Estado nutricional, factores sociodemográficos y de salud en estudiantes de nuevo ingreso a la UAZ / Nutritional status and social-demographical and health factors among newly enrolled students at UAZ / Estado nutricional, fatores sociodemográficos e de saúde em estudantes de novo ingresso à UAZ

Introducción El sobrepeso y obesidad son factores de riesgo para desarrollar complicaciones a corto y largo plazo. La población de nuevo ingreso a la universidad se considera un colectivo, especialmente, vulnerable desde el punto de vista nutricional. Objetivo Describir el estado nutricional, factores sociodemográficos y de salud en estudiantes de nuevo ingreso a la UAZ. Metodología Estudio de tipo observacional, transversal y descriptivo, que se realizó a 3,972 estudiantes universitarios de nuevo ingreso. Se logró el consentimiento verbal de los alumnos. Se capacitaron y estandarizaron a los pasantes de enfermería, medicina y nutrición, para llevar a cabo las mediciones. Se obtuvo información del estado nutricional, factores sociodemográficos y salud, así como mediciones antropométricas. Resultados Los hombres tienen mayor prevalencia de sobrepeso (24.1%) y obesidad (9.2%) que las mujeres (p < 0.001). Los hombres realizan mayor actividad física (73.6% vs 51.1%), consumen más alcohol (58.3% vs 34.3%) y tabaco (20.8% vs 9.5%) (p < 0.000). Se encontró una asociación positiva en los momios de sobrepeso en relación con los hombres (RM=1.22, IC 95% 1.02-1.45), edad de 19 años (RM=1.36, IC 95% 1.02-1.45), en las áreas de ciencias de la salud (RM=1.88, IC 95% 1.05-3.35), ciencias sociales (RM=1.93, IC 95% 1.06-3.48), humanidades y educativas (RM=1.90, IC 95% 1.01-3.53), ingenierías y tecnologías (RM=1.83, IC 95% 1.01-3.30). Discusión y conclusión Se puede contribuir a reducir las prevalencias de sobrepeso y obesidad de los estudiantes, a través de intervenciones dirigidas a modificar las conductas de riesgo durante la estancia universitaria, mejorar la alimentación y promover estilos de vida saludables.

Introduction Obesity and overweight are risk factors to developing short and long-term health-related complications; and newly enrolled university students are considered a vulnerable group in terms of their nutritional progression status. Objective To describe the nutritional status, and social-demographical and health factors among newly enrolled students at UAZ. Methodology This is an observational, transversal, and descriptive study on a sample of 3,972 newly enrolled university students who verbally consented on their participation. Nursing, medicine, and nutrition intern students were trained to carry out diverse assessments related to the nutritional status, social-demographical and health factors, and anthropometric data on the sample. Results Newly enrolled male students showed a higher prevalence of overweight (24.1%) and obesity (9.2%) in comparison to their female counterparts (p < .001). Male students showed having more physical activity (73.6% vs 51.1%) but also consuming more alcohol (58.3% vs 34.3%) and tobacco (20.8% vs 9.5%) (p < .000). Positive associations were found between the overweight numbers and, being male (RM=1.22, CI 95% 1.02-1.45), being 19 years old (RM = 1.36, CI 95% 1.02-1.45), being in the areas of health sciences (RM=1.88, CI 95% 1.05-3.35), being in the areas of social sciences (RM=1.93, CI 95% 1.06-3.48), being in the areas of humanities and education (RM=1.90, CI 95% 1.01-3.53), and being in the areas of engineering and technology (RM=1.83, CI 95% 1.01-3.30). Discussion and conclusion It is necessary to address to obesity and overweight problems among university students through interventions aimed at modifying risky behaviors during their university stay, improving the quality of nutrition, and promoting healthy life-styles.

