Ozone pollution, oxidative stress, synaptic plasticity, and neurodegeneration.

INTRODUCTION: Overpopulation and industrial growth result in an increase in air pollution, mainly due to suspended particulate matter and the formation of ozone. Repeated exposure to low doses of ozone, such as on a day with high air pollution levels, results in a state of chronic oxidative stress, causing the loss of dendritic spines, alterations in cerebral plasticity and in learning and memory mechanisms, and neuronal death and a loss of brain repair capacity. This has a direct impact on human health, increasing the incidence of chronic and degenerative diseases. DEVELOPMENT: We performed a search of the PubMed, Scopus, and Google Scholar databases for original articles and reviews published between 2000 and 2018 and addressing the main consequences of ozone exposure on synaptic plasticity, information processing in cognitive processes, and the alterations that may lead to the development of neurodegenerative diseases. CONCLUSIONS: This review describes one of the pathophysiological mechanisms of the effect of repeated exposure to low doses of ozone, which causes loss of synaptic plasticity by producing a state of chronic oxidative stress. This brain function is key to both information processing and the generation of structural changes in neuronal populations. We also address the effect of chronic ozone exposure on brain tissue and the close relationship between ozone pollution and the appearance and progression of neurodegenerative diseases.

Empleo de la presión positiva continua en la vía aerea en la sedación de la ecobroncoscopia / Use of continuous positive airway pressure in sedation for endobronchial ultrasound-guided transbronchial needle aspiration

Objetivo. Analizar el beneficio del sistema de presión positiva continua en la vía aérea frente a la oxigenoterapia, en sujetos sedados durante ecobroncoscopia. El objetivo primario fue analizar el porcentaje de episodios de desaturación. Objetivos secundarios: duración de sedación, dosis de sedante empleado, grado de sedación, tiempo en despertar, presencia de complicaciones y evolución de parámetros hemodinámicos y respiratorios. Material y método. Estudio observacional retrospectivo (mayo 2016-noviembre 2017) realizado en hospital de tercer nivel sobre una cohorte de 120 pacientes sometidos a ecobroncoscopia para estudio de patología pulmonar, y que precisaron sedación (escala Ramsay), con propofol y fentanilo. No se establecieron criterios de exclusión. Resultados. Globalmente, la duración del procedimiento fue de 50 (40-60) minutos, obteniendo un nivel de sedación moderada-profunda (Ramsay V en 43%, Ramsay VI en 53%). La tasa de complicaciones no fue elevada, destacando los episodios de desaturación en un 25%, con predominio del grupo de oxigenoterapia [11 (50%) vs 19 (19%) en grupo presión positiva continua en la vía aérea, p = 0,005]. En el grupo de presión positiva continua en la vía aérea se observó un mejor nivel de oxigenación frente al grupo de oxigenoterapia. En ambos grupos se apreció un descenso significativo de la tensión arterial en relación a la situación basal. Un sujeto del grupo de presión positiva continua en la vía aérea presentó parada respiratoria no grave. Conclusión. La utilización de presión positiva continua en la vía aérea en la sedación moderada-profunda de la ecobroncoscopia es segura, pudiendo ser recomendada en dicho procedimiento

Endobronchial ultrasound-guided transbronchial needle aspiration (EBUS-TBNA). The primary objective was to analyse the percentage of episodes of oxygen desaturation. Secondary objectives: duration of sedation, dose of sedative used, depth of sedation, time to wake up, presence of complications and evolution of hemodynamic and respiratory parameters. Material and method. A retrospective observational study (May 2016 to November 2017) was carried out in a tertiary hospital. A cohort of 120 subjects undergoing EBUS-TBNA, who were sedated (Ramsay scale) with propofol and fentanyl. No exclusion criteria were established. Results. Overall, the duration of the procedure was 50 (40-60) minutes, obtaining a level of moderate-deep sedation (Ramsay V in 43%, Ramsay VI in 54%). The complication rate was not high, with a percentage of oxygen desaturation in 25% of subjects, mainly in the oxygen therapy group [11 (50%) vs 19 (19%) in the continuous positive airway pressure group, p= 0.005]. During the procedure, the oxygen levels were better in the continuous positive airway pressure group compared to the oxygen therapy group. In both groups there was a significant decrease in blood pressure compared to baseline. One subject in continuous positive airway pressure group suffered from non-severe respiratory arrest. Conclusion. The use of a continuous positive airway pressure in moderate-deep sedation of subjects undergoing EBUS-TBNA is safe, and it could be recommended to patients undergoing this procedure

Ozone pollution, oxidative stress, synaptic plasticity, and neurodegeneration. / Contaminación por ozono, estrés oxidativo, plasticidad sináptica y neurodegeneración.

