The sexual and reproductive health of young people in Latin America: evidence from WHO case studies / La salud sexual y reproductiva de los jóvenes en América Latina: evidencia derivada de estudios de la OMS

This original article addresses the sexual and reproductive health needs of young people aged 15 to 24 in Latin America. It introduces five articles from original research projects in three countries: Argentina, Brazil, and Peru. These projects were funded by the World Health Organization. This article explains the importance of studies that address the sexual and reproductive health of young people in developing countries. It provides an overview of sexual and reproductive health issues in Latin America and a discussion these issues in the three study countries. The five articles deal with difficult and challenging issues, including: knowledge of STIs and HIV/AIDS; pregnancy related practices; quality of care; the role of young men in couple formation, pregnancy and adoption of contraceptive practice; and, the role of obstetricians and gynecologists in public policy debate about family planning and abortion. The four articles in this special section help to improve our understanding of the factors that contribute to risky sexual behavior and negative reproductive health outcomes among youth in Latin America. The findings are useful to help inform and improve health care interventions in various contexts.

Este artículo original trata de las necesidades de salud sexual y reproductiva de jóvenes entre 15 y 24 años de edad en América Latina. Se presentan cuatro artículos derivados de investigaciones originales en tres países: Argentina, Brasil y Perú. Estos proyectos fueron patrocinados por la Organización Mundial de la Salud. Este artículo elucida la importancia de los estudios que tratan de la salud sexual y reproductiva de jóvenes en países en desarollo. Se ilustra el panorama general en cuestiones de salud sexual y reproductiva en América Latina y una discusión de estas cuestiones en los tres países de donde provienen los estudios. Los cinco artículos discuten cuestiones difíciles y controversiales, como los conocimientos sobre ITS y VIH/SIDA; las prácticas asociadas con el parto; la calidad de cuidados; el papel de los hombres jóvenes en la formación de parejas, el embarazo y el uso de métodos anticonceptivos; así como el papel de los tocólogos y ginecólogos en el debate público sobre planificación familiar y aborto. Los cuatro artículos en esta sección especial promueven un mejor entendimiento de los factores que contribuyen a las conductas sexuales de riesgo y a los resultados negativos en salud reproductiva entre los jóvenes en América Latina. Las conclusiones son útiles para informar y mejorar intervenciones de servicios de salud en contextos varios.

Pharmacological models of ADHD.

For more than 50 years, heavy metal exposure during pre- or post-natal ontogeny has been known to produce long-lived hyperactivity in rodents. Global brain injury produced by neonatal hypoxia also produced hyperactivity, as did (mainly) hippocampal injury produced by ontogenetic exposure to X-rays, and (mainly) cerebellar injury produced by the ontogenetic treatments with the antimitotic agent methylazoxymethanol or with polychlorinated biphenyls (PCBs). More recently, ontogenetic exposure to nicotine has been implicated in childhood hyperactivity. Because attention deficits most often accompany the hyperactivity, all of the above treatments have been used as models of attention deficit hyperactivity disorder (ADHD). However, the causation of childhood hyperactivity remains unknown. Neonatal 6-OHDA-induced dopaminergic denervation of rodent forebrain also produces hyperactivity - and this model, or variations of it, remain the most widely-used animal model of ADHD. In all models, amphetamine (AMPH) and methylphenidate (MPH), standard treatments of childhood ADHD, typically attenuate the hyperactivity and/or attention deficit. On the basis of genetic models and the noted animal models, monoaminergic phenotypes appear to most-closely attend the behavioral dysfunctions, notably dopaminergic, noradrenergic and serotoninergic systems in forebrain (basal ganglia, nucleus accumbens, prefrontal cortex). This paper describes the various pharmacological models of ADHD and attempts to ascribe a neuronal phenotype with specific brain regions that may be associated with ADHD.

Proposed animal model of severe Parkinson's disease: neonatal 6-hydroxydopamine lesion of dopaminergic innervation of striatum.

Rats lesioned shortly after birth with 6-hydroxydopamine are posed as a near-ideal model of severe Parkinson's disease, because of the non-lethality of the procedure, near-total destruction of nigrostriatal dopaminergic fibers, near-total dopamine (DA)-denervation of striatum, reproducibility of effect, and relative absence of overt behavioral effects--there is no aphasia, no adipsia, and no change in motor activity. In vivo microdialysis findings reinforce the utility of the animal model, clearly demonstrating L-DOPA beneficial actions without an increase in hydroxyl radical production.

