Integration of a battery of biomarkers to evaluate the health status of field-collected frogs of Leptodactylus luctator living in ecosystems with different anthropogenic disturbances.

Amphibians are the most threatened group of vertebrates because they have certain biological and ecological characteristics that make them sensitive to environmental changes. The aim of this study was to evaluate the health status of field-collected adult frogs of Leptodactylus luctator (Amphibia, Anura) living in sites with different anthropogenic disturbances (florihorticulture, petrochemical industry and sewage discharges) and a reference site without any detectable influence of such activities. To this end, a battery of 21 biomarkers (hematological, biochemical and individual biomarkers) was studied using a multivariate approach that allows us to evaluate the relationship between them and provide information on their usefulness. The frogs at the florihorticulture, petrochemical and sewage discharges sites exhibited several biomarkers far from homeostasis. In addition, we identified 11 of 21 biomarkers that were useful indicators of the health status of the frogs and allowed discrimination between study sites in the following order: lymphocytes (98 %), neutrophils (45 %), hemoglobin (42 %), monocytes (41 %), fat body index (35 %), eosinophils (35 %), hepatosomatic index (33 %), mean corpuscular hemoglobin (32 %), thrombocytes (27 %), catalase in liver (26 %), and GST in liver (26 %). The results suggest that hematological biomarkers contribute the most to site separation, whereas biochemical biomarkers contribute the least. The integral interpretation of the results also allowed us to diagnose the different health status of L. luctator: The frogs from the petrochemical industry were the most negatively affected, followed by the frogs from the sewages discharges and finally the frogs from the florihorticulture and reference sites. This is the first field study with anurans in which so many biomarkers were examined.

Incidence of varicella zoster virus infections of the central nervous system in the elderly: a large tertiary hospital-based series (2007-2014).

The aim of the study was to describe the clinical and epidemiological characteristics of the central nervous system (CNS) infection by varicella zoster virus (VZV) in patients older than 65 years in a tertiary community hospital. We retrospectively analysed the results of cerebrospinal fluid (CSF) testing in patients older than 65 years between 2007 and 2014 with clinically suspected VZV infection with CNS involvement. Patients whose CSF samples were positive for VZV DNA were included, as were those with negative results who simultaneously presented herpes zoster and CSF or magnetic resonance imaging findings suggestive of CNS infection, and in whom other possible aetiologies had been ruled out. The study included 280 patients. The disease was considered to be caused by a VZV infection in 32 patients (11.4%), of which 23 cases were virologically confirmed (detection of VZV DNA in CSF). The most frequent diagnosis of the patients with VZV CNS infection was encephalitis (83.3%), followed by meningitis (13.3%) and cerebellitis (3.3%). The mean annual incidence of VZV CNS infection was 3.0 cases per 100,000 inhabitants. VZV was the most common cause of encephalitis and viral meningitis, ahead of herpes simplex virus (n = 9). At the time of discharge, 12 (40%) patients showed neurological sequelae. Five patients (20%) died during hospitalization, all with encephalitis. Patients with a fatal outcome had significantly higher median age and longer delay before initiating acyclovir. In conclusion, VZV was the first cause of encephalitis in our elderly population. Despite acyclovir treatment, there was a high rate of case fatality and sequelae at discharge.

Tabaco y esclerosis múltiple / Smoking and multiple sclerosis

Introducción. La esclerosis múltiple (EM) es una enfermedad autoinmune de etiología compleja, hoy por hoy desconocida, en la que factores genéticos y ambientales determinan la susceptibilidad. En los últimos años, el efecto del tabaco ha sido uno de los factores ambientales que ha emergido en la EM, y se ha asociado tanto a un aumento de la susceptibilidad como a un aumento de la progresión. Objetivo. Revisar la evidencia actual sobre el papel del tabaco en la EM. Desarrollo. Se incluye una actualización de los estudios publicados que han analizado distintos aspectos del tabaco en laEM: vías patogénicas implicadas, asociación del tabaco y riesgo de EM, interacción con otros factores de riesgo y efecto del tabaco en el curso de la enfermedad. Conclusiones. Los estudios observacionales demuestran que el tabaquismo incrementa de forma significativa el riesgo de EM (odds ratio ~ 1,5) y es un factor de riesgo independiente. Sin embargo, la EM es una enfermedad compleja y el aumento de riesgo por el tabaco puede diferir en función de la interacción con otros factores genéticos y ambientales. El papel del tabaco como factor de progresión es más controvertido, con resultados contradictorios y estudios de gran variabilidad, lo que dificulta establecer una conclusión firme. Los mecanismos por los que el tabaquismo modifica el riesgo y posiblemente la progresión de la enfermedad no son aún conocidos (AU)

Introduction. Multiple sclerosis (MS) is a complex autoimmune disease of unknown etiology, in which genetic and environmental factors interact and determine the disease susceptibility. In recent years, smoking effect has been one of the emerging environmental factors in the study of MS and has been associated with an increased susceptibility and an increase in disease progression. Aim. To review the current evidence on the role of smoking in MS. Development. The review includes an update of studies that have analyzed different aspects of tobacco in MS, including the potential pathogenic pathways involved, association of smoking and risk of MS, interactions with other risk factors and the effect of smoking in the disease course. Conclusions. Observational studies show that smoking significantly increases the risk of MS (odds ratio ~ 1.5) and is an independent risk factor. However, MS is a complex disease and this risk may be modified depending on the interaction with other genetic and environmental factors. The role of smoking as a progression factor is more controversial, with confronted results and highly variable studies, making it difficult to draw any conclusion. The mechanisms by which smoking may modify the risk and progression of the disease have to be further investigated (AU)

