Abnormal eating attitudes in Mexican female students: a study of prevalence and sociodemographic-clinical associated factors.

The objective of the study was to determine the prevalence of abnormal eating attitudes (AEA) in Mexican high school and university students in the city of San Luis Potosí, Mexico. By means of a transversal study with a weighted, random and multistage sampling process, we analyzed a representative sample of female students (N= 2006). The instrument was the Eating Disorder Inventory-2 (EDI-2), validated in Mexican population and a questionnaire of sociodemographic data. The prevalence of AEA was 12.6% and its frequency was significantly higher in high school than in university students. AEA cases were uniformly distributed among public and private institutions and a highly significant relationship between substances consumption and AEA was observed. A logistic regression model for AEA was obtained. Therefore, a profile of highly AEA was built based on sociodemographic data and a solid instrument validated in Mexican population, which can be employed as a screening and secondary prevention tool to design public health programs.

Decreased nitric oxide markers and morphological changes in the brain of arsenic-exposed rats.

Epidemiological studies demonstrate an association between chronic consumption of arsenic contaminated water and cognitive deficits, especially when the exposure takes place during childhood. This study documents structural changes and nitrergic deficits in the striatum of adult female Wistar rats exposed to arsenic in drinking water (3 ppm, approximately 0.4 mg/kg per day) from gestation, throughout lactation and development until the age of 4 months. Kainic acid injected animals (10mg/kg, i.p.) were also analyzed as positive controls of neural cell damage. Morphological characteristics of cells, fiber tracts and axons were analyzed by means of light microscopy as well as immunoreactivity to neuronal nitric oxide synthase (nNOS). As nitrergic markers, nitrite/nitrate concentrations, nNOS levels and expression of nNOS-mRNA were quantified in striatal tissue. Reactive oxygen species (ROS) and lipid peroxidation (LPx) were determined as oxidative stress markers. Arsenic exposure resulted in moderate to severe alterations of thickness, organization, surrounding space and shape of fiber tracts and axons, while cell bodies remained healthy. These anomalies were not accompanied by ROS and/or LPx increases. By contrast, except the expression of nNOS-mRNA, all nitrergic markers including striatal nNOS immunoreactivity presented a significant decrease. These results indicate that arsenic targets the central nitrergic system and disturbs brain structural organization at low exposure levels.

The effects of arsenic exposure on the nervous system.

Arsenic (As) is a common environmental contaminant widely distributed around the world. Human exposure to this metalloid comes from well water and contaminated soil, from fish and other sea organisms rich in methylated arsenic species, and from occupational exposure. It has been reported that human arsenic exposure causes several health problems such as cancer, liver damage, dermatosis, and nervous system disturbances such as polyneuropathy, EEG abnormalities and, in extreme cases, hallucinations, disorientation and agitation. Although there is evidence that arsenic exposure has a toxic effect on the nervous system there are few studies that address this issue. The purpose of this review is to describe what is presently known about the effects of arsenic compounds on the nervous system in humans and rodents and to discuss its possible mechanisms of action.

Methylmercury increases glutamate extracellular levels in frontal cortex of awake rats.

A current hypothesis about methylmercury (MeHg) neurotoxicity proposes that neuronal damage is due to excitotoxicity following glutamate uptake alterations in the astrocyte. By sampling from a microdialysis probe implanted in the frontal cortex of adult Wistar rats, we measured the effects of acute exposure to either 10 or 100 microM MeHg through the microdialysis probe, on glutamate extracellular levels in 15 awake animals. After baseline measurements, the perfusion of MeHg during 90 min induced immediate and significant elevations in extracellular glutamate at 10 microM (9.8-fold, P<.001) and at 100 microM (2.4-fold, P=.001). This in vivo demonstration of increments of extracellular glutamate supports the hypothesis that dysfunction of glutamate neurotransmission plays a key role in MeHg-induced neural damage.

Behavioral effects of exposure to endosulfan and methyl parathion in adult rats.