Introdução O sobrepeso e a obesidade são fatores de risco para desenvolver complicações a curto e longo prazo. A população de novo ingresso à universidade considera-se um coletivo, especialmente, vulnerável desde o ponto de vista nutricional. Objetivo Descrever o estado nutricional, fatores sociodemográficos e de saúde em estudantes de novo ingresso à UAZ. Metodologia Estudo de tipo observacional, transversal e descritivo, que se realizou a 3,972 estudantes universitários de novo ingresso. Conseguiu-se o consentimento verbal dos alunos. Capacitaram-se e padronizaram os formados de enfermagem, medicina e nutrição, para levar a cabo as medições. Obteve-se informação do estado nutricional, fatores sociodemográficos e saúde, assim como medições antropométricas. Resultados Os homens de novo ingresso têm maior prevalência de sobrepeso (24.1%) e obesidade (9.2%) quanto as mulheres (p < 0.001). Homens realizam mais atividade física que mulheres (73.6% vs. 51.1%), consomem mais álcool (58.3% vs. 34.3%) e tabaco (20.8% vs. 9.5%) (p < 0.000). Encontrou-se uma associação positiva nas chances de sobrepeso em relação com aos homens (RM = 1.22, IC 95% 1.02-1.45), ter 19 anos de idade (RM = 1.36, IC 95% 1.02-1.45) nas áreas de ciências da saúde (RM = 1.88, IC 95% 1.05-3.35), ciências sociais (RM = 1.93, IC 95% 1.06-3.48), humanidades e educativas (RM = 1.90, IC 95% 1.01-3.53), engenharias e tecnologias (RM = 1.83, IC 95% 1.01-3.30). Discussão e conclusão Pode-se contribuir a reduzir as prevalências de sobrepeso e obesidade dos estudantes, a través de intervenções dirigidas a modificar as condutas de risco durante a permanência universitária, melhorar a alimentação e promover estilos de vida saudáveis.

Methylmercury reduces synaptic transmission and neuronal excitability in rat hippocampal slices.

In a previous study, we pointed out that the neurotoxic action evoked by methylmercury (MeHg), a potent environmental pollutant responsible for fatal food poisoning, is associated with alterations of cellular excitability by irreversible blockade of sodium and calcium currents. Here, we investigated the MeHg effects on synaptic transmission and neuronal plasticity using extracellular field recording in CA1 area of rat hippocampal slices. MeHg caused a fast and drastic depression of evoked field excitatory postsynaptic potentials (fEPSPs) in a concentration-dependent manner with an IC50 of 25.7 µM. This depression was partially caused by the irreversible reduction of axon recruitment deduced from the decrement of the fiber volley (FV) amplitude. Nevertheless, this MeHg-induced synaptic depression represents a true reduction of synaptic efficacy, as judged by input/output curves. In addition, a reduction on presynaptic release of glutamate was detected with the paradigm of paired-pulse facilitation during MeHg application. Moreover, MeHg also reduced population spike (PS) ampxlitude, and this effect was more prominent when the PS was evoked by ortodromic stimulation than by antidromic stimulation. Interestingly, despite these strong effects of MeHg on synaptic transmission and excitability, this compound did not modify the induction of long-term synaptic potentiation (LTP). The effects described here for MeHg were irreversible or very slowly reversible after drug wash-out. In summary, the blockade of sodium and calcium channels by MeHg affects synaptic transmission and cellular excitability but not synaptic plasticity.

Choline induces opposite changes in pyramidal neuron excitability and synaptic transmission through a nicotinic receptor-independent process in hippocampal slices.

Choline is present at cholinergic synapses as a product of acetylcholine degradation. In addition, it is considered a selective agonist for α5 and α7 nicotinic acetylcholine receptors (nAChRs). In this study, we determined how choline affects action potentials and excitatory synaptic transmission using extracellular and intracellular recording techniques in CA1 area of hippocampal slices obtained from both mice and rats. Choline caused a reversible depression of evoked field excitatory postsynaptic potentials (fEPSPs) in a concentration-dependent manner that was not affected by α7 nAChR antagonists. Moreover, this choline-induced effect was not mimicked by either selective agonists or allosteric modulators of α7 nAChRs. Additionally, this choline-mediated effect was not prevented by either selective antagonists of GABA receptors or hemicholinium, a choline uptake inhibitor. The paired pulse facilitation paradigm, which detects whether a substance affects presynaptic release of glutamate, was not modified by choline. On the other hand, choline induced a robust increase of population spike evoked by orthodromic stimulation but did not modify that evoked by antidromic stimulation. We also found that choline impaired recurrent inhibition recorded in the pyramidal cell layer through a mechanism independent of α7 nAChR activation. These choline-mediated effects on fEPSP and population spike observed in rat slices were completely reproduced in slices obtained from α7 nAChR knockout mice, which reinforces our conclusion that choline modulates synaptic transmission and neuronal excitability by a mechanism independent of nicotinic receptor activation.