Epidermal growth factor receptor tyrosine-kinase inhibitor treatment resistance in nos-small cell lung cancer: biological basis and therapeutic strategies

Lung cancer remains the leading cause of cancer-related death. Non-small cell lung cancer (NSCLC) represents 85 % of all lung cancer cases and it is classified into three major subtypes: adenocarcinoma, squamous cell carcinoma and large-cell carcinoma. In the past years, molecular-targeted therapies have been developed in order to improve response, survival and quality of life in patients with advanced NSCLC. Lung cancers harboring mutations in the epidermal growth factor receptor (EGFR) respond to EGFR tyrosine-kinase inhibitors (TKIs). However, virtually all patients with initial response relapse due to acquired resistance. Better understanding the biology of these tumors and mechanisms of EGFR TKIs resistance could shed some light on research of new therapeutic options in this setting. This review aims to emphasize on EGFR involved lung cancer pathway, primary and acquired mechanisms of TKIs resistance, and discuss agents currently used in clinical development in this emerging scenario (AU)

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Epidermal growth factor receptor tyrosine-kinase inhibitor treatment resistance in non-small cell lung cancer: biological basis and therapeutic strategies.

Lung cancer remains the leading cause of cancer-related death. Non-small cell lung cancer (NSCLC) represents 85 % of all lung cancer cases and it is classified into three major subtypes: adenocarcinoma, squamous cell carcinoma and large-cell carcinoma. In the past years, molecular-targeted therapies have been developed in order to improve response, survival and quality of life in patients with advanced NSCLC. Lung cancers harboring mutations in the epidermal growth factor receptor (EGFR) respond to EGFR tyrosine-kinase inhibitors (TKIs). However, virtually all patients with initial response relapse due to acquired resistance. Better understanding the biology of these tumors and mechanisms of EGFR TKIs resistance could shed some light on research of new therapeutic options in this setting. This review aims to emphasize on EGFR involved lung cancer pathway, primary and acquired mechanisms of TKIs resistance, and discuss agents currently used in clinical development in this emerging scenario.

Respuesta al tratamiento con corticoides en un caso de angiopatía amiloide inflamatoria sin realización de biopsia / Response to treatment with corticoids in a case of inflammatory amyloid angiopathy without performing a biopsy

Introducción. La angiopatía amiloide inflamatoria (AAI) es una forma de presentación infrecuente de la angiopatía amiloide cerebral recientemente reconocida y cuyo diagnóstico definitivo es anatomopatológico. Objetivo. Se presenta un paciente con AAI con buena respuesta clínica, neuropsicológica y de neuroimagen al tratamiento con corticoides y en el que no se consideró necesario practicar biopsia cerebral. Caso clínico. Varón de 68 años con diagnóstico de enfermedad de Alzheimer que sufrió una crisis convulsiva generalizada seguida de trastorno del lenguaje y hemiparesia derecha. La resonancia magnética mostró una lesión de comportamiento infiltrante hemisférica izquierda y múltiples microsangrados. La clínica y radiología fueron sugestivas de AAI y se instauró tratamiento corticoideo. La neuroimagen y los tests neuropsicológicos mostraron una notable mejoría a los 30 días del inicio del tratamiento inmunosupresor. El genotipo fue ApoE ε4/ε4. Se desestimó la realización de biopsia cerebral. Conclusiones. El caso descrito sugiere la posibilidad de, en casos individualizados con clínica y radiología características de AAI, instaurar tratamiento empírico con corticoides con diagnóstico de probabilidad y realizar biopsia cerebral en caso de que no haya respuesta al tratamiento (AU)

Introduction. Inflammatory amyloid angiopathy (IAA) is an infrequent presenting symptom of the recently recognised cerebral amyloid angiopathy and its definitive diagnosis is reached by means of pathological analyses. Aim. We report the case of a male patient with IAA and good clinical, neuropsychological and neuroimaging response to treatment with corticoids; a biopsy of brain tissue was not considered necessary. Case report. The patient, 68 years old and diagnosed with Alzheimer’s disease, suffered from generalised seizures followed by a language disorder and hemiparesis of the right-hand side. A magnetic resonance imaging scan showed a lesion displaying infiltrating behaviour in the left hemisphere and multiple instances of microbleeding. Clinical and radiological features suggested IAA and treatment was established with corticoids. Neuroimaging and neuropsychological tests revealed a notable improvement at 30 days after beginning treatment with immunosuppressants. The genotype was ApoE ε4/ε4. The need to perform a biopsy of brain tissue was ruled out. Conclusions. The case described here suggests that, in individualised cases with clinical and radiological features that are characteristic of IAA, it may be possible to establish an empirical treatment with corticoids with a probability diagnosis and perform a biopsy of brain tissue in the event of a lack of response to treatment (AU)