Going to work with COVID-19 symptoms among non-sanitary (or socio-sanitary) workers: an issue of social inequality.

OBJECIVES: To describe the characteristics of the workers of activity sectors other than sanitary and socio-sanitary, who go to work with COVID-19 symptoms (GWC19S) during the lockdown or first phase of the lockdown de-escalation in Spain. STUDY DESIGN: An observational cross-sectional study based on a convenience sample selected from the COTS online survey. METHODS: A cross-sectional study based on a sample of n = 9601 workers. Descriptive analyses were performed calculating GWC19S prevalences and fitting robust Poisson regressions to obtain crude and adjusted prevalence ratios. RESULTS: The overall GWC19S prevalence is 5.6%, greater in young people (8.7%), manual workers (8.7%), workers with low salaries (9.5%), and workers of essential sectors (7.4%). Among those workers who went to work regularly to their workplaces, the GWC19S prevalence is 10.0%, greater in young (15.1%), workers with low salaries (14.2%), and women (13.2%). CONCLUSIONS: The axes of inequality of the labor market are clearly represented in the GWC19S phenomenon.

Activated macrophages utilize glycolytic ATP to maintain mitochondrial membrane potential and prevent apoptotic cell death.

This corrects the article DOI: 10.1038/cdd.2010.27.

Intensification and isolation: psychosocial work environment changes in Spain 2005-10.

BACKGROUND: Work organization in Spain has traditionally been based on a high proportion of passive work. Changes in the labour market in Europe and the economic crisis that began in 2008 may have had an impact on the pace of work in Spain. AIMS: To estimate the prevalence of exposure to high-strain work and passive work in 2010 compared with 2005 and to analyse the distribution by gender, age and occupation of workers exposed to high strain and iso-strain in 2010 compared with 2005. METHODS: Two representative samples of the Spanish working population were compared. Unweighted and weighted prevalences in 2010 were calculated and compared with those in 2005. RESULTS: In the 2010 sample of 5110 workers, 29% (95% CI 27.8; 30.7) were exposed to high strain (of whom 83% had low social support). There was an increase of 6% (95% CI 3.8; 7.1) in high strain, and of 7% (95% CI 5.2; 8.3) to iso-strain, compared with 2005 (n = 7612). In 2010, as in 2005, the proportion of manual workers exposed to strain and iso-strain was more than double the corresponding proportion in non-manual workers. CONCLUSIONS: There has been an intensification of work, reduction in social support and a notable increase in exposure to high strain and iso-strain. The class inequalities reflect the segmentation of the Spanish labour market.

Empleo precario en España: prevalencia, distribución social y riesgo atribuible poblacional porcentual para mal estado de salud mental / Employment precariousness in Spain: prevalence, social distribution, and population-attributable risk percent of poor mental health

Como consecuencia de la flexibilización del mercado laboral se ha hecho muy extensiva la utilización de diversas modalidades de empleo atípico y ha retrocedido el empleo estándar. En muchos casos, estas transformaciones suponen una precarización de las condiciones de empleo, consideradas un determinante fundamental de la salud y de las desigualdades en salud. Utilizando la Escala de Precariedad Laboral (EPRES), el objetivo de este estudio es determinar la prevalencia de empleo precario en la población laboral asalariada en España, describir su distribución por grupos sociales según ocupación, género, edad y estatus de inmigrante, y estimarla proporción de casos con afectación de la salud mental potencialmente atribuibles a la precariedad laboral. Los datos proceden de la Encuesta de Riesgos Psicosociales realizada por el Instituto Sindical de Trabajo, Ambiente y Salud (ISTAS)en 2004-05 sobre una muestra representativa de trabajadores en España. Los resultados indican una elevada prevalencia de precariedad laboral, afectando a cerca de 6,5 millones de trabajadores, de los que casi 900,000 están expuestos a situaciones de elevada precariedad. Estas estimaciones superan el número de empleados temporales que aparecen en las estadísticas oficiales, pero pueden estar por debajo de los valores actuales dada la presente situación de crisis económica. Adicionalmente, una proporción importante de los casos con afectación de la salud mental serían potencialmente atribuibles a la precariedad en el empleo. Tanto los casos de salud mental deteriorada atribuibles a la precariedad como la prevalencia de precariedad laboral están distribuidos de forma muy desigual en la muestra, lo que sugiere que se trata de factores que contribuyen de forma importante a las desigualdades sociales en salud mental(AU)