Modulation of calcium channels by taurine acting via a metabotropic-like glycine receptor.

Taurine is one of the most abundant free amino acids in the central nervous system, where it displays several functions. However, its molecular targets remain unknown. It is well known that taurine can activate GABA-A and strychnine-sensitive glycine receptors, which increases a chloride conductance. In this study, we describe that acute application of taurine induces a dose-dependent inhibition of voltage-dependent calcium channels in chromaffin cells from bovine adrenal medullae. This taurine effect was not explained by the activation of either GABA-A, GABA-B or strychnine-sensitive glycine receptors. Interestingly, glycine mimicked the modulatory action exerted by taurine on calcium channels, although the acute application of glycine did not elicit any ionic current in these cells. Additionally, the modulation of calcium channels exerted by both taurine and glycine was prevented by the intracellular dialysis of GDP-ß-S. Thus, the modulation of voltage-dependent calcium channels by taurine seems to be mediated by a metabotropic-like glycinergic receptor coupled to G-protein activation in a membrane delimited pathway.

Dimorphic histopathology of long-standing childhood-onset diabetes.

AIMS/HYPOTHESIS: Childhood diabetes is thought to usually result from autoimmune beta cell destruction (type 1A) with eventual total loss of beta cells. Analysis of C-peptide in children characterised at diabetes onset for autoantibodies shows heterogeneous preservation of insulin secretion in long-standing diabetes. The aim of this study was to characterise the pancreases of childhood-onset diabetes in order to define the pathological basis of this heterogeneity. METHODS: We evaluated 20 cadaveric organ donor pancreases of childhood-onset long-term patients for disease heterogeneity and obtained corresponding C-peptide measurements. RESULTS: Pancreases from the majority of cadaveric donors contained only insulin-deficient islets (14 of 20). The remaining six patients (30%) had numerous insulin-positive cells within at least some islets, with two different histological patterns. Pattern A (which we would associate with type 1A diabetes) had lobular retention of areas with 'abnormal' beta cells producing the apoptosis inhibitor survivin and HLA class I. In pattern B, 100% of all islets contained normal-appearing but quantitatively reduced beta cells without survivin or HLA class I. CONCLUSIONS/INTERPRETATION: Our data demonstrate that C-peptide secretion in long-standing diabetic patients can be explained by two different patterns of beta cell survival,possibly reflecting different subsets of type 1 diabetes.

[Value of autopsy in a neonatal intensive care unit]. / Valor de la autopsia en una unidad de cuidados intensivos neonatológicos.

OBJECTIVES: 1) To identify the profile of the cases requested for autopsy; 2) to analyze the clinocopathological discordance; 3) to investigate predictive factors for unsuspected clinically relevant diagnoses. PATIENTS AND METHOD: All autopsies performed between January 1999 and December 2005 in a tertiary neonatal intensive care unit, were retrospectively reviewed. Clinicopathological concordance was assessed independently by two neonatologists and two pathologists, according to a modification of the Goldman classification. A comparison was made between newborns who had an autopsy performed and those who did not and predictive factors for unsuspected findings were investigated. RESULTS: During the study period, there were 309 deaths, and autopsies were performed in 128 (41.4 %) of these cases. Autopsies were more common in newborns who had gestational age > 36 weeks (p < 0.001), birthweight > 1500 g (p < 0.001) and congenital defects (p < 0.007). However, the probability that the autopsy was granted decreased with increasing death age (p < 0.016). Unsuspected diagnoses were observed in 49.2 % of the autopsies, being a major finding in 21.1 % of the cases. A clinicopathological discordance involving the prognosis was found in four cases (3.1 %). Relevant unsuspected findings could not be predicted from the ante-mortem clinical diagnosis, gestational age, birthweight, sex, and death age. CONCLUSION: The autopsy remains the "gold standard" method to reveal major and unsuspected diagnoses and there is no substitute for it. Postmortem examination should be requested systematically in every neonatal death. However, several factors such as gestational age, birthweight, presence of congenital defects and death age, influence the likelihood of autopsy being granted.

