La Escuela de Salud Pública de México: innovación educativa y tecnológica en el nuevo milenio / School of Public Health of Mexico: Educational and technological innovation in the new millennium

Este artículo fue concebido para analizar la función de la Escuela de Salud Pública de México (ESPM) desde el año 2000 hasta el presente. Uno de sus puntos centrales es el análisis del proceso de reorientación de la labor educativa de la escuela con la finalidad de responder a los retos en materia de salud y educación surgidos a finales del siglo XX. Para exponer cómo ha evolucionado dicho proceso, retomamos tres ejes rectores que caracterizan la labor de la escuela en la actualidad: el cambio de modelo pedagógico, la incorporación de las tecnologías de la información y las comunicaciones, y la profesionalización de la docencia. Con la exposición de este tema, y a través del contraste entre el pasado y el presente, buscamos completar la historia de trabajo ininterrumpido de la Escuela durante sus 92 años de existencia, que ha trascendido los confines del país.

This article was conceived to analyze the work of the School of Public Health of Mexico (ESPM for is acronym in Spanish) from the year 2000 to the present day. One of the highlights that we will examine is the reorientation of the educational work of the school in order to meet the challenges in health and education that emerged during the end of the twentieth century. In order to explain the evolution of this process, we will describe the three main guiding principles that characterize the present work of the school: the pedagogical model's change, the incorporation of the information and communication technologies, and the professionalization in teaching. The purpose of this work is to define those guiding principles, and to expose, through the contrast between past and present, the complete history of uninterrupted work of the School of Public Health of Mexico during its ninety-two years of existence, that has gone beyond the boundaries of the country.

Mechanism of intragastric amoxicillin protection against 96 percent ethanol damage in rat stomach

The purpose of this study was to investigate the role played by endogenous prostaglandins, sulfhydryls, gastric motility, fluid volume, and mucus volume retained in the gastric lumen in the protection offered by intragastric amoxicillin against ethanol-induced gastric lesions. It has been demonstrated that intragastric administration of amoxicillin (Amx) dose-dependently protected the rat gastric mucosa from 96 per cent ethanol-induced lesions. The inhibition of the lesions was 28, 41.4, 84.7 and 90 per cent at doses of 50, 100, 200 and 400 mg/Kg, respectively. The gastroprotective effect of Amx was significantly reversed by pretreatment with both indomethacin (5 mg/Kg, subcutaneously), a cyclooxygenase inhibitors, and iodoacetamide (100 mg/Kgm subcutaneously), a sulfhydryl blocker. Gastric motility was measured by a ballon method. There was not any significant differences between Amx (50-400 mg/Kg)-induced and spontaneous motility with regard to both amplitudes and frequently of gastric contraction. One milliliter of 96 per cent ethanol produced hemorrhagic bandlike lesions in the corpus mucosa with the occurrence of a complete inhibition of the amplitude and frequency of gastric contraction. This inhibition of gastric motility caused by ethanol was not modified by pretreatment of Amx (400 mg/Kg) alone, indomethacin plus Amx or iodoacetamide plus Amx. In addition, there was a significant increase in the mucus volume retained in the gastric lumen for Amx (200 and 400 mg/Kg) at 30 min after its adminitration. We conclude that the intragastric Amx prospective effect aginst 96 per cent athanol-induced mucosal lesions may be mediated by endogenous prostaglandins, sulfhydryl compounds of the gastric mucosa, an increase in mucus volume retained in the gastric lumen at the time when ethanol is administered, and is not associated with the gastric motor activity.

Thioctic acid protection against ethanol-induced gastric mucosal lesions involves sulfhydryl and prostagladin participation

Thioctic acid, a sulfhydryl agent, given orally macroscopically protected the gastric mucosa from 96 percent ethanol-induced lesions in a dose-and time dependent fashion. The inhibition of the lesions was 56.0 and 90.3 percent at doses of 25 and 50 mg/Kg, respectively. The duration of its protective effect was appoximately 120 minutes. Histopathologically, the oral administration of thioctic acid prevented necrotic mucosal lesions in the deeper part of the mucosa but did not protect the surface epithelial cells against ethanol challenge. Gastric motility measured by a ballon method, was dose-dependently inhibited by the oral administration of thioctic acid. Thioctic acid protection was suppressed by pretreatment with indomethacin (30 mg/Kg), a cyclooxygenase inhibitor, and iodoacetamide (100 mg/Kg), a sulfhydryl bloker. The gastric motility inhibited by oral thioctic acid was not reversed by indomethacin or iodoacetamide. These doses of indomethacin or iodomethamide were administered because previously they had been used to suppress endogenous prostagladins, and nonprotein sulfhydryls of the gastric mucosa, respectively. There was an increase in the fluid volume retained in the gastric lumen for thioctic acid (50 mg/Kg) at 30,60,90, and 120 minutes after administration. There was an increase in the mucus volume retained in the gastric lumen for thioctic acid (50, 25 mg/Kg) at 120 minutes after administration. The lesion area in the rats treated with 70 mul of vehicle and in the rats treated with 250 mul of vehicle were significantly higher than in the rats treated with 450 mul of vehicle. The present study suggests that thioctic acid administered orally, affered protection to the rat gastric mucosa against 96 percent ethanol-induced lesions. This protective effect appears to be dependent on prostagladin-and sulfhydryl-sensitive mechanisms, together with an increase in both the fluid volume and the mucus volume retained in the gastric lumen, and is not associated with the inhibition of gastric motor activity.

Inactivation of a beta-glucosidase from Arthrobotrys conoides by diethyl pyrocarbonate: evidence of histidine at the active site.

Modification of A. conoides beta-glucosidase by diethylpyrocarbonate caused rapid inactivation of the enzyme. The kinetic analyses showed that the inactivation by diethylpyrocarbonate resulted from the modification of an average of one histidine residue per mole of enzyme. The modified enzyme showed an increase in absorbance at 240 nm. Sulphydryl, lysine and tyrosine residues were not modified by diethylpyrocarbonate treatment. The substrate offered significant protection against diethylpyrocarbonates modification. The results indicate that diethylpyrocarbonate was interacting with the enzyme at or near the active site.