As a consequence of labor market flexibilization, nonstandard employment has expanded and standard employment has declined. In many cases, these transformations are best described as an evolution toward precarious employment, which is considered a major determinant of health and health inequalities. Using the Employment Precariousness Scale (EPRES), this study aims to determine the prevalence of precarious employment in the waged and salaried workforce in Spain, to describe its distribution across social groups defined by occupational class, gender, age, and immigrant status, and to estimate the proportion of cases of poor mental health potentially attributable to employment precariousness. Data are from the Psychosocial Work Environment Survey conducted in 2004-5 on a representative sample of the Spanish workforce. Findings indicate a high prevalence of employment precariousness, affecting nearly6.5 million workers, with almost 900,000 of them exposed to high precariousness. These estimates are higher than the proportion of fixed-term employment reported in regular statistical sources but may today be an underestimation, given the current economic crisis. Additionally, a significant proportion of cases of poor mental health are potentially attributable to employment precariousness. Both the proportion of cases of poor mental health attributable to and the prevalence of employment precariousness were highly unequally distributed across the study sample, indicating that this may be a significant contributor to social inequalities in mental health(AU)

Nitric oxide inhibition of Drp1-mediated mitochondrial fission is critical for myogenic differentiation.

During myogenic differentiation the short mitochondria of myoblasts change into the extensively elongated network observed in myotubes. The functional relevance and the molecular mechanisms driving the formation of this mitochondrial network are unknown. We now show that mitochondrial elongation is required for myogenesis to occur and that this event depends on the cellular generation of nitric oxide (NO). Inhibition of NO synthesis in myogenic precursor cells leads to inhibition of mitochondrial elongation and of myogenic differentiation. This is due to the enhanced activity, translocation and docking of the pro-fission GTPase dynamin-related protein-1 (Drp1) to mitochondria, leading also to a latent mitochondrial dysfunction that increased sensitivity to apoptotic stimuli. These effects of NO inhibition were not observed in myogenic precursor cells containing a dominant-negative form of Drp1. Both NO-dependent repression of Drp1 action and maintenance of mitochondrial integrity and function were mediated through the soluble guanylate cyclase. These data uncover a novel level of regulation of differentiation linking mitochondrial morphology and function to myogenic differentiation.

Mitochondria as pharmacological targets.

In the last decade, mitochondria have provided a vast area of research for the pharmacologist, with a wealth of potential targets for drug action. Correct target identification and subsequent pharmacological manipulation might greatly help in the prevention and/or treatment of a number of the most prevalent diseases of our time including cancer, neurodegenerative disease and myocardial infarction. This is a commentary to accompany the publication of three papers in this issue of the BJP by Kurz et al., Pravdic et al. and Puerta et al. on different aspects of pharmacology involving mitochondria.

Activated macrophages utilize glycolytic ATP to maintain mitochondrial membrane potential and prevent apoptotic cell death.

We have previously analysed the bioenergetic consequences of activating J774.A1 macrophages (MΦ) with interferon-γ (IFN-γ) and lipopolysaccharide (LPS) and found that there is a nitric oxide (NO)-dependent mitochondrial impairment and stabilization of hypoxia-inducible factor (HIF)-1α, which synergize to activate glycolysis and generate large quantities of ATP. We now show, using tetramethylrhodamine methyl ester (TMRM) fluorescence and time-lapse confocal microscopy, that these cells maintain a high mitochondrial membrane potential (ΔΨ(m)) despite the complete inhibition of respiration. The maintenance of high ΔΨ(m) is due to the use of a significant proportion of glycolytically generated ATP as a defence mechanism against cell death. This is achieved by the reverse functioning of F(o)F(1)-ATP synthase and adenine nucleotide translocase (ANT). Treatment of activated MΦ with inhibitors of either of these enzymes, but not with inhibitors of the respiratory chain complexes I to IV, led to a collapse in ΔΨ(m) and to an immediate increase in intracellular [ATP], due to the prevention of ATP hydrolysis by the F(o)F(1)-ATP synthase. This collapse in ΔΨ(m) was followed by translocation of Bax from cytosol to the mitochondria, release of cytochrome c into the cytosol, activation of caspases 3 and 9 and subsequent apoptotic cell death. Our results indicate that during inflammatory activation 'glycolytically competent cells' such as MΦ use significant amounts of the glycolytically generated ATP to maintain ΔΨ(m) and thereby prevent apoptosis.