Hippocampal synaptic plasticity and water maze learning in cocaine self-administered rats.

Previously, we have shown that long-term potentiation (LTP) in hippocampus of Lewis rats was significantly modulated by cocaine self-administration. Using a single train of high-frequency stimulation of 100 Hz for 1s (HFS), we found an enhancement of LTP after cocaine self-administration that was maintained even during the extinction of this behavior. However, the effects of cocaine self-administration on a hippocampal-dependent spatial learning task were unknown. Therefore, in the present study our first objective was to analyze if cocaine self-administration might affect the performance in a hippocampus-dependent task, such as the Morris water maze test. Male adult Lewis (LEW) rats self-administered cocaine (1 mg/kg/injection) or saline (0.9% NaCl) for 3 weeks. Three hours after finishing the last self-administration session, animals were submitted to Morris water maze training for 3 consecutives days. A memory test was carried out 24 h after the last training session. No significant differences were found in escape latencies and time spent in the quadrant where the platform was located during training. Given that we did not find any cocaine effect on this spatial learning task, our second objective was to estimate indirectly if brain cocaine levels have failed to modulate LTP in animals that were performing the water maze trials. To this end, we tested if cocaine application to hippocampal slices of naïve subjects was able to evoke LTP. The results indicated that cocaine produced an enhanced LTP in these hippocampal slices. Taking together, the results of the present study suggest that hippocampal LTP-like processes generated after cocaine self-administration are not related to spatial learning hippocampal-dependent tasks, such as the water maze test.

Taurine-induced synaptic potentiation and the late phase of long-term potentiation are related mechanistically.

The application of taurine (2-aminoethanesulfonic acid) induces a long-lasting increase of synaptic efficacy and axon excitability (LLP-TAU) in rat hippocampal CA1 area. After taurine withdrawal, LLP-TAU lasted at least 3 h. This fact prompted us to assess whether the mechanisms involved in the maintenance of this particular potentiation were similar to those implicated in the late phase of long-term potentiation (L-LTP). In the presence of KN-62, an inhibitor of calcium/calmodulin-dependent protein kinase, taurine perfusion (10 mM, 30 min) did not affect the induction of LLP-TAU. However, LLP-TAU maintenance was completely suppressed by KT5720, an inhibitor of the cAMP-dependent protein kinase (PKA). Moreover, the late phase of LLP-TAU was blocked by inhibiting protein synthesis with anisomycin. In addition, taurine perfusion increased the phosphorylation of cAMP response element-binding protein (CREB), although did not affect cAMP levels. These features of LLP-TAU do not appear to be caused by the activation of D1/D5 dopamine receptors, as taurine also induced synaptic potentiation in the presence of SCH23390, an antagonist of this type of receptors. Finally, the late phase of both L-LTP and LLP-TAU occluded mutually. These results suggest that taurine triggers the sequence of some of the molecular events involved in the induction of L-LTP.

Mecanismos de acción del topiramato y su importanciaen el tratamiento del dolor / Mechanisms of action of topiramate and their relevance for the ma nagement of pain

Los fármacos con actividad anticonvulsivante vienen siendo usados desde hace tiempo para el tratamiento del dolor. El topiramato, un nuevo anticonvulsivante, presenta múltiples mecanismos de acción que pueden intervenir en el control de la hiperexcitabilidad neuronal: disminuye la actividad de los canales de sodio y calcio dependientes del voltaje, hiperpolariza la membrana por la apertura de canales de potasio, reduce las corrientes generadas por la activación de los receptores para glutamato del tipo AMPA y kainato, aumenta el flujo de cloruro a través de los canales para este ión en el receptor GABAA, e inhibe la anhidrasa carbónica. Esta plétora de mecanismos de acción puede ser relevante para explicar el efecto beneficioso que tiene el topiramato en varios tipos de síndromes dolorosos como cefaleas, neuralgias y dolor neuropático (AU)

An osmotic-sensitive taurine pool is localized in rat pancreatic islet cells containing glucagon and somatostatin.