INTRODUCTION: Overpopulation and industrial growth result in an increase in air pollution, mainly due to suspended particulate matter and the formation of ozone. Repeated exposure to low doses of ozone, such as on a day with high air pollution levels, results in a state of chronic oxidative stress, causing the loss of dendritic spines, alterations in cerebral plasticity and in learning and memory mechanisms, and neuronal death and a loss of brain repair capacity. This has a direct impact on human health, increasing the incidence of chronic and degenerative diseases. DEVELOPMENT: We performed a search of the PubMed, Scopus, and Google Scholar databases for original articles and reviews published between 2000 and 2018 and addressing the main consequences of ozone exposure on synaptic plasticity, information processing in cognitive processes, and the alterations that may lead to the development of neurodegenerative diseases. CONCLUSIONS: This review describes one of the pathophysiological mechanisms of the effect of repeated exposure to low doses of ozone, which causes loss of synaptic plasticity by producing a state of chronic oxidative stress. This brain function is key to both information processing and the generation of structural changes in neuronal populations. We also address the effect of chronic ozone exposure on brain tissue and the close relationship between ozone pollution and the appearance and progression of neurodegenerative diseases.

Frequency shift in topography of spontaneous brain rhythms from childhood to adulthood.

It has been described that the frequency ranges at which theta, mu and alpha rhythms oscillate is increasing with age. The present report, by analyzing the spontaneous EEG, tries to demonstrate whether there is an increase with age in the frequency at which the cortical structures oscillate. A topographical approach was followed. The spontaneous EEG of one hundredand seventy subjects was recorded. The spectral power (from 0.5 to 45.5 Hz) was obtained by means of the Fast Fourier Transform. Correlations of spatial topographies among the different age groups showed that older groups presented the same topographical maps as younger groups, but oscillating at higher frequencies. The results suggest that the same brain areas oscillate at lower frequencies in children than in older groups, for a broad frequency range. This shift to a higher frequency with age would be a trend in spontaneous brain rhythm development.

Análisis retrospectivo sobre la extubación en pacientes con patología neurológica aguda / Retrospective analysis on the extubation in patients with acute neurological pathology

Objetivo: Evaluar la idoneidad de la prueba de respiración espontánea para predecir el fracaso de la extubación de pacientes neurológicos y determinar los factores predictivos de fracaso. Diseño: Casos y controles. De enero de 2001 a diciembre de 2010. Ámbito: Unidad de Cuidados Intensivos. Pacientes: Enfermos neurológicos agudos sometidos a ventilación mecánica y posterior extubación. Se excluyeron: pacientes con cirugías neurológicas programadas, con patología neuromuscular, lesión medular, traqueotomía, politraumatismos con predominio de afectación del resto de los sistemas sobre el neurológico, aquellos que murieron en la Unidad de Cuidados Intensivos o que fueron trasladados. Variables de interés: Tasa de fracaso, infección intrahospitalaria, necesidad de traqueotomía, duración de la ventilación mecánica, estancia en la Unidad de Cuidados Intensivos y en el hospital, mortalidad en esta Unidad, en el hospital y a los 90 días, y factores asociados al fracaso. Resultados: De 479 pacientes, 208 fueron sometidos a prueba de respiración espontánea y posterior extubación. Cincuenta y cuatro (26%) fracasaron, la tasa de complicaciones, la estancia, la duración de la ventilación mecánica y la mortalidad fueron mayores que en el grupo de éxito. Los pacientes con accidente cerebrovascular [OR 4,256 (IC95% 1,442-12,561), p = 0,009] y necesidad de aspiraciones frecuentes [OR 5,699 (IC95% 1,863-17,432), p = 0,002] son más propensos al fracaso [ROC 0,73 (IC95% 0,628-0,840)]. Conclusiones: Los pacientes neurológicos presentan una elevada tasa de fracaso de la extubación con numerosas complicaciones asociadas y muerte. La prueba de respiración espontánea no predijo el éxito de la extubación. Los pacientes con accidente cerebrovascular y necesidad de aspiraciones frecuentes de secreciones se verían abocados a un mayor fracaso de extubación.(AU)

