Indications for the Use of the Miller–Abbott Tube

Long-tube insertion with the ropeway method facilitated by a guidewire placed by transnasal ultrathin endoscopy for bowel obstruction: a prospective, randomized, controlled trial

“…Although bowel obstruction had long been a fatal condition, since Wangsteen 2-4 reported a technique for advancing a long tube through the jejunum in 1933 to decompress the obstructed intestine, the development of various long tubes for this purpose 11,12 has resulted in a decrease in the mortality rate of bowel obstruction from 50% to 3%. 5 Although a randomized trial indicated no advantage of decompression by a long tube compared with such treatment with a short nasogastric tube, 13 there have been reports from many countries describing the usefulness of long-tube decompression for the management of bowel obstruction.…”

The management of acute intestinal obstruction: A critical review of 179 personal cases

“…It profits a patient but little if in spite of adequate replacement of fluid and electrolyte loss, and removal of the cause of his obstruction, he dies with paralytic ileus from unrelieved overdistension of his bowel. At the beginning of this series an extensive trial of Miller -Abbott intubation (Miller and Abbott, 1934;Abbott and Johnston, 1938;Johnston, Penberthy, Noer, and Kenning, 1938;Wilson, 1938;Penberthy, Johnston, and Noer, 1939;Abbott, 1941) was made in all those patients who had gross abdominal distension and were deemed to be suffering from a simple occlusion rather than a strangulation obstruction. Whilst, given time, little difficulty was encountered in passing the tube in the unobstructed patient, it was found to be almost impossible in those with faeculent vomiting.…”

Resultados preliminares del estudio de la muerte neuronal y de la expresión de la proteína bcl-2 en la enfermedad de Alzheimer

“…(•];H~I ffilfj 1 ~--------------Estos res ultados concuerdan con los hallazgos ele muerte ne uronal por apoptosis mediante la técnica TlJNEL en los cerebros con EA y la relativa indemnidad de los astrocitos incluso al rededor de las placas seniles y con los hallazgos en cultivos celulares que de muestran que la exposición a beta-amiloide produce muerte ele neuronas pero no de astrocitos (18,25 ). Los astrocitos tienen como funciones retirar excitotoxinas, producir matriz extracelular y proteínas de adhesión, restaura r el medio iónico y son un componente esencial ele la barrera hematoencefálica (26). Un aumento en la actividad de los astrocitos a través del aumento e n la expresión de bcl-2 podría tene r un efecto beneficioso aumentando las actividades previas o podría tener también un efecto adverso ya que pueden segregar citoquinas como el factor de necrosis tumoral y componentes del comple mento (27).…”