Taxonomic Revision of Living Boring Bivalves Belonging to the Family Pholadidae Lamarck, 1809, (Bivalvia: Myida) from the Southwestern Atlantic.

Boring bivalves of the family Pholadidae Lamarck, 1809 living in Argentinean and Uruguayan waters are herein revised. The literature research revealed twelve nominal species of Pholadidae mentioned as living in the study area. Type material of all nominal taxa were examined when it was possible. Additional specimens from field works and malacological collections were studied, illustrated and re-described. Details of type localities, repositories, and distribution range are provided for each valid taxa. This work revealed the presence of five native and one introduced species belonging to Pholadidae in Argentinean and Uruguayan waters. Barnea (Anchomasa) lamellosa, Cyrtopleura (Scobinopholas) lanceolata, Pholas (Thovana) campechiensis and Martesia fragilis belonging to the Argentine biogeographical province; Netastoma darwinii from Magellan province; and Barnea (Anchomasa) truncata introduced in the Bahía Blanca estuary. Finally, morphological comparison with congeneric species distributed in American seas are provided.

Sequence analysis of in vivo defective interfering-like RNA of influenza A H1N1 pandemic virus.

Influenza virus defective interfering (DI) particles are naturally occurring noninfectious virions typically generated during in vitro serial passages in cell culture of the virus at a high multiplicity of infection. DI particles are recognized for the role they play in inhibiting viral replication and for the impact they have on the production of infectious virions. To date, influenza virus DI particles have been reported primarily as a phenomenon of cell culture and in experimentally infected embryonated chicken eggs. They have also been isolated from a respiratory infection of chickens. Using a sequencing approach, we characterize several subgenomic viral RNAs from human nasopharyngeal specimens infected with the influenza A(H1N1)pdm09 virus. The distribution of these in vivo-derived DI-like RNAs was similar to that of in vitro DIs, with the majority of the defective RNAs generated from the PB2 (segment 1) of the polymerase complex, followed by PB1 and PA. The lengths of the in vivo-derived DI-like segments also are similar to those of known in vitro DIs, and the in vivo-derived DI-like segments share internal deletions of the same segments. The presence of identical DI-like RNAs in patients linked by direct contact is compatible with transmission between them. The functional role of DI-like RNAs in natural infections remains to be established.

Mapping the effects of three dopamine agonists with different dyskinetogenic potential and receptor selectivity using pharmacological functional magnetic resonance imaging.

The mechanisms underlying dopamine agonist-induced dyskinesia in Parkinson's disease remain poorly understood. Similar to patients, rats with severe nigrostriatal degeneration induced by 6-hydroxydopamine are more likely to show dyskinesia during chronic treatment with unselective dopamine receptor agonists than with D2 agonists, suggesting that D1 receptor stimulation alone or in conjunction with D2 receptor stimulation increases the chances of experiencing dyskinesia. As a first step towards disclosing drug-induced brain activation in dyskinesia, we examined the effects of dopamine agonists on behavior and blood oxygenation level-dependent (BOLD) signal in the striatum and motor cortex of rats with unilateral nigrostriatal lesions. Rats were rendered dyskinetic before pharmacologic functional magnetic resonance imaging by means of a repeated treatment regime with dopamine agonists. The unselective agonist apomorphine and the selective D1/D5 agonist SKF-81297 induced strong forelimb dyskinesia (FD) and axial dystonia and increased BOLD signal in the denervated striatum. Besides, SKF-81297 produced a significant but smaller BOLD increase in the intact striatum and a symmetric bilateral increase in the motor cortex. The D2 family agonist quinpirole, which induced mild dyskinesia on chronic treatment, did not produce BOLD changes in the striatum or motor cortex. Further evidence to support an association between BOLD changes and dyskinesia comes from a direct correlation between scores of FD and magnitude of drug-induced BOLD increases in the denervated striatum and motor cortex. Our results suggest that striatal and cortical activation induced by stimulation of D1/D5 receptors has a primary role in the induction of peak dose dyskinesia in parkinsonism.