Endosulfan (ES) and methyl parathion (MP) are widely used in Latin America, and simultaneous exposure to both products is documented. This exposure may have effects on the nervous system because their targets include the GABAergic and cholinergic systems, which are main modulators of neuronal excitability in the cortex and hippocampus. We tested whether low-level, repeated exposure of adult rats to commercial formulations containing ES and MP disrupts spatial learning in the water maze. Five groups of eight animals received subcutaneously appropriate dilutions of the commercial formulations to yield the following treatments during 10 days: saline, 25 mg/kg ES, 2 mg/kg MP (MP(2)), 25 mg/kg ES plus 1 mg/kg MP (ES+MP(1)) and 25 mg/kg ES plus 2 mg/kg MP (ES+MP(2)). In addition, markers of neurological function, renal and hepatic damage were explored as potential consequences of exposure. In the absence of overt toxicity, the groups exposed to the ES plus MP showed significantly longer escape latencies, higher number of failures to reach the platform and more time in the periphery of the tank than the control and single-exposed groups. This finding shows that commercial formulations of ES and MP have marginal effects when administered individually but can produce behavioral alterations when given in combination.

In vivo hydroxyl radical formation after quinolinic acid infusion into rat corpus striatum.

We studied the effect of an acute infusion of quinolinic acid (QUIN) on in vivo hydroxyl radical (.OH) formation in the striatum of awake rats. Using the microdialysis technique, the generation of.OH was assessed through electrochemical detection of the salicylate hydroxylation product 2,3-dihydroxybenzoic acid (2,3-DHBA). The .OH extracellular levels increased up to 30 times over basal levels after QUIN infusion (240 nmol/microl), returning to the baseline 2 h later. This response was attenuated, but not abolished, by pretreatment with the NMDA receptor antagonist MK-801 (10 mg/kg, i.p.) 60 min before QUIN infusion. The mitochondrial toxin 3-nitropropionic acid (3-NPA, 500 nmol/microl) had stronger effects than QUIN on .OH generation, as well as on other markers of oxidative stress explored as potential consequences of .OH increased levels. These results support the hypothesis that early .OH generation contributes to the pattern of toxicity elicited by QUIN. The partial protection by MK-801 suggests that QUIN neurotoxicity is not completely explained through NMDA receptor overactivation, but it may also involve intrinsic QUIN oxidative properties.

Exposure to arsenic and lead and neuropsychological development in Mexican children.

This cross-sectional study examined the effects of chronic exposure to lead (Pb), arsenic (AS) and undernutrition on the neuropsychological development of children. Two populations chronically exposed to either high (41 children) or low (39 children) levels of As and Pb were analyzed using the Wechsler Intelligence Scale for Children, Revised Version, for México (WISC-RM). Geometric means of urinary arsenic (AsU) and lead in blood (PbB) were 62.9+/-0.03 (microgAs/g creatinine) and 8.9+/-0.03 (microg/dl) for the exposed group and 40.2+/-0.03 (microgAs/g creatinine) and 9.7+/-0.02 (microg/dl) for the reference group. The height for age index (HAI) was used as an indicator of chronic malnutrition and sociodemographic information was obtained with a questionnaire. Lead and arsenic were measured by atomic absorption spectrophotometry. Data on full, verbal, and performance intelligence quotients (IQ) scores, long-term memory, linguistic abstraction, attention span, and visuospatial organization were obtained through the WISC-RM. After controlling for significant potential confounders verbal IQ (P<0.01) decreased with increasing concentrations of AsU. The HAI correlated positively with full-scale and performance IQ (P<0.01). Higher levels of AsU were significantly related to poorer performance on WISC-RM factors examining long-term memory and linguistic abstraction, while lower scores in WISC-RM factors measuring attention were obtained at increasing values of PbB. Our results suggest that exposure to As and chronic malnutrition could have an influence on verbal abilities and long-term memory, while Pb exposure could affect the attention process even at low levels.

Effects of arsenite on central monoamines and plasmatic levels of adrenocorticotropic hormone (ACTH) in mice.

We studied the effects of chronic arsenic exposure on brain monoamines and plasma levels of adrenocorticotropic hormone (ACTH) of mice. After weaning, mice received arsenic (0, 20, 40, 60 or 100 ppm) in drinking water over a period of 9 weeks. Monoamine content was quantified in different brain regions, arsenic was quantified in brain tissue and ACTH levels in plasma. Brain arsenic concentrations up to 200 ng/g showed a significant correlation with exposure levels and produced slight modifications in regional monoamine levels. ACTH plasma levels were significantly associated with norepinephrine (NE) concentrations in the medulla and pons, but not with hypothalamic NE levels. ACTH levels were significantly higher in the group exposed to 20 ppm. Dopamine showed significant dose-related decreases in the hypothalamus. These results show that chronic sodium arsenite exposure produces changes in central monoamines, which are not associated on a dose-dependent basis with major alterations in plasma ACTH.