Peculiarities of L: -DOPA treatment of Parkinson's disease.

L-Dihydroxyphenylalanine (L: -DOPA), the anti-parkinsonian drug affording the greatest symptomatic relief of parkinsonian symptoms, is still misunderstood in terms of its neurotoxic potential and the mechanism by which generated dopamine (DA) is able to exert an effect despite the absence of DA innervation of target sites in basal ganglia. This review summaries important aspects and new developments on these themes. On the basis of L: -DOPA therapy in animal models of Parkinson's disease, it appears that L: -DOPA is actually neuroprotective, not neurotoxic, as indicated by L: -DOPA's reducing striatal tissue content of the reactive oxygen species, hydroxyl radical (HO(*)), and by leaving unaltered the extraneuronal in vivo microdialysate level of HO(*). In addition, the potential beneficial anti-parkinsonian effect of L: -DOPA is actually increased because of the fact that the basal ganglia are largely DA-denervated. That is, from in vivo microdialysis studies it can be clearly demonstrated that extraneuronal in vivo microdialysate DA levels are actually higher in the DA-denervated vs. the intact striatum of rats - owing to the absence of DA transporter (i.e., uptake sites) on the absent DA nerve terminal fibers in parkinsonian brain. In essence, there are fewer pumps removing DA from the extraneuronal pool. Finally, the undesired motor dyskinesias that commonly accompany long-term L: -DOPA therapy, can be viewed as an outcome of L: -DOPA's sensitizing DA receptors (D(1)-D(5)), an effect easily replicated by repeated DA agonist treatments (especially agonist of the D(2) class) in animals, even if the brain is not DA-denervated. The newest findings demonstrate that L: -DOPA induces BDNF release from corticostriatal fibers, which in-turn enhances the expression of D(3) receptors; and that this effect is associated with motor dyskinesias (and it is blocked by D(3) antagonists). The recent evidence on mechanisms and effects of L: -DOPA increases our understanding of this beneficial anti-parkinsonian drug, and can lead to improvements in L: -DOPA effects while providing avenues for reducing or eliminating L: -DOPA's deleterious effects.

Neuroprotective and neurotoxic roles of levodopa (L-DOPA) in neurodegenerative disorders relating to Parkinson's disease.

Despite its being the most efficacious drug for symptom reversal in Parkinson's disease (PD), there is concern that chronic levodopa (L-DOPA) treatment may be detrimental. In this paper we review the potential for L-DOPA to 1). autoxidize from a catechol to a quinone, and 2). generate other reactive oxygen species (ROS). Overt toxicity and neuroprotective effects of L-DOPA, both in vivo and in vitro, are described in the context of whether L-DOPA may accelerate or delay progression of human Parkinson's disease.

Dopaminergic denervation enhances susceptibility to hydroxyl radicals in rat neostriatum.

To determine if greater amounts of hydroxyl radical (*OH) are formed by dopamine (DA) denervation and treatment with L-dihydroxyphenylalanine (L-DOPA), the neostriatum was DA denervated (99% reduction in DA content) by 6-hydroxydopamine treatment (134microg icv, desipramine pretreatment) of neonatal rats. At 10 weeks the peripherally restricted dopa decarboxylase inhibitor carbidopa (12.5mg/kg i.p.) was administered 30min before vehicle, L-DOPA (60mg/kg i.p.), or the known generator of reactive oxygen species, 6-hydroxydopa (6-OHDOPA) (60mg/kg i.p.); and this was followed 30min later (and 15 min before termination) by the spin trap, salicylic acid (8micromoles icv). By means of a high performance liquid chromatographic method with electrochemical detection, we found a 4-fold increase in the non-enzymatically formed spin trap product, 2,3-dihydroxybenzoic acid (2,3-DHBA), with neither L-DOPA nor 6-OHDOPA having an effect on 2,3-DHBA content of the neostriatum. Basal content of 2,5-DHBA, the enzymatically formed spin trap product, was 4-fold higher vs. 2,3-DHBA in the neostriatum of untreated rats, while L-DOPA and 6-OHDOPA each reduced formation of 2,5-DHBA. We conclude that DA innervation normally suppresses *OH formation, and that the antiparkinsonian drug L-DOPA has no effect (2,3-DHBA) or slightly reduces (2,5-DHBA) *OH formation in the neostriatum, probably by virtue of its bathing the system of newly formed *OH.