[The neural networks of facial expression]. / Redes neuronales de la expresion facial.

INTRODUCTION: Face perception involves a broad network of connections between cortical and subcortical regions for the exchange and synchronization of information using white matter fibers. This precise communication system can be affected by the structures and the pathways that connect them. AIMS: To establish the neural substrate underlying the perception of facial expression and to analyze the different factors involved in modulating the integrity of this neural network, with the aim being to introduce improvements into rehabilitation programs. DEVELOPMENT: When the complex neural network involved in the perception of facial expression is altered by trauma, neurodegenerative disorders, developmental disorders, social isolation or negative contexts, the adaptive capacity to interact with the environment also deteriorates. CONCLUSIONS: Maintaining the neural network integrity responsible for processing facial expression requires considering different variables. To a greater or lesser extent, these variables modify the structure or function of neural networks, such as aerobic training, transcranial magnetic stimulation, transcranial electrical stimulation, and learning. These variables are affected by age, and the type and course of the condition or generator context, and raise the need for rehabilitation protocols that are adapted and designed to delimit the deficient neuronal substrate.

TITLE: Redes neuronales de la expresion facial.Introduccion. La percepcion de caras involucra una amplia red de conexiones entre regiones corticales y subcorticales que intercambian y sincronizan informacion a traves de haces de sustancia blanca. Este preciso sistema de comunicacion puede verse afectado tanto a traves de las propias estructuras como por las vias que las conectan. Objetivos. Delimitar el sustrato neuronal que subyace a la percepcion de la expresion facial y analizar los diferentes factores que participan modulando la integridad de esta red neuronal, con el fin de proponer mejoras en los programas de rehabilitacion. Desarrollo. Cuando la compleja red de conexiones que participa en la percepcion de la expresion facial se altera por traumatismos, patologias neurodegenerativas, trastornos del desarrollo, incluso por aislamiento social o contextos negativos, se deteriora tambien la capacidad para interactuar de manera adaptativa con el entorno. Conclusiones. La posibilidad de restaurar la integridad de la red neuronal encargada del procesamiento de la expresion facial pasa por tener en cuenta diferentes variables que en mayor o menor grado se han mostrado capaces de modificar la estructura o funcionalidad de las redes neuronales, como el entrenamiento aerobico, la estimulacion magnetica transcraneal, la estimulacion electrica transcraneal y el aprendizaje, sin bien estas variables estarian condicionadas por la edad, el tipo y evolucion del trastorno o el contexto generador, lo que plantearia la necesidad de protocolos de rehabilitacion ajustados y orientados a delimitar el sustrato neuronal del deficit.

Análisis de la fluencia lectora en pacientes con la enfermedad de Alzheimer y controles asintomáticos / Oral reading fluency analysis in patients with Alzheimer disease and asymptomatic control subjects

Introducción: Numerosos estudios han puesto de manifiesto que la alteración en la capacidad comunicativa es uno de los síntomas característicos de la enfermedad de Alzheimer (EA). Objetivo: Estudiar la organización temporal del habla en una tarea de lectura en un grupo de pacientes con EA y otro de controles sanos, utilizando un procedimiento semiautomático, así como valorar su capacidad para discriminar entre ambos grupos. Sujetos y método: Se aplicó una prueba de lectura a 70 sujetos: 35 con EA y otros tantos controles. Antes del registro del habla, los sujetos fueron sometidos a una batería de pruebas neuropsicológicas. Los grupos no diferían en edad, sexo o nivel de estudios. Resultados: Todas las variables analizadas se mostraron alteradas en el grupo con EA. Los resultados señalan que la lectura de los pacientes con EA se caracteriza por una reducida velocidad de elocución y articulación, una baja efectividad del tiempo de fonación, así como en un incremento del número y la proporción de las pausas. Los algoritmos de procesamiento de la señal aplicados a las grabaciones de fluidez lectora demostraron su capacidad para discriminar entre ambos grupos con una precisión del 80% (especificidad 74,2%; sensibilidad 77,1%) mediante la velocidad de elocución. Conclusión: El análisis de la fluidez de lectura oral puede representar una herramienta potencial para el análisis objetivo y la cuantificación de los déficits del lenguaje en la EA (AU)