Poly(ADP-ribose) polymerase-1 protects neurons against apoptosis induced by oxidative stress.

In neurons, DNA is prone to free radical damage, although repair mechanisms preserve the genomic integrity. However, activation of the DNA repair system, poly(ADP-ribose) polymerase (PARP-1), is thought to cause neuronal death through NAD+ depletion and mitochondrial membrane potential (delta psi(m)) depolarization. Here, we show that abolishing PARP-1 activity in primary cortical neurons can either enhance or prevent apoptotic death, depending on the intensity of an oxidative stress. Only in severe oxidative stress does PARP-1 activation result in NAD+ and ATP depletion and neuronal death. To investigate the role of PARP-1 in an endogenous model of oxidative stress, we used an RNA interference (RNAi) strategy to specifically knock down glutamate-cysteine ligase (GCL), the rate-limiting enzyme of glutathione biosynthesis. GCL RNAi spontaneously elicited a mild type of oxidative stress that was enough to stimulate PARP-1 in a Ca2+-calmodulin kinase II-dependent manner. GCL RNAi-mediated PARP-1 activation facilitated DNA repair, although neurons underwent delta psi(m) loss followed by some apoptotic death. PARP-1 inhibition did not prevent delta psi(m) loss, but enhanced the vulnerability of neurons to apoptosis upon GCL silencing. Conversely, mild expression of PARP-1 partially prevented to GCL RNAi-dependent apoptosis. Thus, in the mild progressive damage likely occur in neurodegenerative diseases, PARP-1 activation plays a neuroprotective role that should be taken into account when considering therapeutic strategies.

Antigenic cross-reactivity between sixteen venoms from scorpions belonging to six genera.

Venoms of 15 scorpion species from Venezuela and one from Brazil were compared in their antigenic cross-reactivity with specific F(ab')2 against Tityus discrepans (Td-antibodies), using the method of King and collaborators (1). Our results show that Tityus venoms cross-reactivity (shared epitopes) with the venoms of other species within the genus tended to be less for a greater distance between the habitat of the species. A nonparametric linear regression of free Td-antibody binding to T. discrepans venom immobilized to a solid phase in the presence of other Tityus venoms versus distance showed binding = a + b x log10 (distance) where: median (95% confidence interval) for a = 0.92 (7.43, 9.80) and b = 17.20 (4.15, 22.57) binding/log10(Km); Spearman rS = 0.783 with associated P = 0.006. Our results show that toxins from different Tityus species, targeting mammalian Na+ and K+ channels, are antigenically very similar. Venoms from species from other genera such as Centruroides, Broteas, Diplocentrus, Chactas, and Rhopalurus did not cross-react with Td-antibodies.

Nitric oxide and the vascular endothelium.

The vascular endothelium synthesises the vasodilator and anti-aggregatory mediator nitric oxide (NO) from L-arginine. This action is catalysed by the action of NO synthases, of which two forms are present in the endothelium. Endothelial (e)NOS is highly regulated, constitutively active and generates NO in response to shear stress and other physiological stimuli. Inducible (i)NOS is expressed in response to immunological stimuli, is transcriptionally regulated and, once activated, generates large amounts of NO that contribute to pathological conditions. The physiological actions of NO include the regulation of vascular tone and blood pressure, prevention of platelet aggregation and inhibition of vascular smooth muscle proliferation. Many of these actions are a result of the activation by NO of the soluble guanylate cyclase and consequent generation of cyclic guanosine monophosphate (cGMP). An additional target of NO is the cytochrome c oxidase, the terminal enzyme in the electron transport chain, which is inhibited by NO in a manner that is reversible and competitive with oxygen. The consequent reduction of cytochrome c oxidase leads to the release of superoxide anion. This may be an NO-regulated cell signalling system which, under certain circumstances, may lead to the formation of the powerful oxidant species, peroxynitrite, that is associated with a variety of vascular diseases.