[A method for assessing health risks in mining sites]. / Un método para la evaluación de riesgos para la salud en zonas mineras.

OBJECTIVE: Considering the health risk associated with mining areas, in this work a methodology for the health assessment of this kind of hazardous sites is proposed. MATERIAL AND METHODS: The methodology includes a toxicological assessment, an environmental monitoring of metals, and the exposure assessment of the high risk population. The scheme was evaluated in the mining area of Villa de la Paz, San Luis Potosi, Mexico. The toxicological studies were done in rats treated with mining waste, biomarkers of effect for liver and central nervous tissue were analyzed. Metals levels in surface soil, household dust and water were studied. Finally, urinary arsenic was quantified in children. RESULTS: Neurotoxicity and hepatotoxicity of the mining waste were shown in rats. Then, arsenic and lead levels were analyzed in surface soil, household dust, and water. In all three media, exposure points, heavily contaminated with both metals, were localized. Finally, high levels of urinary arsenic were found in children living in the vicinity of the mine. CONCLUSIONS: Taking into account all these results, the Mexican authorities concluded that a high health risk is present in Villa de la Paz, and a remediation program is in progress.

Effects of oral exposure to mining waste on in vivo dopamine release from rat striatum.

Several single components of mining waste (arsenic, manganese, lead, cadmium) to which humans are exposed at the mining area of Villa de la Paz, Mexico, are known to provoke alterations of striatal dopaminergic parameters. In this study we used an animal model to examine neurochemical changes resulting from exposure to a metal mixture. We used microdialysis to compare in vivo dopamine release from adult rats subchronically exposed to a mining waste by oral route with those from a control group and from a sodium arsenite group (25 mg/kg/day). We found that arsenic and manganese do accumulate in rat brain after 2 weeks of oral exposure. The mining waste group showed significantly decreased basal levels of dihydroxyphenylacetic acid (DOPAC; 66.7 +/- 7.53 pg/ microl) when compared to a control group (113.7 +/- 14.3 pg/ microl). Although basal dopamine release rates were comparable among groups, when the system was challenged with a long-standing depolarization through high-potassium perfusion, animals exposed to mining waste were not able to sustain an increased dopamine release in response to depolarization (mining waste group 5.5 +/- 0.5 pg/ microl versus control group 21.7 +/- 5.8 pg/ microl). Also, DOPAC and homovanillic acid levels were significantly lower in exposed animals than in controls during stimulation with high potassium. The arsenite group showed a similar tendency to that from the mining waste group. In vivo microdialysis provides relevant data about the effects of a chemical mixture. Our results indicate that this mining waste may represent a health risk for the exposed population.

Changes in extracellular levels of dopamine metabolites in somatosensory cortex after peripheral denervation.

This study examined the effects of a nerve transection on monoamine release from primary somatosensory cortex. The technique of microdialysis was employed to sample extracellular levels of norepinephrine (NE), 3,4-dihydroxyphenylacetic acid (DOPAC), 5-hydroxyindole-3-acetic acid (5-HIAA) and homovanillic acid (HVA) in the barrel field of freely moving rats following the surgical transection of the contralateral infraorbital nerve. Microdialysates obtained 3, 4, and 5 days after deafferentation were analyzed using high-performance liquid chromatography with electrochemical detection. We found a significant increase in the release of the dopamine metabolites, DOPAC and HVA from the deafferented cortex. Three days after deafferentation the release of DOPAC was three-fold higher in the deafferented than in the control animals, and remained about 100% higher in the next two days in this group of animals. The release of HVA showed a gradual increase following the deafferentation procedure, since a 92% larger value on day 3 increased to a 338% difference on day 5. On the other hand, the release rate of NE and the levels of the serotonin metabolite 5-HIAA were not significantly affected by the deafferentation procedure. These results are discussed in the context of the possible participation of dopamine in the reorganization of the deafferented somatosensory cortex.