Previous reports have dealt with the hypoglycemic properties of taurine and its effects on insulin secretion by adult and fetal isolated islets. We have studied the presence and cellular distribution of taurine in rat islets, the conditions to evoke its release, and its possible modulatory action on insulin secretion. We localized taurine by techniques of double immunolabeling in most glucagon-positive cells and in some somatostatin-positive cells, whereas insulin-positive cells were not labeled with the taurine antibody. Although high-glucose stimulation did not evoke any taurine release, a hyposmotic solution (17% osmolarity reduction) induced a specific phasic release of taurine and GABA (34 and 52% increase on their basal release rate). On the other hand, taurine (10 mmol/l) application slightly reduced the second phase of insulin secretion induced by glucose stimulation. In conclusion, taurine is highly concentrated in glucagon-containing cells of the islet periphery. It is not liberated by glucose stimulation but is strongly released under hyposmotic conditions. All of these data suggest that taurine plays an osmoregulatory role in alpha-cells.

Taurine activates GABA(A) but not GABA(B) receptors in rat hippocampal CA1 area.

We investigated if taurine, an endogenous GABA analog, could mimic both hyperpolarizing and depolarizing GABA(A)-mediated responses as well as pre- and postsynaptic GABA(B)-mediated actions in the CA1 region of rat hippocampal slices. Taurine (10 mM) perfusion induced changes in membrane potential and input resistance that are compatible with GABA(A) receptor activation. Local pressure application of taurine and GABA from a double barrel pipette positioned along the dendritic shaft of pyramidal cells revealed that taurine evoked a very small change of membrane potential and resistance compared with the large changes induced by GABA in these parameters. Moreover, in the presence of GABA(A) antagonists, local application of GABA on the dendrites evoked a GABA(B)-mediated hyperpolarization while taurine did not induce any change. Taurine neither mimicked baclofen inhibitory actions on presynaptic release of glutamate and GABA as judging by the lack of taurine effect on paired-pulse facilitation ratio and slow inhibitory postsynaptic potentials, respectively. These results show that taurine mainly activates GABA(A) receptors located on the cell body, indicating therefore that if taurine has any action on the dendrites it will not be mediated by either GABA(A) or GABA(B) receptors activation.

Taurine-induced synaptic potentiation: role of calcium and interaction with LTP.

Taurine induces a long-lasting potentiation of excitatory synaptic potentials due to the enhancement of both synaptic efficacy and axon excitability in the CA1 area of rat hippocampal slices. In this study, we characterized the role of Ca2+ in the generation of these long-lasting taurine effects. Taurine perfusion in a free-Ca2+ medium did not induce changes in either field excitatory synaptic potentials (fEPSP) slope or fiber volley (FV) amplitude. Intracellular recordings with a micropipette filled with the Ca2+ chelator BAPTA, prevented the EPSP potentiation induced by taurine in the impaled cell, whereas a long-lasting potentiation of the simultaneously recorded fEPSP was obtained. The depletion of intracellular Ca2+ stores by thapsigargin (1 microM), an inhibitor of endosomal Ca2+-ATPase, transformed the taurine-induced potentiation into a transitory process that declined to basal values after taurine withdrawal. Taurine-induced potentiation was not significantly affected by kynurenate (glutamate receptor antagonist), or nifedipine (high-voltage-activated Ca2+ channel antagonist). But, the presence of nickel (50 microM), an antagonist of low-voltage-activated Ca2+ channel, inhibited the taurine-induced potentiation, indicating that Ca2+ influx through this type of Ca2+ channels could account for the Ca2+ requirement of the taurine-induced potentiation. Occlusion experiments between tetanus-induced long-term potentiation (LTP) and taurine-induced potentiation indicate that both processes share some common mechanisms during the maintenance period.

Study of the parameters affecting the binding of metals in solution by Chlorella vulgaris.

The ability of Chlorella vulgaris to accumulate heavy metals in solution (Mn, Cr, Ni, Zn and Cu) was investigated. Various parameters (algal biomass, pH and contact time of the algae with the sample) have been studied. Nine mg of algal biomass, pH 8 and 15 min of contact time, with 1 ppm of each metal, were the optimized conditions. At pH 8, the optimum value to rise the maximum binding, a fraction of metals in solution precipitates forming hydroxides. Combining both processes, a chemical-biological system for the removing of metals at ppb levels from the environment is obtained. The simultaneous determination of these five metals was performed by capillary electrophoresis (CE) with a UV/Vis detector.