Objective: To assess the adequacy of the spontaneous breathing test to predict extubation failure in neurological patients undergoing mechanical ventilation and to determine factors associated with extubation failure. Design: Case-control study. Between January 2001 and December 2010. Setting: Intensive Care Unit. Patients: Acute neurological patients who underwent mechanical ventilation and were subsequently extubated. Patients with scheduled neurosurgery intervention, neuromuscular disease, spinal cord injury, tracheotomy, multiple trauma with less neurological damage than in other systems, those who died in the Intensive Care Unit or in hospital or those transferred to other hospital, were excluded. Variables of interest: Extubation failure rate, nosocomial infection, need for tracheostomy, duration of mechanical ventilation, ICU and hospital stay, mortality in the ICU or hospital, and at day 90, as well as failure-related factors. Results: Two-hundred and eight patients underwent spontaneous breathing trial, and were subsequently extubated. Fifty-four (26%) patients failed. Patients who failed extubation had a higher complication rate, received mechanical ventilation for more days, their hospitalization was longer, and the mortality rate was higher than in the success group. Patients with stroke [OR 4.256 (95%CI, 1.442-12.561), p=0.009] and those who required a greater number of aspirations during weaning [OR 5.699 (95%CI, 1.863-17.432), p=0.002] were susceptible to extubation failure [ROC curve 0.73 (0.628-0.840)]. Conclusion: Extubation failure in neurological patients is common and frequently associated with severe complications. The spontaneous breathing trial does not predict a successful extubation. Patients with stroke and those who need frequent aspiration of secretions would be doomed to further failure of extubation(AU)

Sequential projection pursuit with kernel matrix update and symbolic model selection.

This paper proposes a novel way for generating reliable low-dimensional features with improved class separability in a kernel-induced feature space. The feature projections rely on a very efficient sequential projection pursuit method, adapted to support nonlinear projections using a new kernel matrix update scheme. This enables the gradual removal of structure from the space of residual dimensions to allow the recovery of multiple projections. An adaptive kernel function is employed to unfold different types of data characteristics. We follow a holistic model selection procedure that, together with the optimal projections, dimensionality, and kernel parameters, additionally optimizes symbolically the projection index that controls the actual measurement of the data interestingness without user interaction. We tackle the underlying complex bi-level optimization model as a mixture of evolutionary and gradient search. The effectiveness of the proposed algorithm over existing approaches is demonstrated with benchmark evaluations and comparisons.

Mitochondrial dysfunction in the hippocampus of rats caused by chronic oxidative stress.

The aim of this study was to analyze the effects of chronic oxidative stress on mitochondrial function and its relationship to progressive neurodegeneration in the hippocampus of rats chronically exposed to ozone. Animals were exposed to 0.25 ppm ozone for 7, 15, 30, or 60 days. Each group was tested for (1) protein oxidation and, manganese superoxide dismutase (Mn-SOD), glutathione peroxidase (GPx) and succinate dehydrogenase (SDH) activity using spectrophotometric techniques, (2) oxygen consumption, (3) cytochrome c, inducible nitric oxide synthase (iNOS), peroxisome proliferator-activated receptor γ Co-activator 1α (PGC-1α), B-cell lymphoma (Bcl-2), and Bax expression using Western blotting, (4) histology using hematoxylin and eosin staining, and (5) mitochondrial structure using electron microscopy. Our results showed increased levels of carbonyl protein and Mn-SOD activity after 30 days of ozone exposure and decreased GPx activity. The SDH activity decreased from 7 to 60 days of exposure. The oxygen consumption decreased at 60 days. Western blotting showed an increase in cytochrome c at 60 days of ozone exposure and an increase in iNOS up to 60 days of ozone exposure. The expression of PGC-1α was decreased after 15, 30, and 60 days compared to the earlier time Bcl-2 was increased at 60 days compared to earlier time points, and Bax was increased after 30 and 60 days of exposure compared to earlier time points. We observed cellular damage, and mitochondrial swelling with a loss of mitochondrial cristae after 60 days of exposure. These changes suggest that low doses of ozone caused mitochondrial abnormalities that may lead to cell damage.

Propuesta de acciones de capacitación para la prevención de VIH/SIDA enestudiantes de Servicios Farmacéuticos / Training proposed actions to prevent hiv / aids among students of pharmacy services

Para el desarrollo de esta investigación se realiza un estudio con el objetivo de elaborar un conjunto de acciones de capacitación que permita elevar el nivel de conocimientos sobre el VIH/sida en estudiantes del perfil de Servicios Farmacéuticos de la Filial de Ciencias Médicas de Guantánamo. Teóricamente se aporta el conjunto de acciones dirigidas a estos estudiantes, las cuales son aceptadas desde su estructura, posibilidades metodológicas y factibilidad de aplicación en cualquier población (AU)

A study is done in order to develop a set of training activities that will raise the level of knowledge about HIV / AIDS among students of the profile of the Pharmaceutical Services at Medical Sciences in Guantanamo. Theoretically is provided a set of actions aimed at these students, which are accepted from its structure, methodological possibilities and feasibility of implementation in any population

Automatic induction of projection pursuit indices.