Adventures in vascular biology: a tale of two mediators.

I would like to thank the Royal Society for inviting me to deliver the Croonian Lecture. In so doing, the Society is adding my name to a list of very distinguished scientists who, since 1738, have preceded me in this task. This is, indeed, a great honour. For most of my research career my main interest has been the understanding of the normal functioning of the blood vessel wall and the way this is affected in pathology. During this time, our knowledge of these subjects has grown to such an extent that many people now believe that the conquering of vascular disease is a real possibility in the foreseeable future. My lecture concerns the discovery of two substances, prostacyclin and nitric oxide. I would like to describe the moments of insight and some of the critical experiments that contributed significantly to the uncovering of their roles in vascular biology. The process was often adventurous, hence the title of this lecture. It is the excitement of the adventure that I would like to convey in the text that follows.

The discovery of nitric oxide and its role in vascular biology.

Nitric oxide (NO) is a relative newcomer to pharmacology, as the paper which initiated the field was published only 25 years ago. Nevertheless its impact is such that to date more than 31,000 papers have been published with NO in the title and more than 65,000 refer to it in some way. The identification of NO with endothelium-derived relaxing factor and the discovery of its synthesis from L-arginine led to the realisation that the L-arginine: NO pathway is widespread and plays a variety of physiological roles. These include the maintenance of vascular tone, neurotransmitter function in both the central and peripheral nervous systems, and mediation of cellular defence. In addition, NO interacts with mitochondrial systems to regulate cell respiration and to augment the generation of reactive oxygen species, thus triggering mechanisms of cell survival or death. This review will focus on the role of NO in the cardiovascular system where, in addition to maintaining a vasodilator tone, it inhibits platelet aggregation and adhesion and modulates smooth muscle cell proliferation. NO has been implicated in a number of cardiovascular diseases and virtually every risk factor for these appears to be associated with a reduction in endothelial generation of NO. Reduced basal NO synthesis or action leads to vasoconstriction, elevated blood pressure and thrombus formation. By contrast, overproduction of NO leads to vasodilatation, hypotension, vascular leakage, and disruption of cell metabolism. Appropriate pharmacological or molecular biological manipulation of the generation of NO will doubtless prove beneficial in such conditions.

ISTAS21: Versión en lengua castellana del cuestionario psicosocial de Copenhague (COPSOQ) / ISTAS21: the Spanish version of the Copenhagen psychosocial questionnaire (COPSOQ)

Objetivos: Adaptar y validar las tres versiones del Cuestionario Psicosocial de Copenhague a la lengua castellana. Métodos: La adaptación se realizó por el método de traducción y retro-traducción. El estudio de la validez del constructo y de la fiabilidad y la reducción de escalas se realizó mediante encuesta a una muestra (N = 859) representativa de la población ocupada en la Comunidad Autónoma de Navarra. El análisis incluyó técnicas descriptivas uni y bivariadas, análisis factorial y de reducción de escalas, evaluación de concordancias y ajuste de modelos logísticos. Resultados: Consistencia interna de las escalas: la alfa de Chronbach osciló entre 0,65 y 0,92 para la mayoría de ellas, excepto dos que presentaron un índice inferior debido al bajo número de ítems que contenían. Concordancia entre versiones: el índice Kappa osciló entre 0,64 y 0,89. Validez de constructo: Se consiguieron reproducir las hipótesis principales de asociación entre 19 dimensiones psicosociales y las de salud y estrés. Para las dimensiones de exigencias psicológicas sensoriales e influencia se encontraron menos asociaciones de las esperadas. Algunas de las OR ajustadas por edad y sexo más relevantes fueron: exigencias emocionales y salud mental ORaj= 6,15 (IC 95%:3,85-9,84), Inseguridad y salud mental ORaj=2,28 (IC 95%=1,49- 3,48), Previsibilidad y síntomas cognitivos de estrés ORaj=3,02 (IC95%=1,81-5,04). Conclusiones: La versión castellana del COPSOQ "ISTAS21 COPSOQ" se corresponde con el original y presenta un nivel excelente validez, fiabilidad y concordancia entre versiones