Introduction: Many studies highlight that an impaired ability to communicate is one of the key clinical features of Alzheimer disease (AD). Objective: To study temporal organisation of speech in an oral reading task in patients with AD and in matched healthy controls using a semi-automatic method, and evaluate that method's ability to discriminate between the 2 groups. Subjects and methods: A test with an oral reading task was administered to 70 subjects, comprising 35 AD patients and 35 controls. Before speech samples were recorded, participants completed a battery of neuropsychological tests. There were no differences between groups with regard to age, sex, or educational level. Results: All of the study variables showed impairment in the AD group. According to the results, AD patients’ oral reading was marked by reduced speech and articulation rates, low effectiveness of phonation time, and increases in the number and proportion of pauses. Signal processing algorithms applied to reading fluency recordings were shown to be capable of differentiating between AD patients and controls with an accuracy of 80% (specificity 74.2%, sensitivity 77.1%) based on speech rate. Conclusion: Analysis of oral reading fluency may be useful as a tool for the objective study and quantification of speech deficits in AD (AU)

Oral reading fluency analysis in patients with Alzheimer disease and asymptomatic control subjects.

INTRODUCTION: Many studies highlight that an impaired ability to communicate is one of the key clinical features of Alzheimer disease (AD). OBJECTIVE: To study temporal organisation of speech in an oral reading task in patients with AD and in matched healthy controls using a semi-automatic method, and evaluate that method's ability to discriminate between the 2 groups. SUBJECTS AND METHODS: A test with an oral reading task was administered to 70 subjects, comprising 35 AD patients and 35 controls. Before speech samples were recorded, participants completed a battery of neuropsychological tests. There were no differences between groups with regard to age, sex, or educational level. RESULTS: All of the study variables showed impairment in the AD group. According to the results, AD patients' oral reading was marked by reduced speech and articulation rates, low effectiveness of phonation time, and increases in the number and proportion of pauses. Signal processing algorithms applied to reading fluency recordings were shown to be capable of differentiating between AD patients and controls with an accuracy of 80% (specificity 74.2%, sensitivity 77.1%) based on speech rate. CONCLUSION: Analysis of oral reading fluency may be useful as a tool for the objective study and quantification of speech deficits in AD.

Time-related efficacy of liver cell isografts in fulminant hepatic failure.

We and others have reported that dispersed liver cells transplanted into the spleen parenchyma of syngeneic rats remained functional and viable for a long time. This report describes our results with hepatocellular transplantation as a therapeutic method in a model of fulminant hepatic failure (FHF) in the rat. 60 male Sprague-Dawley rats weighing 200-250 g were used. The FHF was reached through an Eck's fistula with 2/3 hepatectomy at the same time. This model produced lethal hepatic failure in a highly reproducible manner. Liver cells were isolated by the collagenase method. 40 X 10(6) hepatocytes suspended in Hanks' balanced salt solution were transplanted into the spleen parenchyma 24 hr before (group 1), at the same time as (group 2), and 24 hr after (group 3) FHF was achieved. Additional sham-operated animals (groups 4 and 5) and a control group (group 6) were used. The hepatocellular transplantation markedly increased the survival of the animals with induced FHF to 80% (group 1) and 60% (group 2)--but not in group 3 (20%),--compared with 10% in the control group. This study shows that dispersed liver cells transplanted into the spleen can provide sufficient support to allow animals with lethal hepatic failure to survive and recover. Nevertheless the efficacy of transplantation is a time-related phenomenon with the FHF induction.

Hepatocyte damage induced by lymphocytes from patients with chronic liver diseases, as detected by LDH release.

