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In Chile, sex work takes place covertly in a variety of venues and locations. Formative research using time-location sampling methods is important in order to understand the nature of this diversity. This study used qualitative methods to develop a typology of female sex work in the Metropolitan Region of Santiago, Chile, using semi-structured interviews, focus groups and ethnographic fieldwork during visits to sex work venues. The study identified seven types of venue, which reflect the context and regulatory framework of the country and the structural vulnerabilities that affect female sex workers in Chile. These venues and locations include: cafés con piernas (coffee with legs); nightclubs, topless bars and cabarets; brothels; hotels; street and highway soliciting; massage parlours; and private residences. Formative research methods were helpful in identifying and characterising the venues and locations in which sex work occurred. Barriers to accessing and mapping specific locations were also identified. Recommendations for addressing these barriers include working with non-governmental organisations to map venues and initiate contact with the populations of interest. A comprehensive typology of sex work in the Metropolitan Region of Santiago, Chile, is an essential element for future time-location sampling and bio-behavioural research in the context of second-generation surveillance for HIV and sexually transmitted infections in Chile.

Depressed immune response is well documented in protein-calorie malnutrition (PCM). Also, central and peripheral noradrenaline (NA) activities have been reported to be increased in malnourished animals. Since increases in central and peripheral NA may inhibit immune function, it is possible that malnutrition-induced immunodepression could be mediated by noradrenergic hyperactivity. To address this hypothesis the effect of malnutrition on cell-mediated immune response, as well as on NA levels of the median eminence, spleen and thymus was studied in PCM rats. Decreased lymphoproliferative response and IL-1 production by mononuclear macrophages was observed in PCM. Besides, increased NA concentration was detected in thymuses of PCM rats, while unchanged levels of this neurotransmitter were observed in median eminence and spleen. These data suggest a positive correlation between malnutrition-induced immunodepression and sympathetic noradrenergic activity in thymus, an organ implicated in immune cell differentiation during early development.

It has been shown that prenatal malnutrition results at birth in increased concentration of noradrenaline (NA) in the brain. Besides, it is known that NA is an important regulator of normal regressive processes occurring during synaptogenesis such as cell death, axonal pruning and synaptic elimination. The present study was designed to investigate (i) whether prenatal malnutrition enhances the NA release in the visual cortex and (ii) whether or not chronic administration of clonidine during gestation may prevent long-term deleterious effects of fetal malnutrition on functional properties of interhemispheric connections of the visual cortex and on the interhemispheric asymmetry of visual evoked responses. Prenatal malnutrition was induced by restricting food consumption to pregnant rats from Day 8 postconception to parturition. Results show that at birth, prenatally malnourished rats had higher NA release than normals. At 45-50 days of age, the malnourished group exhibited (a) reduced peak-to-peak amplitude and diminished extent of the projecting field of transcallosal evoked responses, and (b) abolished interhemispheric asymmetry of visual evoked responses. Clonidine administration to malnourished mothers from Day 14 postconception to parturition (10 g/kg/day s.c.), prevented in the offspring disorders induced by prenatal malnutrition on cortical NA release, on interhemispheric connectivity of visual areas and on interhemispheric bioelectrical asymmetry, probably by restoring the normal trophic role of NA during synaptogenesis. Results are discussed in relationship to normal regressive events occurring during early brain development.

A great body of evidence indicates that malnutrition early in life induces central noradrenergic hyperactivity (CNH). On the other hand, it is known that noradrenaline (NA) is an important regulator of the regressive processes occurring during synaptogenesis such as cell death, axonal pruning and synaptic elimination. This leads to the hypothesis that some of the morphofunctional modifications induced by malnutrition on the brain could be due, at least in part, to an increase of NA activity during the period of accelerated brain growth. This study evaluates whether early reduction of CNH by the alpha-2 presynaptic adrenoreceptor agonist clonidine, prevents long-term morphofunctional deficits induced by protein-energy malnutrition in the rat. Results of experiments performed on 45 day-old malnourished animals that received clonidine during the suckling period, show that the pharmacological treatment prevented: (i) deficits in both NA levels and NA release in the visual cortex; (ii) deficit in brain weight but not in body weight; and (iii) reduction of the normal brain interhemispheric asymmetry of visual cortical evoked potentials. It is suggested that administration of clonidine early in life prevents brain morphofunctional deficits by malnutrition, by restoring the normal tropic role of NA during synaptogenesis.

The influence of early protein-energy malnutrition on the induced release of noradrenaline in the rat prefrontal cortex was studied: (i) by evaluating in vivo the release of the neurotransmitter as revealed by changes in the ability of pyramidal cells to integrate transient transmembrane currents generated by discrete packets of noradrenaline released by repetitive electrical stimulation of the locus coeruleus; and (ii) by measuring in vitro the potassium-induced release of 3H-noradrenaline in slices obtained from the brain frontal pole. Both electrophysiological and neurochemical data show that, in malnourished rats, weak stimulation produces an increased release, whereas strong stimulation results in a decreased release of the neurotransmitter. The results provide direct evidence that malnutrition alters the release of noradrenaline at the cortical level. Since the prefrontal cortex is involved in cognitive processing, the present results could provide functional evidence linking nutritional and behavioral deficits.