Objectives: To adapt and validate the three Spanish versions of the Copenhagen Psychosocial Questionnaire. Methods: The adaptation process was based on the translation and back translation method. A representative populationbased survey of the employed population in the Autonomous Community of Navarra (N=859) was carried out in order to assess validity and reliability and to reduce scales. Analysis included univariate and bivariate descriptive techniques, factor analysis, scale reduction, and concordance analysis techniques, and logistic models were adjusted. Results: Internal consistency of the scales: Cronbach alpha values ranged from 0.65 to 0.92 for all scales except two that showed lower alpha values due to a low number of items. Concordance between versions: kappa scores ranged from 0.64 to 0.89. Construct validity: main associations between 19 psychosocial dimensions and those of health and stress were reproduced. Influence and sensorial psychological demands showed fewer associations than expected. Some of the most relevant odds ratios (OR), adjusted for sex and age were found between: emotional psychological demands and mental health [OR= 6.15 (95% CI: 3.85-9.84)], insecurity and mental health [OR=2.28 (95% CI =1.49-3.48)], predictability and cognitive stress symptoms [OR=3.02 (95% CI =1.81-5.04]. Conclusions: the Spanish version of the COPSOQ "ISTAS21 COPSOQ" is equivalent to the original English version, with excellent validity, reliability and concordance between the two versions

Synergistic action of advanced glycation end products and endogenous nitric oxide leads to neuronal apoptosis in vitro: a new insight into selective nitrergic neuropathy in diabetes.

AIMS/HYPOTHESIS: We have previously shown that in diabetes nitrergic neurones innervating the urogenital and gastrointestinal organs undergo a selective degenerative process. This comprises an initial insulin-reversible decrease in neuronal nitric oxide synthase (nNOS) in the axons, followed by apoptosis of the nitrergic neurones, a process that is not reversible by insulin. Since apoptosis was independent of serum glucose concentrations, and advanced glycation endproducts (AGEs) have been implicated in the pathogenesis of diabetic complications, we have now measured AGEs in the serum and penis, pyloric sphincter and pelvic ganglia of diabetic animals at different times after streptozotocin treatment. Furthermore, we have studied their effect in vitro on human neuroblastoma (SH-SY5Y) cells in the presence or absence of nNOS expression. METHODS: Serum AGEs were measured using fluorometry and ELISA. Accumulation of AGEs in the tissues was evaluated with immunohistochemistry. The viability, apoptosis and oxidative stress in SH-SY5Y cells were measured upon exposure to AGEs or high concentrations of glucose. RESULTS: AGEs increased gradually in the serum and tissues of streptozotocin-induced diabetic rats; this process was not affected by delayed insulin treatment. In SH-SY5Y cells, AGEs, but not high glucose concentrations, increased the reactive oxygen species and caspase-3-dependent apoptosis in a synergistic fashion with endogenous nitric oxide (NO). Apoptosis was prevented by treatment with a NOS inhibitor, a pan-caspase inhibitor, a soluble receptor of AGEs or an anti-oxidant, but not an inhibitor of soluble guanylate cyclase. CONCLUSIONS/INTERPRETATION: The synergistic actions of NO and AGEs account for the irreversible nitrergic degeneration in diabetes.

Differential effect of nitric oxide on glutathione metabolism and mitochondrial function in astrocytes and neurones: implications for neuroprotection/neurodegeneration?

