Biomedical subjects
Publications and source records attributed to Z Gombos.
The metal ion-induced inhibition of tetrapyrrole biosynthesis was studied in the cyanobacterium Anacystis nidulans. The accumulation of protoporphyrin and Mg protoporphyrin due to the effect of Co(2+) and Mn(2+) treatment, respectively, pointed to two different sites of inhibition.
Testosterone, progesterone, thyroxine and triiodothyronine levels in peripheral plasma of cocks and capons were determined by RIA, corticosteroid contents by CPB method 10, 20 and 30 min as well as 1, 2 and 4 hr following a single intravenous injection of 0.5 micrograms/kg D-Lys6-LH-RH ethylamide. Testosterone level increased after 30 min, reached a peak after 1 hr, and returned after 4 hr to the control level in cocks. Plasma concentrations of progesterone and triiodothyronine did not change in response to the treatment. Thyroxine plasma level increased in cocks simultaneously with the decrease of testosterone contents between 1 and 2 hr. In capons, the increase of thyroxine did not occur, thus the promoting factor was probably not LH-RH but rather the decrease of the high testosterone level. Corticosterone level increased between the 2nd and the 4th hr in cocks and between the 1st and 4th hr in capons. This increase might have been due to the increase in thyroxine level (cocks) and the immediate stimulatory effect of the LH-RH analogue of not the C-RH type (cocks, capons).
Gastroduodenal ulceration is still poorly understood and changes in gene expression may provide new mechanistic insights. Previously, we demonstrated that angiogenic growth factors are potent ulcer healing agents, and the synthesis of bFGF, PDGF and VEGF is enhanced early in duodenal ulcer healing. The initial molecular event in duodenal ulceration seems to be the organ-specific early release of ET-1 in the pre-ulcerogenic stages after the administration of duodenal ulcerogen cysteamine in rats. We also briefly review here data from literature indicating a central role of ET-1 in gastroduodenal ulceration. After studying the involvement of immediate early genes (e.g. egr-1, Sp1) in ulcer development, we now investigated expression of other genes in the duodenal mucosa in the early stages of chemically induced duodenal ulceration in rats. Following a brief review of principles of gene expression and gene therapy, we review our preliminary gene expression studies, involving monitoring about 1200 genes which revealed about 160 signals and prominent changes in about 30 genes in the early stages of experimental duodenal ulceration. Cysteamine enhanced ET-B receptor gene expression in 30 min, while transcription factors (MAX, STAT 3) showed increased expression in 12 h. We recently also initiated gene therapy studies to enhance the local synthesis of PDGF and VEGF to accelerate duodenal ulcer healing, using a single dose of naked DNA (ND) or adenoviral (AV) vectors of VEGF and PDGF in rats with cysteamine-induced duodenal ulcers. Gene therapy with ND or AV of VEGF or PDGF significantly accelerated chronic duodenal ulcer healing, and increased levels of VEGF and PDGF were detected by Western blotting and ELISA in duodenal mucosa after both VEGF and PDGF gene therapy. Thus, gene expression studies provide new insights into the molecular mechanisms of duodenal ulceration and VEGF or PDGF gene therapy seems to be a new option to achieve a rapid ulcer healing.