Shiga Toxin Detection Methods : A Short Review

The Shiga toxins comprise a family of related protein toxins secreted by certain types of bacteria. Shigella dysenteriae, some strain of Escherichia coli and other bacterias can express toxins which caused serious complication during the infection. Shiga toxin and the closely related Shiga-like toxins represent a group of very similar cytotoxins that may play an important role in diarrheal disease and hemolytic-uremic syndrome. The outbreaks caused by this toxin raised serious public health crisis and caused economic losses. These toxins have the same biologic activities and according to recent studies also share the same binding receptor, globotriosyl ceramide (Gb3). Rapid detection of food contamination is therefore relevant for the containment of food-borne pathogens. The conventional methods to detect pathogens, such as microbiological and biochemical identification are time-consuming and laborious. The immunological or nucleic acid-based techniques require extensive sample preparation and are not amenable to miniaturization for on-site detection. In the present are necessary of techniques of rapid identification, simple and sensitive which can be employed in the countryside with minimally-sophisticated instrumentation. Biosensors have shown tremendous promise to overcome these limitations and are being aggressively studied to provide rapid, reliable and sensitive detection platforms for such applications.Comment: 16 pages, 2 figure

CIBERER : Spanish national network for research on rare diseases: A highly productive collaborative initiative

Altres ajuts: Instituto de Salud Carlos III (ISCIII); Ministerio de Ciencia e Innovación.CIBER (Center for Biomedical Network Research; Centro de Investigación Biomédica En Red) is a public national consortium created in 2006 under the umbrella of the Spanish National Institute of Health Carlos III (ISCIII). This innovative research structure comprises 11 different specific areas dedicated to the main public health priorities in the National Health System. CIBERER, the thematic area of CIBER focused on rare diseases (RDs) currently consists of 75 research groups belonging to universities, research centers, and hospitals of the entire country. CIBERER's mission is to be a center prioritizing and favoring collaboration and cooperation between biomedical and clinical research groups, with special emphasis on the aspects of genetic, molecular, biochemical, and cellular research of RDs. This research is the basis for providing new tools for the diagnosis and therapy of low-prevalence diseases, in line with the International Rare Diseases Research Consortium (IRDiRC) objectives, thus favoring translational research between the scientific environment of the laboratory and the clinical setting of health centers. In this article, we intend to review CIBERER's 15-year journey and summarize the main results obtained in terms of internationalization, scientific production, contributions toward the discovery of new therapies and novel genes associated to diseases, cooperation with patients' associations and many other topics related to RD research

Changes in oxidative metabolism and memory and learning in a cerebral hypoperfusion model in rats

Introduction: Chronic hypoperfusion in rats produces memory and learning impairments due to permanent occlusion of commun carotid arteries (POCCA). Molecular mechanisms leading to behavioural disorders have been poorly studied. For this reason, the aim of the present study was to characterise oxidative metabolism disorders and their implications in memory and learning impairments. Methods: Superoxide dismutase (SOD) and catalase (CAT) activities were determined in cortex, hippocampus and striatum homogenates at 24 hours and at 22 days after the lesion. Haematoxylin–eosin staining and glial fibrillary acidic protein (GFAP) immunoreactivity were performed on coronal sections. Behavioural impairments were explored using the Morris water maze (MWM). Escape latencies were determined in all behavioural studies. Results: The lesion induced a significant increase (P < .01) in CAT activity in the cortex at 24 hours, while SOD activity was significantly higher (P < .01) in the cortex and hippocampus at 22 days. An intense vacuolization was observed in the cortex and striatum as a result of the lesion. A neuronal loss in the striatum and hippocampus was observed. The glial reaction increased in the cortex and striatum. Visual alterations were observed in the lesion group with the lowest evolution time (P < .001). Escape latencies, corresponding to MWM schemes for long-term and short-term memory evaluation increased significantly (P < .05) in both groups of lesioned animals. Conclusion: It was concluded that changes in SOD and CAT activities indicate a possible implication of oxidative imbalance in the pathology associated with chronic cerebral hypoperfusion. In addition, the POCCA model in rats is useful for understanding mechanisms by which cerebral hypoperfusion produces memory and learning impairments. Resumen: Introducción: La hipoperfusión cerebral en ratas, mediante la oclusión permanente de las arterias carótidas comunes (OPACC), induce alteraciones de la memoria y el aprendizaje. Los mecanismos moleculares han sido poco estudiados y el objetivo del trabajo consiste en caracterizar las alteraciones del metabolismo oxidativo, de la memoria y del aprendizaje. Métodos: Mediante la OPACC se determinó a las 24 h y 22 días de la lesión la actividad de la superóxido dismutasa y la catalasa en el hipocampo, la corteza y el cuerpo estriado. Se realizó una tinción con hematoxilina-eosina y un marcaje con GFAP de cortes coronales. Los trastornos conductuales se exploraron mediante la prueba del laberinto acuático de Morris. Resultados: La lesión indujo un incremento (p < 0,01) de la actividad de la catalasa en la corteza a las 24 h, mientras que la superóxido dismutasa aumentó significativamente (p < 0,01) en la corteza y el hipocampo a los 22 días. Se observó una intensa vacuolización y pérdida neuronal. La respuesta glial estuvo incrementada en la corteza y el cuerpo estriado. Fue perceptible la afectación en la visión (p < 0,001), y las latencias de escape al evaluar la memoria a largo y corto plazo aumentaron considerablemente (p < 0,05) en ambos grupos de animales lesionados. Conclusiones: Los cambios en las actividades de las enzimas apuntan a una posible implicación del disbalance oxidativo en la patología asociada a la hipoperfusión cerebral crónica. La OPACC resulta útil para entender los mecanismos por los cuales la hipoperfusión cerebral conduce a las alteraciones de los procesos de memoria y aprendizaje. Keywords: Hypoperfusion, Rats, Oxidative metabolism, Behavioural disorders, Morris maze, Learning impairments, Palabras clave: Hipoperfusión, Ratas, Oxidativo, Oclusión, Carótidas, Morri