Primary culture rat astrocytes exposed to the long acting nitric oxide donor (Z)-1-[2-aminoethyl)-N-(2-ammonioethyl)amino]diazen-1-ium-1,2-diolate (DETA-NO) for 24 h approximately double their concentration of glutathione (GSH) and show no sign of cell death. In contrast, GSH was depleted by 48%, and significant loss of mitochondrial respiratory chain complex activity and cell death were observed in primary culture rat neurones subjected to DETA-NO for 18 h. Northern blot analysis suggested that mRNA amounts of both subunits of glutamate-cysteine ligase (GCL), the rate-limiting enzyme in GSH synthesis, were elevated in astrocytes following nitric oxide (NO) exposure. This correlated with an increase in astrocytic GCL activity. Neurones on the other hand did not exhibit increased GCL activity when exposed to NO. In addition, the rate of GSH efflux was doubled and gamma-glutamyltranspeptidase (gamma-GT) activity was increased by 42% in astrocytes treated with NO for 24 h. These results suggest that astrocytes, but not neurones, up-regulate GSH synthesis as a defence mechanism against excess NO. It is possible that the increased rate of GSH release and activity of gamma-GT in astrocytes may have important implications for neuroprotection in vivo by optimizing the supply of GSH precursors to neurones in close proximity.

Relationship between plasmatic levels of various cytokines, tumour necrosis factor, enzymes, glucose and venom concentration following Tityus scorpion sting.

A sandwich enzyme-linked immunosorbent assay was developed for measuring Tityus venom levels in plasma. The method proved capable of distinguishing patients with only local symptoms from controls, and was used to quantify venom in 205 accidental human envenomations. Our results show that the severity of envenoming is related to the patient plasma venom concentration. This depends on time elapsed between the sting and when the plasma was drawn. We observed that 46 and 49% of patients with moderate to severe symptoms (MS, n=41) showed hyperamylasemia and hyperglycemia, respectively. In addition, 39% of cases with MS symptoms had partial thromboplastin time values prolonged or shorted and 6.5% of patients with local symptoms (LS, n=164) had only prolonged prothrombin time values. Interleukin 6 (IL6) increased significantly in patients with MS symptoms. IL6 values increased with hyperamylasemia, envenoming severity and time hyperamylasemia.

Cyclic GMP-dependent inhibition of acid sphingomyelinase by nitric oxide: an early step in protection against apoptosis.

Activation of acid and neutral sphingomyelinases, and the ensuing generation of ceramide, contributes to the biological effects of tumour necrosis factor-alpha (TNF-alpha), one of which is apoptosis. While the mechanisms of activation of sphingomyelinases by the cytokine are being unravelled, less is known about regulation of their activity. Nitric oxide has previously been shown to exert a cyclic GMP-dependent inhibition of early apoptotic events triggered by TNF-alpha in the U937 monocytic cell line. We therefore investigated whether inhibition of sphingomyelinases by nitric oxide plays a role in regulating such early events. We found that activation of both acid and neutral sphingomyelinases, triggered in the first minutes after U937 cell stimulation with TNF-alpha, is regulated in an inhibitory fashion by nitric oxide, working through generation of cyclic GMP and activation of protein kinase G. Using a range of inhibitors selective for either sphingomyelinase we found that the acid sphingomyelinase contributes to activation of the initiator caspase-8 and early DNA fragmentation and that inhibition of the acid enzyme by nitric oxide accounts for cyclic GMP-dependent early protection from apoptosis. We also found that the protective effect by both cGMP and acid sphingomyelinase inhibitors progressively disappeared at later stages of the apoptotic process. Inhibition of sphingomyelinases represents a novel action of nitric oxide, which might be of physiological relevance in regulating initial phases of apoptosis as well as other biological actions of ceramide.

Estrategias de reducción de riesgos con usuarios de drogas inyectadas: talleres de sexo más seguro / Harm reduction strategies with injecting drug users: safe sex workshops

Objetivo: El objetivo es evaluar los resultados de, y la satisfacción de los usuarios con, 25 Talleres de sexo más seguro diseñados para reducir los riesgos asociados a la conducta sexual entre la población de usuarios de drogas inyectadas (UDIs). Material y Método: La muestra incluye 387 UDIs (68.7 por ciento hombres y 31.3 por ciento mujeres) con una edad promedio de 32.4 años, asignados de forma no aleatoria a los grupos de intervención y comparación. Los sujetos fueron evaluados en pre-test, post-test y seguimiento utilizando un cuestionario autoaplicados sobre conductas sexuales de riesgo y variables mediadoras en estas conductas. Resultados: Los Talleres de sexo más seguro están asociados a un aumento en la frecuencia del uso del preservativo en las relaciones coitales, tanto con al pareja habitual como con pareja ocasional. También están asociados a un aumento en las variables mediadoras para las prácticas de seco seguro: conocimientos sobre el uso adecuado del preservativo, conocimientos sobre la transmisión del VIH/SIDA y expectativas de resultados del uso del preservativo. Adicionalmente, la satisfacción de los usuarios de estos Talleres es muy elevada. Conclusión: Estos resultados proporcionan apoyo empírico a la eficacia de este tipo de intervenciones cortas diseñadas para recudir los riesgos asociados a las prácticas sexuales entre los UDIs. Indirectamente proporcionan apoyo a la formación en redes realizada con profesionales sanitarios que trabajan en drogodependencias para fomentar las intervenciones de reducción de los riesgos entre sus pacientes UDIs (AU)