Heparina con vancomicina en la prevención de bacteremias asociadas a cateter venoso permanente en pacientes oncológicos: resultados preliminares de un estudio randomizado de doble ciego / Heparin plus vancomycin in prophylaxis of catheter associated bacteremias in oncological patients: preliminar results of a double blind, randomized study

Objetivos: probar si la adición de vancomicina en microdosis (25 mcg/ml) a la solución de heparinización de catéteres venosos centrales permanentes (CVP) previene la ocurrencia de bacteremias por gérmenes vancomicina sensibles en pacientes oncológicos. Métodos: 39 pacientes con patología oncológica portadores de CVP externo (Hickman-Broviac) participaron en un estudio prospectivo, randomizado de doble ciego y fueron asignados a recibir una solución de heparina sola (Hep) o de heparina-vancomicina (HepVan). Todos los episodios febriles fueron registrados, realizándose hemograma y hemocultivo central y periférico. Los episodios febriles fueron tratados con antibióticos según normas establecidas. Resultados: se observaron en 14 meses 6.519 días catéter. Hubo 70 episodios febriles y 16 episodios de bacteremia, de los cuales 9 fueron por gérmenes sensibles a la vancomicina, 6 en el grupo Hep y 3 en el grupo HepVan (p = 0,31). En los episodios no neutropénicos (recuento absoluto de neutrófilos > 500/cm3) hubo 4 bacteremias en el grupo Hep y 0 en el grupo HepVan (p = 0,057). Conclusiones: la adición de vancomicina a la solución de heparinización de CVP no previene bacteremia asociada a CVP. La menor incidencia de bacteremias por gérmenes sensibles a la vancomicina en pacientes no neutropénicos versus neutropénicos en el grupo HepVan apoya la hipótesis de que la colonización intraluminal del CVP es un factor importante en las bacteremias en pacientes no neutropénicos

[Infective complications of the use of permanent central venous catheters in oncology]. / Complicaciones infecciosas del uso de catéteres venosos centrales permanentes en oncología.

We analyzed the infectious complications associated with the use of permanent central venous catheters (PVC) in pediatric and adult cancer patients. 62 patients used 74 PVC (54 external, 20 subcutaneous), which were in place for an average of 200 days with a total observation period of 14,876 days, 152 febrile episodes occurred during this period, 87 in neutropenic patients (less than 500 neutrophils/mu, FN+) and 65 in non neutropenic patients (FN-). The incidence of bacteremia was 32% in febrile episodes in the first group (FN+C+ and 41% in the second (FN-C+). Overall there were 3.7 episodes of bacteremia per 1000 catheter days. We found a statistically significant difference in the incidence of bacteremia between the external and subcutaneous PVC in favor of the latter among patients over 15 years of age but not in the pediatric group. 14 PVC had to be removed due to an infection, 8 in patients with bacteremia and 6 in patients with exit site infections. We conclude that the use of PVC in the care of cancer patients is beneficial and safe, with a low incidence of infectious complications.

Respuesta cutánea de lactantes a 2 y 10 unidades de tuberculina / Cutaneous response to 2 and 10 units of tuberculin in infants

Se estudiaron 322 lactantes sanos, eutróficos, entre 3 y 18 meses de edad, que habían sido inmunizados con BCG en el período neonatal y procedían de salas-cunas de la Región Metropolitana. Entre ellos, 304 (92,4%) tenían cicatriz BCG y fueron ingresados a un estudio doble ciego aleatorio, para determinar eventuales variaciones en las respuestas cutáneas a PPD 2 UT y 10 UT. No se encontraron diferencias en el tamaño de las respuestas cutáneas ni el porcentaje de respuestas positivas (* 10 mm), excepto para las reacciones * 15 mm, que fueron más frecuentes en los niños inoculados con PPD 10 UT. En 184/304 (60,5%) se obtuvo respuesta cutánea negativa (* 10 mm). Los 18/322 (5,6%) que no tenían cicatriz BCG fueron inoculados con PPD 2 UT: ninguno mostró respuesta cutánea positiva y en 3/18 ésta fue de 6 a 9 mm. Al administrar una segunda dosis de PPD a 55 lactantes cuya respuesta inicial había sido * 5 mm, se obtuvieron reacciones de mayor tamaño que en la primera en los niños que tenían cicatriz BCG cuando la segunda dosis era igual o mayor potencia que la primera, sugiriendo un mecanismo de refuerzo