The phenylephrine blood pressure clamp in pharmacologic magnetic resonance imaging: reduction of systemic confounds and improved detectability of drug-induced BOLD signal changes.

RATIONALE: Peripheral physiologic changes accompany many central pharmacologic manipulations and can interact with brain activity and cerebral perfusion in complex ways. This considerably complicates the interpretation of drug-induced brain activity changes. OBJECTIVES: To evaluate a method whereby drug-induced blood pressure (BP) changes are prevented. METHODS: A continuously adjusted infusion of the peripheral vasoconstrictor phenylephrine (PEP) was used to counter-regulate BP changes elicited by application of the dopamine receptor agonist apomorphine (APO) in the rat. Central effects of APO were measured using pharmacologic magnetic resonance imaging (phMRI) with blood oxygenation level dependent (BOLD) contrast at a field strength of 7 T. RESULTS: Compared to a NOPEP control group, the PEP blood pressure clamp successfully prevented BP changes and improved the detectability of central APO effects. Moreover, APO-induced central changes no longer correlated with BP time courses. CONCLUSIONS: The method is suitable for isolating central drug effects from peripherally originating (BP) confounds in high-field functional magnetic resonance imaging (fMRI) studies. It may also be useful in fMRI studies of autonomic regulation, cognition, and emotion if the experimental manipulation entails BP changes.

Differential gene expression induced by chronic levodopa treatment in the striatum of rats with lesions of the nigrostriatal system.

Levodopa, the major treatment for patients with Parkinson's disease, has been shown to induce a variety of compensatory effects, including facilitation of sprouting by dopaminergic neurons, in experimental animals with lesions leading to denervation of the striatum. To better understand the cellular and molecular environment where most of these compensatory changes take place, in particular elements that might contribute to the recovery of dopaminergic innervation, we have constructed a differential expression library enriched in transcripts from the striata of rats with lesions of the medial forebrain bundle treated with levodopa for 6 months. We have used this library to screen an expression array of rat genes representing the major cell functions, and have identified several that are involved in neurotrophic mechanisms and plasticity. We have confirmed the differential expression of selected transcripts by non-radioactive in situ hybridization, and report that the growth factor pleiotrophin, myelin basic protein and calmodulin are overexpressed in the denervated striatum of levodopa-treated rats.

Effects of orally administered levodopa on mesencephalic dopaminergic neurons undergoing a degenerative process.

Although the issue of in vivo levodopa toxicity appears to be settled by now in the light of recent findings, a crucial aspect was not accounted for the experiments designed to tackle that question. Levodopa could in fact be non-toxic on surviving dopamine neurons, but that could not be the case when the drug is administered at the same time those neurons are undergoing degeneration, which is what happens in the clinical setting. Dopaminergic neurons could in that situation be more vulnerable to levodopa's potential toxic action. Our aim was to determine if oral administration of levodopa is toxic for mesencephalic dopaminergic neurons that are actively involved in a degenerative process. We induced delayed retrograde degeneration of the nigrostriatal system in rats by injecting 6-hydroxydopamine (6-OHDA) intrastriatally. Treatment was started the day after the injection. Dopaminergic markers were histologically studied at the striatal and nigral levels, to determine degree of damage of the nigrostriatal dopaminergic system in levodopa- and vehicle-treated rats. No significant differences between levodopa or vehicle-treated rats were found in: (i) striatal immunoautoradiographic labeling for tyrosine hydroxylase (TH) and the membrane dopamine transporter (DAT); (ii) cell counts of TH-immunoreactive (TH-ir) neurons remaining in the substantia nigra and ventral tegmental area (VTA); (iii) surface area of remaining TH-immunoreactive neurons in the substantia nigra. The present experiments demonstrate that levodopa does not enhance delayed retrograde degeneration of dopaminergic neurons induced by intrastriatal administration of 6-OHDA.