Objective: The objective is to evaluate the results and user satisfaction with 25 safer-sex workshops designed to reduce the risks associated with sexual behaviours among injecting drug users (IDUs). Method: The sample includes 387 individuals (68.7% male and 32.3% female IDUs) with an average of 32.4 years, assigned non-randomly to a comparison group or to a workshop user-group. They were assessed at pretest, postest and followup using a questionnaire that includes questions on high-risk sexual behaviours and mediating variables for these behaviours. Results: Workshops designed for safer sex practices were associated with higher frequencies of condom use with a habitual or occasional partner. Also, these interventions were related to significant improvements in mediating variables for safer sex practices: knowledge on an adequate use of a preservative, knowledge on HIV and AIDS, and outcome expectancies about using a condom. Moreover, users of these workshops reported high satisfaction levels. Conclusions: The findings provide encouraging support for the efficacy and user satisfaction of this type of short intervention, designed for risk-reduction associated with sex practices among injecting drug users. Indirectly, they provide support for training in networks, carried out by health professionals working in drug dependency to foster risk reduction interventions among their IDU patients (AU)

Cognición, actitud y conducta: cambio en UDIs hacia la reducción de los riesgos asociados al uso de drogas / Cognition, attitudes and behavior: changing towards harm reduction associated with drug use among injection drug users

Objetivo: El objetivo es evaluar 15 Talleres diseñados para la reducción de los riesgos asociados a la inyección de drogas. Material y Método: La muestra incluye 229 hombres y mujeres con una edad promedio de 34 años, policonsumidores de drogas por la vía parenteral. Los sujetos fueron evaluados en pretest, postest y seguimiento utilizando un cuestionario autoaplicado sobre conductas de riesgo asociadas a la inyección y variables mediadoras en estas conductas. Resultados: Los Talleres de Consumo de Menor Riesgo están asociados a una disminución en las conductas de riesgo y a un aumento en las conductas de protección en la inyección de drogas. También están asociados a un aumento en los conocimientos sobre la transmisión del VIH/SIDA, a una mayor autoedificada de afrontamiento ante situaciones de riesgo y a un mantenimiento de la motivación para reducir estos riesgos. Adicionalmente, la satisfacción de los usuarios de estos Talleres es muy elevada. Conclusión: Estos resultados proporcionan apoyo a la eficacia de estos Talleres de Consumo de Menor Riesgo, e indirectamente en favor del Programa de Formación en redes para profesionales sanitarios para el diseño, implementación y evaluación de los Talleres para la reducción de riesgos asociados al uso de drogas (AU)

Objective: Objective is to evaluate 15 workshops designed to improve injection practices among injecting drug users. Method: Sample includes 229 male and female injecting drug users assigned non-randomly to one comparison group or to one workshop user-group. They were assessed three times using a questionnaire including questions on injection patterns and mediating variables for risk-injecting. Results: Workshops designed for improving injection practices were associated with significant reductions in risk-injecting behaviors and a significant increase in using a new syringe. They were also associated with significant improvements in mediating variables for injection patterns: knowledge on injection-risk and AIDS, self-efficacy and motivation for risk-reduction in injecting drug use. Moreover, users of these workshops reported high satisfaction levels. Conclusions: The findings provide encouraging support for these short-interventions designed for risk-reduction among injecting drug users, and also for previous efforts in training a network of health professionals involved in risk reduction among drug users (AU)