A classical model of educational cooperation in Human Anatomy: the Table Leaders.

This project has been developed for many years in the Human Anatomy courses.Its good outcomes have been confirmed by years of evidence of excellent resultsobtained through the learning of Human Anatomy. This method of teaching andlearning as one allows students who are taking Human Anatomy classes to receivepractical training in small groups and transmit it to their colleagues in the practicaltraining established in the Medical degree. Table Leaders feel rewarded as theylearn to speak in public, regularly transmitting the knowledge obtained, and byhaving to be up to date with their studies. These are all aspects that help, not onlythe Table Leaders process of learning, but also that of their colleagues, who seeclosely and carefully anatomical details that help them understand the subject.This method of supporting practical training is always under the supervision ofthe teacher who develops the practical classes. These Leaders used to pass thetest without additional problems. Thus the note was significantly increased versusthe class colleagues.

A useful experimental model of short bowel syndrome.

The short bowel syndrome is a well-known human clinical entity that produces serious metabolic disorders. This syndrome arises after a massive resection of more than 50% of the small intestine, when the intestine attempts to minimize the consequent irregularities by means of compensatory mechanisms. Many reports suggest that an exocrine and endocrine pancreatic dysfunction is associated with enterohormones and an abnormal altered nutrient flow. In this report, we present an experimental model of short bowel syndrome in rats. A massive intestine resection was performed in rats, followed by a histological study of the small intestine. We report the histological changes related to the compensatory changes that occurred in the remaining intestine. The residual intestine produces a hyperplasic response, and hypertrophy was seen in the portion proximal to the anastomosis. We believe this experimental model of short bowel syndrome could be a very useful tool for studying the enterohormonal changes related to an abnormal blood flow of nutrients.

A Useful Experimental Model of Short Bowel Syndrome.

The short bowel syndrome is a well-known human clinical entity that produces serious metabolic disorders. This syndrome arises after a massive resection of more than 50% of the small intestine, when the intestine attempts to minimize the consequent irregularities by means of compensatory mechanisms. Many reports suggest that an exocrine and endocrine pancreatic dysfunction is associated with enterohormones and an abnormal altered nutrient flow. In this report, we present an experimental model of short bowel syndrome in rats. A massive intestine resection was performed in rats, followed by a histological study of the small intestine. We report the histological changes related to the compensatory changes that occurred in the remaining intestine. The residual intestine produces a hyperplasic response, and hypertrophy was seen in the portion proximal to the anastomosis. We believe this experimental model of short bowel syndrome could be a very useful tool for studying the enterohormonal changes related to an abnormal blood flow of nutrients.

Ontogenic attendance of neuropeptides in the embryo chicken retina.

We have examined the ontogeny of somatostatin-, Glucagon-, Vasoactive Intestinal Polypeptide-, Substance P-, Neuropeptide Y, and Calcitonin gene-related peptide-Iike structures in the chicken retina by immunocytochemistry. Neuroblastic cells containing Substance P-Iike immunoreactivity (IR) first appeared at embryonic day 5 in the peripheral portion of the retina. Somatostatin-like immunoreactivity was detected as early as embryonic day 11 in the innermost level of the inner neuroblastic layer. The distribution pattern of amacrine cells containing Vasoactive Intestinal Peptide-Iike immunoreactivity was similar to that for Neuropeptide Y- and Calcitonin gene-related peptide-Iike immunoreactive cells. These three types of IR cell appeared at embryonic day 13. Glucagon-like immunoreactive cells first appeared in the retina at embryonic day 15, in the innermost part of the inner nuclear layer. From the 13th to 15th day of incubation, the number and intensity of Calcitonin gene-related peptide-, Somatostatin-, Neuropeptide Y- and Substance P-Iike immunoreactive cells increased and then decreased progressively before hatching. Glucagon immunoreactive cells increased in number on the last day before hatching. After embryonic day 15, the amacrine cells containing Vasoactive intestinal peptide-Iike immunoreactivity decreased notably in number. Our study showed that development of these immunoreactive structures was different for each neuropeptide. These differences in development may reflect the diverse neurophysiological roles of these neuroactive peptides, which could act as neurotransmitters/neuromodulators at the chick retinal level. Their presence may indicate roles as neuronal differentiation or growth factors.