We have used a cytoplasmic enzyme system in the study of the in vitro cytotoxic activity of human peripheral blood leucocytes against isolated liver cells in patients with chronic liver diseases. Lymphocytes from primary biliary cirrhosis and chronic active liver disease patients were shown to have an in vitro capacity to induce a cytolitic effect on isolated hepatocytes, as demonstrated by the enhanced release of lactate dehydrogenase (LDH), a cytoplasmic marker enzyme. No significant LDH release was seen with control lymphocytes of normal persons or with lymphocytes from patients with alcoholic cirrhosis. Our results corroborate, in a different assay system, by a simple, reproducible and different method, that lymphocyte-mediated liver cell damage "in vitro" occurs in both primary biliary cirrhosis and chronic active liver disease.

Injurious effect on rat liver mitochondria by lymphocytes from patients with primary biliary cirrhosis.

Lymphocytes from primary biliary cirrhosis (PBC) patients were shown to have an injurious effect on rat liver mitochondria, as was demonstrated by the inhibition of mitochondrial respiratory control by these cells. The incubation of the PBC patients' lymphocytes with isolated rat liver mitochondria produced a significant inhibition of mitochondrial respiration in the presence of ADP. However, no significant effect on respiration was seen with control lymphocytes of normal persons or with lymphocytes from patients with alcoholic cirrhosis and miscellaneous liver diseases. The results suggest that this injurious effect of PBC lymphocytes on mitochondria might be a consequence of sensitization in vivo of the PBC patients' lymphocytes by the mitochondrial antigens.

Primary biliary cirrhosis. Study of the action of mitochondrial antibody plus complement on mitochondrial membrane functions.

It has been described that mitochondrial antibodies can be detected in the serum of primary biliary cirrhosis patients (over 90%) and that these antibodies are directed specifically against a component of the mitochondrial inner membrane. In the present study whole mitochondria isolated from rat liver were exposed to mitochondrial antibodies from patients with primary biliary cirrhosis, and to antibodies induced experimentally in rabbits to mitochondrial antigens of rat liver. This was an attempt to study the action of these antibodies and complement on mitochondrial functions. By studying respiratory control and oxidative phosphorylation of mitochondria, no significant, nor specific effect on mitochondrial membranes functions could be detected, after the incubation of suspensions of mitochdondria with normal or immune gamma-globulin (neither from rabbits nor from human) nor with the addition of complement. Furthermore, the respiration of fragmental mitochondria using succinate and NADH substrates was unaffected by the antibodies and complement. Similarly, mitochondrial APT-ase activity and swelling and contraction were not affected by antibody. Experiments are in progress to study the hypothesis of a lymphocyte dependent antibody mediated cytotoxicity in this system. In order to demonstrate that this autoimmune phenomenon might be associated with cellular immunity to a mitochondrial component, we have in a previous report demonstrated impairment of mitochondrial respiratory control by lymphocytes from rabbits sensitized in vivo with mitochondrial antigens. Subsequently we have recently shown evidence of sensitization. In-vivo of lymphocytes from patients with primary biliary cirrhosis as demonstrated by an injurious effect on rat liver mitochondria by lymphocytes from patients with this disease. Further studies are necessary to clarify the involvement of this phenomena in the possible mechanisms responsible for the pathogenesis of the lesions.

[Radiological appearances of cancer of the gastric stump (author's transl)]. / Aspects radiologiques du cancer du moignon gastrique

The authors report 35 cases of primary carcinoma of the gastric stump, describing the technique they use for radiography, noting the main diagnosis signs and discussing the importance of the various methods for their study. They emphasize the importance of periodic post-operative control in these cases.

Impairment of mitochondrial respiratory control by activated lymphocytes.

Mitochondria isolated from rat livers were used as a source of antigens capable of producing in vitro activation of lymphocytes that had previously been sensitized in vivo with the same antigen. Such lymphocytes were shown to have an injurious effect on target mitochondria, as was demonstrated by a new biochemical approach based on the study of the inhibition by these cells of mitochondrial respiratory control. A somewhat milder injurious capacity was also observed in normal and sensitized lymphocytes activated in vitro with the mitogen PHA. The lateration of the respiratory control of mitochondria by lymphocytes correlated with an increase in DNA synthesis in these cells.