Projection techniques are frequently used as the principal means for the implementation of feature extraction and dimensionality reduction for machine learning applications. A well established and broad class of such projection techniques is the projection pursuit (PP). Its core design parameter is a projection index, which is the driving force in obtaining the transformation function via optimization, and represents in an explicit or implicit way the user's perception of the useful information contained within the datasets. This paper seeks to address the problem related to the design of PP index functions for the linear feature extraction case. We achieve this using an evolutionary search framework, capable of building new indices to fit the properties of the available datasets. The high expressive power of this framework is sustained by a rich set of function primitives. The performance of several PP indices previously proposed by human experts is compared with these automatically generated indices for the task of classification, and results show a decrease in the classification errors.

[Urinary disorders, sexual dysfunction and hypersexuality in Parkinson's disease]. / Trastornos urinarios, disfunción sexual e hipersexualidad en la enfermedad de Parkinson.

INTRODUCTION: As Parkinson's disease progresses, its non-motor manifestations become increasingly more apparent to the point where, in advances phases of the disease, they are the most important clinical symptoms. A very wide range of non-motor symptoms can appear in Parkinson's disease. Impairment of the urinary function and the sexual function (understood as the capacity to carry out sexual activity) can be seen as belonging to the dysautonomic disorders. Hypersexuality would be included within the group of impulse control disorders. DEVELOPMENT: This study reviews the epidemiology, phenomenology and treatment of urinary disorders, sexual dysfunction and hypersexuality as non-motor symptoms of Parkinson's disease. CONCLUSIONS: Urinary disorders are the most frequent non-motor symptom in Parkinson's disease. They usually present as nocturia, urgency and increased mictional frequency (pollakiuria). Preferred treatment is with anticholinergic agents. Sexual dysfunction is a frequent complaint in patients with Parkinson. It has a multifactorial aetiology and is more frequent in males than in females. In males it manifests mainly as incapacity to achieve an erection, premature ejaculation or loss of the capacity to ejaculate, whereas in females the predominant signs are decreased libido, lowered arousal and difficulty in reaching an orgasm. Hypersexuality affects young males above all and has been related to the use of dopamine agonists.

[Update on chorea]. / Actualización en coreas.

INTRODUCTION: Chorea is a brief, random, involuntary movement that can affect any muscle group and flows in an unpredictable manner from one part of the body to another. Choreic movements are present at rest, increase with distracting manoeuvres, can be partially suppressed and often disappear during sleep. The differential diagnosis of choreic syndromes is very wide and includes both genetic and acquired causes (cerebrovascular disease and space-occupying lesions, immune-based choreas, choreas caused by infection, toxic and metabolic encephalopathies, and choreas induced by pharmaceuticals). DEVELOPMENT: We review the phenomenology and pathophysiology of choreic movements, the most frequent causes, the diagnostic process and the most important recent findings in its treatment. CONCLUSIONS: Huntington's disease is the most frequent cause of hereditary chorea. In patients with a familial picture suggesting Huntington's disease, but with a negative genetic study, the chances of reaching a definitive diagnosis are, today, very low. Medication is the most frequent cause of acquired chorea. When dealing with a case of hemichorea, it is essential to rule out structural insult of the basal ganglia or their connections. Treatment of choreas must be aimed at correcting their cause if it is reversible, although the patient must always be given symptomatic treatment if the intensity and functional repercussions of the chorea require it. In cases of hereditary choreas, prevention could involve genetic counselling aimed at affected patients and their relatives.