Alteraciones del metabolismo oxidativo y de la memoria y el aprendizaje en un modelo de hipoperfusión cerebral en ratas

Resumen: Introducción: La hipoperfusión cerebral en ratas, mediante la oclusión permanente de las arterias carótidas comunes (OPACC), induce alteraciones de la memoria y el aprendizaje. Los mecanismos moleculares han sido poco estudiados y el objetivo del trabajo consiste en caracterizar las alteraciones del metabolismo oxidativo, de la memoria y del aprendizaje. Métodos: Mediante la OPACC se determinó a las 24 h y 22 días de la lesión la actividad de la superóxido dismutasa y la catalasa en el hipocampo, la corteza y el cuerpo estriado. Se realizó una tinción con hematoxilina-eosina y un marcaje con GFAP de cortes coronales. Los trastornos conductuales se exploraron mediante la prueba del laberinto acuático de Morris. Resultados: La lesión indujo un incremento (p < 0,01) de la actividad de la catalasa en la corteza a las 24 h, mientras que la superóxido dismutasa aumentó significativamente (p < 0,01) en la corteza y el hipocampo a los 22 días. Se observó una intensa vacuolización y pérdida neuronal. La respuesta glial estuvo incrementada en la corteza y el cuerpo estriado. Fue perceptible la afectación en la visión (p < 0,001), y las latencias de escape al evaluar la memoria a largo y corto plazo aumentaron considerablemente (p < 0,05) en ambos grupos de animales lesionados. Conclusiones: Los cambios en las actividades de las enzimas apuntan a una posible implicación del disbalance oxidativo en la patología asociada a la hipoperfusión cerebral crónica. La OPACC resulta útil para entender los mecanismos por los cuales la hipoperfusión cerebral conduce a las alteraciones de los procesos de memoria y aprendizaje. Abstract: Introduction: Chronic hypoperfusion in rats produces memory and learning impairments due to permanent occlusion of commun carotid arteries (POCCA). Molecular mechanisms leading to behavioural disorders have been poorly studied. For this reason, the aim of the present study was to characterise oxidative metabolism disorders and their implications in memory and learning impairments. Methods: Superoxide dismutase (SOD) and catalase (CAT) activities were determined in cortex, hippocampus and striatum homogenates at 24 hours and at 22 days after the lesion. Haematoxylin-eosin staining and glial fibrillary acidic protein (GFAP) immunoreactivity were performed on coronal sections. Behavioural impairments were explored using the Morris water maze (MWM). Escape latencies were determined in all behavioural studies. Results: The lesion induced a significant increase (P<.01) in CAT activity in the cortex at 24 hours, while SOD activity was significantly higher (P<.01) in the cortex and hippocampus at 22 days. An intense vacuolization was observed in the cortex and striatum as a result of the lesion. A neuronal loss in the striatum and hippocampus was observed. The glial reaction increased in the cortex and striatum. Visual alterations were observed in the lesion group with the lowest evolution time (P<.001). Escape latencies, corresponding to MWM schemes for long-term and short-term memory evaluation increased significantly (P<.05) in both groups of lesioned animals. Conclusion: It was concluded that changes in SOD and CAT activities indicate a possible implication of oxidative imbalance in the pathology associated with chronic cerebral hypoperfusion. In addition, the POCCA model in rats is useful for understanding mechanisms by which cerebral hypoperfusion produces memory and learning impairments. Palabras clave: Hipoperfusión, Ratas, Oxidativo, Oclusión, Carótidas, Morris, Keywords: Hypoperfusion, Rats, Oxidative metabolism, Behavioural disorders, Morris maze, Learning impairment