Institution
University of Texas System
Education•Austin, Texas, United States•
About: University of Texas System is a education organization based out in Austin, Texas, United States. It is known for research contribution in the topics: Cancer & Population. The organization has 13901 authors who have published 10925 publications receiving 319328 citations. The organization is also known as: UT System.
Topics: Cancer, Population, Antigen, Gene, Antibody
Papers published on a yearly basis
Papers
More filters
••
01 Jan 2006
131 citations
••
TL;DR: Central nervous system relapse generally did not shorten BM CR or survival, although early primary CNS relapse was associated with early BM relapse, and leukocyte count was important, reflecting the common origin of BM and CNS leukemic cells.
Abstract: Central nervous system (CNS) involvement occurred in 45 of 222 (20.3%) leukemic adults achieving bone marrow (BM) complete remission (CR), including 12 of 23 (52%) acute undifferentiated leukemia (AUL), 12 of 32 (39%) lymphoma leukemia, 5 of 26 (19%) acute lymphoblastic leukemia, and 16 of 142 (11%) acute myelogenous leukemia. Risk factors for CNS disease were lactic dehydrogenase (LDH) greater than or equal to 25,000/mm3. AUL morphology, age less than 20 years, and extramedullary involvement were most significant. Pattern of CNS involvement varied with morphology. Survival after CNS relapse depended most on BM status and symptoms. Duration of CNS CR was longest for asymptomatic patients with low CSF cell counts. Also important were duration of first BM CR, ease of achievement of initial BM CR, and leukocyte count (original and at most closely antecedent BM involvement), reflecting the common origin of BM and CNS leukemic cells. Central nervous system relapse generally did not shorten BM CR or survival, although early primary CNS relapse was associated with early BM relapse.
131 citations
••
TL;DR: Although the pH of storage granules in exocrine and endocrine cells is different, the pH is acidic, the trans Golgi condensing vacuoles in both cells is acidic.
Abstract: A number of intracellular, membrane-bound compartments in both the endocytic and exocytic pathways of eukaryotic cells have an acidic internal pH. In endocrine cells, the mature secretory vesicle has an acidic pH; secretory vesicles isolated from exocrine cells, however, appear to have a neutral pH. Recently we have used a newly developed immunocytochemical technique to map low-pH compartments in insulin-secreting islet cells with the electron microscope and find that during the maturation of the secretory vesicle there is a progressive acidification of these vesicles that begins as soon as the trans Golgi condensing vacuoles form. Now we have used this technique to examine two exocrine cells: the pancreatic acinar cell and the parotid serous cell. In both cell types, the trans Golgi condensing vacuoles are acidic and accumulate the low-pH probe to the same extent as condensing vacuoles of insulin-secreting islet cells. Unlike insulin-secreting cells, however, maturation of the granules is accompanied by a return of luminal pH to near neutrality. Therefore, although the pH of storage granules in exocrine and endocrine cells is different, the pH of the condensing vacuoles in both cells is acidic.
130 citations
••
TL;DR: Concurrent administration of triacetyloleandomycin with drugs whose metabolism is known to be affected or that could potentially be affected should be avoided unless appropriate adjustments in dosage are made, and Coadministration of erythromycin with Drugs believed to interact should be undertaken with caution and with appropriate patient monitoring.
Abstract: The macrolide antibiotics erythromycin and triacetyloleandomycin (troleandomycin) are prescribed for many types of infections. As such they are often added to other preexisting drug therapy. Thus, there are frequent opportunities for the interaction of these antibiotics with other drugs. Both erythromycin and triacetyloleandomycin appear to have the potential to inhibit drug metabolism in the liver and also drug metabolism by micro-organisms in the gut, either through their antibiotic effect or through complex formation and inactivation of microsomal drug oxidising enzymes. Of the two agents, triacetyloleandomycin appears to be the more potent inhibitor of microsomal drug metabolism. Published studies indicate that triacetyloleandomycin can significantly decrease the metabolism of methylprednisolone, theophylline and carbamazepine. Its ability to cause ergotism in patients receiving ergot alkaloids and cholestatic jaundice in patients on oral contraceptives may also be related to its inhibitory effect on drug metabolism. Erythromycin appears to be a much weaker inhibitor of drug metabolism. There are numerous reports describing apparent interactions of erythromycin with theophylline and a lesser number of reports dealing with carbamazepine, warfarin methylprednisolone and digoxin. There are sufficient data to suggest that erythromycin can, in some individuals, inhibit the elimination of methylprednisolone, theophylline, carbamazepine and warfarin. The mean change in drug clearance is about 20 to 25% in most cases, with some patients having a much larger change than others. Like tetracycline, erythromycin also appears to have the potential for increasing the bioavailability of digoxin in patients who excrete high amounts of reduced digoxin metabolites, apparently through destruction of the gut flora that form these compounds. Concurrent administration of triacetyloleandomycin with drugs whose metabolism is known to be affected or that could potentially be affected should be avoided unless appropriate adjustments in dosage are made. Coadministration of erythromycin with drugs believed to interact should be undertaken with caution and with appropriate patient monitoring. Among the other macrolide antibiotics, josamycin has seldom been involved in causing drug interactions, while midecamycin and the older derivative spiramycin have not so far been incriminated.
130 citations
Authors
Showing all 13902 results
Name | H-index | Papers | Citations |
---|---|---|---|
Yi Chen | 217 | 4342 | 293080 |
Joseph L. Goldstein | 207 | 556 | 149527 |
Eric N. Olson | 206 | 814 | 144586 |
Hagop M. Kantarjian | 204 | 3708 | 210208 |
Thomas C. Südhof | 191 | 653 | 118007 |
Gordon B. Mills | 187 | 1273 | 186451 |
Michael S. Brown | 185 | 422 | 123723 |
Eric Boerwinkle | 183 | 1321 | 170971 |
Russel J. Reiter | 169 | 1646 | 121010 |
John D. Minna | 169 | 951 | 106363 |
Timothy A. Springer | 167 | 669 | 122421 |
Gabriel N. Hortobagyi | 166 | 1374 | 104845 |
Rodney S. Ruoff | 164 | 666 | 194902 |
Ralph A. DeFronzo | 160 | 759 | 132993 |
Ronald A. DePinho | 160 | 486 | 104039 |