The chronic effects of nicotine monomethidide on gastric secretion in pylorus-ligated rats

Résumé L'action de la nicotine monométhyliodine (NMI) sur la sécrétion gastrique basique et sur les concentrations de choline de cervelles, d'acétylcholine et de nicotine et sur l'activité de la transacétylcholinestérase a été étudiée chez des rats. Le NMI, sel quaternaire de nicotine, qui ne traverse pas la barrière hématoencéphalique, a été administré dans de la gélatine à 6% en dosage sous-cutané de 1000 g/ml/kg/jour pendant 14 jours. Le NMI n'a pas changé de paramètres et aucune trace de nicotine n'a été découverte dans les homogénates de cervelles complètes.     

Gastric secretory response of Shay rats to ICI-50123

Zusammenfassung An männlichen Ratten wurden nach 2 h Pylorusligatur Magensaftmenge, Volumen/100 g Körpergewicht, pH, Azidität, gesamte Azidität und Säureproduktion bestimmt und als Funktion von ICI-50123 studiert. Eine maximale Stimulation erfolgte bei einer Dosierung von 1000.0 g/kg s.c. Eine Abnahme der Säureproduktion zeigte sich bei supramaximaler Dosis.     

Fluorometric detection of serotonin using o-phthaldialdehyde: An improvement

Résumé Dans la détermination fluorimétrique du complexe sérotonine-OPT, le lavage des spécimens avec un volume égal de chloroforme, avant de l'évaluation, réduit l'interférence des blancs et la dispersion primaire. Cela permet une évaluation plus exacte de la fluorescence de la sérotonine et, dans quelques cas, l'usage de spectres autrement illisibles.     

Bowel serotonin levels in the fasted and non-fasted Sprague-Dawley rat

Zusammenfassung Der Serotoningehalt der Darmmucosa aus 14 Schnittpräparaten von Sprague-Dawley Rattenweibchen nach 16-stündigem Fasten und nach normaler Fütterung wurde bestimmt. Grössere Serotoningehalte wurden im oberen Teil des Verdauungstraktus (ausschliesslich den Magenblindsack) der Hungertiere gefunden.     

Analysis of fibroblast proteins from patients with Duchenne muscular dystrophy by two-dimensional gel electrophoresis.

Duchenne muscular dystrophy (DMD), the most common and severe form of the muscular dystrophies, is an X-linked inborn error of metabolism with multiple tissue involvement. Although the major pathological changes are observed in skeletal muscle, abnormalities have also been detected in the heart, nervous system, red blood cells, lymphocytes and cultured skin fibroblasts. For many reasons, such as readily available tissue material, fewer secondary changes and the potential for prenatal diagnosis, cultured skin fibroblasts should be the tissue of choice to search for the primary defect. Several abnormalities have been reported in DMD fibroblasts, suggesting that the genetic abnormality is expressed in these cells. To search for potentially mutant protein(s) we have compared the protein composition of normal and DMD fibroblasts by two-dimensional gel electrophoresis and have now found one protein spot consistently missing in DMD cells. The nature of this protein and its relation to the DMD gene are unknown.     

Protein encoded by v-erbA functions as a thyroid-hormone receptor antagonist

The thyroid-hormone receptor can, in the absence of its ligand, suppress activity of a responsive promoter. Addition of thyroid hormone, however, results in the stimulation of expression. The oncogenic derivative of the thyroid-hormone receptor, v-erbA, acts as a constitutive repressor and, when coexpressed with the receptor, blocks activation by thyroid hormone. Thus, v-erbA may be the first example of a dominant negative oncogene.     

A bivalent Huntingtin binding peptide suppresses polyglutamine aggregation and pathogenesis in Drosophila

Huntington disease is caused by the expansion of a polyglutamine repeat in the Huntingtin protein (Htt) that leads to degeneration of neurons in the central nervous system and the appearance of visible aggregates within neurons. We have developed and tested suppressor polypeptides that bind mutant Htt and interfere with the process of aggregation in cell culture. In a Drosophila model, the most potent suppressor inhibits both adult lethality and photoreceptor neuron degeneration. The appearance of aggregates in photoreceptor neurons correlates strongly with the occurrence of pathology, and expression of suppressor polypeptides delays and limits the appearance of aggregates and protects photoreceptor neurons. These results suggest that targeting the protein interactions leading to aggregate formation may be beneficial for the design and development of therapeutic agents for Huntington disease.