptic endings of rubrospinal fibers mediate the release of D-[3H]aspartate in the spinal cord. Therefore, these fibers may be glutamatergic and/or aspartatergic. Because other evidence suggests that rubrospinal neurons are probably not GABAergic, the depression of [14C]GABA release probably reflects changes in the activity of spinal interneurons following the loss of rubrospinal input.