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Biomedical subjects

G Jonas

Publications and source records attributed to G Jonas.

10 recordsLinked to original sources

Binding of phage-displayed HIV-1 Tat to TAR RNA in the presence of cyclin T1.

The transactivator protein (Tat) of the human immunodeficiency virus (HIV) is a key regulatory protein in the viral replication cycle. Together with cellular cyclin T1 and an RNA element (transactivation response; TAR) located at the 5' end of all viral transcripts, it forms a ternary complex that ultimately enhances the expression of all viral genes. In this ternary complex, cyclin T1 interacts directly with Tat and TAR. The presence of cyclin T1 is essential for high TAR RNA affinity and specificity of Tat. To study protein-protein and protein-RNA interaction, we developed a phage display system that displays functional Tat on the surface of bacteriophage M13. The addition of recombinant cyclin T1 to the selections yielded a phage display system that mirrors all binding properties of the cyclin T1-Tat-TAR complex known from cell assays and biochemical studies. Phage-displayed Tat protein as well as the cyclin T1 are fully functional. The relative binding capabilities of wild-type- and mutant Tat-displaying phages show that the presence of cyclin T1 significantly reduces the importance of basic residues in the basic sequence region of Tat for its binding to TAR.

Amino Acid Sequence↗

Chronic omeprazole treatment increases duodenal susceptibility to ethanol injury in rats.

To test whether omeprazole would increase the susceptibility of the duodenum to damage, 200 to 250-g male Sprague-Dawley rats were given 10 mg/kg of omeprazole (Losec) by gavage every morning for 29 days. Control rats were given gavage buffer alone. After fasting overnight, half the rats received 10 mg/kg indomethacin intraperitoneally; then all rats were given 2 ml of 50% ethanol by gavage. Three hours later the rats were killed and the stomach and duodenum removed and histologic injury to the duodenal mucosal was quantitated. In omeprazole pretreated rats, gavage with ethanol resulted in a significant twofold worsening of duodenal injury. Pretreatment with indomethacin to decrease endogenous prostaglandin production resulted in more severe ethanol-induced duodenal injury in both groups; however, there were no longer statistically significant differences between the omeprazole and control groups. Measurement of duodenal mucosal synthesis of prostaglandin E2 showed no difference between the omeprazole and control groups. Thus chronic administration of omeprazole appears to increase the susceptibility of the duodenal mucosa to ethanol injury in rats. The mechanism of this effect is as yet unknown but does not appear to be prostaglandin-mediated.

Animals↗

Nurses in the Gulf.

A year ago, the nurses of the 18th Airborne COSCOM, 44th Med Brigade, 5th Mobile Army Surgical Hospital Unit, and the 46th Combat Support Hospital with the 24th Infantry Division arrived in the Saudi Arabian desert. Their experiences left some of them challenging accepted stateside nursing procedures.

Anecdotes as Topic↗

Effect of portal hypertension on in vivo bile acid-mediated small intestinal mucosal injury in the rat.

This study's purpose was to determine whether portal hypertension adversely affects small intestinal mucosal injury. Portal hypertension was produced in male Sprague-Dawley rats by two-stage ligation of the portal vein. Sham-operated rats were used as controls. Two weeks later, intestinal injury was produced by in vivo perfusion with 5 mM chenodeoxycholic acid for 30 min. Intestinal injury was assessed by quantitative morphometry and by measuring intestinal water and mannitol absorption. Portal hypertension resulted in more injury in the distal perfused intestine as manifested by increased villus tip denudation [portal hypertensive 52.5 +/- 9.6 (SEM) vs controls 28.1 +/- 5.7 microns, P = 0.05). Additionally there was a significant decrease in the unperfused duodenal villus height in portal hypertensive rats (portal hypertensive 755 +/- 22 vs controls 848 +/- 28 microns, P less than 0.02). Portal hypertension had no significant effect on the increase in mannitol absorption or water secretion caused by chenodeoxycholic acid perfusion. This study suggests that portal hypertension alters small intestinal mucosa and increases susceptibility to injury.

Absorption↗

Chemical colitis due to endoscope cleaning solutions: a mimic of pseudomembranous colitis.

A unique form of colitis was observed during endoscopy of the lower gastrointestinal tract in 21 patients. The patients were prepared using either tap-water enemas or standard lavage solutions. Patients were found to have discrete or confluent white plaques adherent to the colonic mucosa, mild to severe erythema of the surrounding mucosa, and variable amounts of foamy liquid upon withdrawal of the endoscope. Stool assays for Clostridium difficile toxin and bacterial cultures were negative. Mucosal biopsies revealed vacuolar changes in the lamina propria, with slight to moderate vascular congestion and foci of intramucosal hemorrhage. Five patients developed rectal bleeding, tenesmus, and increased frequency of stools, lasting up to 12 days. We believe these cases were due to contamination of the endoscope's air-water channel with solutions used during endoscope cleaning. Recognition of this entity is important, as it is preventable and may mimic pseudomembranous colitis.

Colitis↗

Candida albicans arthritis in a healthy adult.

Candida arthritis developed postoperatively in a healthy man in whom initial operative cultures had shown no infection. The possibility of iatrogenic infection with fungus should be considered.

Arthritis, Infectious↗