Actualización en coreas / Update on chorea

Resumen. Introducción. La corea consiste en movimientos involuntarios, breves, aleatorios, que pueden afectar a cualquier grupo muscular, fluyendo de forma impredecible de una parte del cuerpo a otra. Los movimientos coreicos están presentes en reposo, aumentan con maniobras de distracción, se pueden suprimir parcialmente y con frecuencia desaparecen durante el sueño. El diagnóstico diferencial de los síndromes coreicos es muy amplio, incluyendo tanto cuadros de causa genética como formas adquiridas (enfermedad cerebrovascular y lesiones ocupantes de espacio, coreas de base inmune, coreas de causa infecciosa, encefalopatías tóxicas y metabólicas y coreas inducidas por fármacos). Desarrollo. Se revisa la fenomenología y la fisiopatología de los movimientos coreicos, las causas más frecuentes, el proceso diagnóstico y las principales novedades en su terapéutica. Conclusiones. La enfermedad de Huntington es la causa más frecuente de corea hereditaria. En los pacientes con un cuadro familiar sugestivo de enfermedad de Huntington, pero con un estudio genético negativo, la probabilidad de llegar a un diagnóstico definitivo es, a fecha de hoy, muy baja. Los fármacos son la causa más frecuente de corea adquirida. Ante un caso de hemicorea, es obligado descartar una lesión estructural de los ganglios basales o sus conexiones. El tratamiento de las coreas debe ir encaminado a corregir su causa en el caso de que ésta sea reversible, aunque siempre hay que ofrecer un tratamiento sintomático si la intensidad y la repercusión funcional de la corea así lo requieren. En las coreas hereditarias se podrá hacer prevención mediante el consejo genético dirigido a los pacientes afectados y sus familiares (AU)

Summary. Introduction. Chorea is a brief, random, involuntary movement that can affect any muscle group and flows in an unpredictable manner from one part of the body to another. Choreic movements are present at rest, increase with distracting manoeuvres, can be partially suppressed and often disappear during sleep. The differential diagnosis of choreic syndromes is very wide and includes both genetic and acquired causes (cerebrovascular disease and space-occupying lesions, immunebased choreas, choreas caused by infection, toxic and metabolic encephalopathies, and choreas induced by pharmaceuticals). Development. We review the phenomenology and pathophysiology of choreic movements, the most frequent causes, the diagnostic process and the most important recent findings in its treatment. Conclusions. Huntington’s disease is the most frequent cause of hereditary chorea. In patients with a familial picture suggesting Huntington’s disease, but with a negative genetic study, the chances of reaching a definitive diagnosis are, today, very low. Medication is the most frequent cause of acquired chorea. When dealing with a case of hemichorea, it is essential to rule out structural insult of the basal ganglia or their connections. Treatment of choreas must be aimed at correcting their cause if it is reversible, although the patient must always be given symptomatic treatment if the intensity and functional repercussions of the chorea require it. In cases of hereditary choreas, prevention could involve genetic counselling aimed at affected patients and their relatives (AU)

Isquemia intestinal por émbolos de colesterol / No disponible

No disponible

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.

Comparative analysis of superoxide dismutase activity between acute pharmacological models and a transgenic mouse model of Huntington's disease.

We examined the activity of striatal superoxide dismutase (SOD) in two acute pharmacological models of Huntington's disease (HD), and compared it with SOD activity in the striata of mice transgenic for the HD mutation. Total SOD, and Cu/ZnSOD activities increased in young transgenic mice, but decreased in older (35 week) mice. We consider that the increased enzyme activity represents a compensatory mechanism to protect cells from free radical-induced damage, but the system becomes insufficient in older animals. Major decreases in SOD activity were also observed both after quinolinic acid and 3-nitropropionic acid intrastriatal injections. The present results indicate that in both types of HD models striatal oxidative damage occurs, and that it is associated with alterations in the cellular antioxidant system.

Effect of quinolinic acid on endogenous antioxidants in rat corpus striatum.

The response of endogenous antioxidants to the N-methyl-D-aspartate (NMDA) receptor agonist and excitotoxin, quinolinic acid (QUIN), was investigated in rat corpus striatum. Animals treated with QUIN (240 nmol/microl), were sacrificed at 120 min after a single intrastriatal injection to examine the alterations in the levels of both reduced (GSH) and oxidized (GSSG) glutathione, and the activities of the antioxidant enzymes, superoxide dismutase (SOD) and glutathione peroxidase (Gpx). Changes in the rate of lipid peroxidation (LP) were also measured after exposure to different doses of QUIN (60, 120, 240 and 480 nmol/microl) as an index of oxidative stress. When compared to control, lipid peroxidation was increased at QUIN doses of 240 and 480 nmol/microl. Striatal levels of GSH and GSSG were decreased and increased, respectively, after QUIN injection; whereas GPx activity was unchanged. Cytosolic copper/zinc SOD (CuZn-SOD) activity decreased after treatment, while mitochondrial manganese SOD (Mn-SOD) was unchanged. The alterations observed on these antioxidant systems suggest that QUIN toxicity is mediated by specific mechanisms leading to oxidative stress.