Colon cancer screening and the evaluation and follow-up of colonic polyps.

Approximately 150,000 new cases of colon cancer are diagnosed each year, and the mortality rate continues to be greater than 50% of those diagnosed. Screening for colon cancer should be part of the routine health maintenance program of the primary physician. Use of history, physical examination, and sigmoidoscopy is part of a complete program. Colonoscopic removal of polyps reduces cancer risk.

Cytoprotection and stress ulceration.

The stomach possesses many mechanisms for protection against stress ulceration. The gastric microcirculation, prostaglandins, mucus secretion, epithelial cell renewal, and muscle tone are factors involved in gastric cytoprotection. Therapy is partially directed at augmenting these natural physiologic defense mechanisms to prevent and promote healing of stress ulceration. Drugs such as sucralfate, carbenoxalone, colloidal bismuth, and prostaglandins are used. Stress ulceration is an important cause of upper gastrointestinal tract hemorrhage in postoperative and critically ill patients in the intensive care unit setting. Preventive therapy includes neutralization of gastric acid by antacids, suppression of gastric acid secretion by H2-receptor blockers, administration of cytoprotective agents, and correction of the underlying stress state. Active bleeding requires accurate diagnosis by gastroscopy. Additional therapy may be necessary, including intra-arterial administration of vasopressin and occasionally surgery. Dieulafoy's lesion is an unusual stress-related cause for upper gastrointestinal bleeding. The area of mucosal injury is minute but underneath lies a large submucosal gastric artery. It can cause massive bleeding and is often missed at initial gastroscopy. The pathogenesis of Dieulafoy's lesion is complex and the mainstay of therapy has been surgical. Ligation of the vessel, wedge resection, or proximal gastric resection is performed. Therapeutic endoscopy with endoscopic cauterization or injection has changed the approach to this lesion.

Axonal transport and transcellular transfer of nucleosides and polyamines in intact and regenerating optic nerves of goldfish: speculation on the axonal regulation of periaxonal cell metabolism.

The axonal transport, metabolism, and transcellular transfer of uridine, adenosine, putrescine, and spermidine have been examined in intact and regenerating optic nerves of goldfish. Following intraocular injection of labeled nucleosides, axonal transport was determined by comparing left-right differences in tectal radioactivity, and transcellular transfer was indicated by light autoradiographic analysis. The results demonstrated axonal transport, transcellular transfer, and periaxonal cell utilization of both nucleosides in intact axons and severalfold increases of all of these processes in regenerating axons. Experiments in which the metabolism of the nucleosides was studied resulted in data which suggested that uridine and adenosine, when delivered to the tectum by axonal transport, are protected from degradation and thus are relatively more available for periaxonal cell utilization than nucleosides reaching these cells via the blood. In intact axons, the majority of the nonmetabolized radioactivity was present as UMP, UDP, and UTP following [3H]uridine injections, whereas the majority of the radioactivity following [3H]adenosine injections was present as adenosine, with the phosphorylated derivatives constituting a smaller proportion. During nerve regeneration, the relative proportion of nucleosides to nucleotides was reversed, with uridine being the principal labeled compound in the first case, and AMP, ADP, and ATP being the major labeled compounds in the latter case. The nucleosides also were found to be different from each other in that adenosine, but not uridine, can be taken up by optic axons and transported retrogradely from the tectum to retinal ganglion cell bodies in the eye. Following intraocular injection of [3H]spermidine, radioactivity was transported to the optic tectum and transferred to tectal cells in the vicinity of the regenerating axons. Following [3H]putrescine injections, silver grains were found over periaxonal glia, but preliminary findings suggest that they are not present over tectal neurons nor over radial glial cells in the periependymal layers. Analysis of tectal radioactivity showed in each case that it was composed primarily of the injected compounds. These studies indicate that, following axonal transport, the polyamines do not remain within regenerating axons but are transferred to cells surrounding the axon. On the basis of these and previous findings, we speculate that the axonal transport and transcellular transfer of uridine, adenosine, polyamines, and perhaps other small molecules are means of communication between axons and periaxonal cells; that the axon can affect RNA and protein synthesis in periaxonal cells by regulating the availability of these small molecules; and that, during nerve regeneration, the increased metabolic needs of periaxonal cells are met by an increased axonal supply of precursors (adenosine and uridine) and other molecules (polyamines) critical for protein synthesis.