PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Drug Stability”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 145 records · Page 8Linked to original sources
PubMed1990

[The effect of an aortocoronary bypass on the physical capacity of drug-stabilized patients with unstable angina pectoris].

To 51 patients with unstable angina pectoris a submaximum symptom-limited bicycle ergometry [correction of veloergometric] test was performed 3 to 6 days after stabilization by medicamentous treatment was achieved and 2 to 6 months after an aortocoronary bypass had been accomplished. During the first veloergometric test myocardial ischemia was induced in all patients--9 patients were in the IV, 18--in the III and 24--in the II functional class according to NYHA. During the second veloergometric test myocardial ischemia was induced only in 5 patients. At the end of the first year after the aortocoronary bypass had been performed 45 (88.2%) of the patients were without complaints. The predictive value of the positive veloergometric test after an aortocoronary bypass for a poor prognosis is 80% and that of the veloergometric test without induced myocardial ischemia for a favorable prognosis is 95.6%. Aortocoronary bypass in combination with medicamentous treatment improves the symptomatic state, physical capacity and the prognosis of patients with unstable angina pectoris up to the end of the first year to a considerably greater degree than the medicamentous treatment alone.

Angina, Unstable↗
PubMed1985

The effects of taxol, a microtubule-stabilizing drug, on steroidogenic cells.

The effects of taxol on steroid production and microtubule polymerization were examined using Y-1 adrenocortical tumor cells, MLTC-1 Leydig tumor cells, and primary cultures of bovine adrenocortical cells. Taxol inhibited the following steroidogenic processes within the Y-1 and MLTC-1 cells: (1) hormonal increase of steroid production, (2) dibutyryl cyclic AMP-increased steroid production, and (3) hormone-stimulated pregnenolone production. The inhibitory action of taxol was concentration dependent and also resulted in an increase in cytoplasmic microtubules. In addition, the inhibitory action of taxol on hormone-stimulated steroid production was reversible. Taxol appeared to inhibit cholesterol movement to the mitochondrial site of cholesterol side-chain cleavage enzyme but did not affect overall protein synthesis. Interestingly, taxol did not affect hormone-stimulated steroid production in bovine adrenocortical cells. This lack of inhibition may correspond to the ultrastructural observation that microtubule bundling after taxol treatment was observed in the tumor cells but not in similarly treated bovine adrenal cells. With this conflicting information between cell types, a direct relationship between taxol treatment and inhibition of steroid production has not been established. However, these results suggest that taxol alters the rate of transport of cholesterol to the cholesterol side-chain cleavage enzyme within the steroidogenic tumor cells.

Adrenal Cortex↗
PubMed1995

Distribution of acetylated tubulin in cultured cells and tissues from the Atlantic cod (Gadus morhua). Role of acetylation in cold adaptation and drug stability.

The Atlantic cod (Gadus morhua) is a poikilothermic animal living at temperatures between 2-15 degrees C. Isolated cod brain tubulin is, in contrast to mammalian brain tubulin, posttranslationally modified by acetylation to a high extent. To investigate the role of acetylation in cold adaptation, microtubules were isolated by a taxol-dependent procedure from different organs of the cod, and cells from different tissues were cultured. All cells from skin and brain were able to grow between 4 degrees C and room temperature. Microtubules in the cultured cells were sometimes severed near the periphery of the cells. Microtubules in brain cells were in general more stable to vinblastine and colchicine, when compared to skin cells. Acetylated microtubules were found only in brain cells, in peripheral nerves on scales and in nerves of the intestinal tract and in microtubules isolated from neuronal tissue. Our results show that acetylated microtubules are found both in the central and peripheral nervous system, but that there is no correlation between acetylation and cold-adaptation.

Acetylation↗
PubMed2005

Resistance to microtubule-stabilizing drugs involves two events: beta-tubulin mutation in one allele followed by loss of the second allele.

Resistance to Taxol (paclitaxel) or the epothilones (Epo) occurs via the acquisition of point mutations in beta-tubulin residues important for drug-tubulin binding. We have isolated four drug-resistant clones selected with Taxol or Epo A, which harbor distinct beta-tubulin mutations. During the development of a stable drug-resistant phenotype, early clones expressing both wild-type (wt) and mutant beta-tubulin sequences exhibited a 10-fold drug resistance, while more advanced clones expressing only the mutant beta-tubulin sequence exhibited 30 to 50-fold drug resistance. The drug-sensitive parental 1A9 ovarian carcinoma cell line and the drug resistant clones (1A9-A8, 1A9-PTX10 and 1A9-PTX22) were evaluated for loss of heterozygosity (LOH) for beta-tubulin (6p25) by single nucleotide polymorphism (SNP) and fluorescent in situ hybridization (FISH) analyses. Functional assays such as drug-induced tubulin polymerization, cell cycle analysis by FACS, DNA sequencing for beta-tubulin and mitotic index by immunofluorescence were performed to correlate the beta-tubulin LOH status with drug response in the early- and late-step drug-resistant clones. Late-step drug resistant clones revealed LOH in one allele for wt beta-tubulin in addition to a beta-tubulin mutation in the other allele leading to increased levels of drug resistance, while the early-step clones that contained both a wt and a mutant beta-tubulin allele were considerably less drug resistant. The LOH and functional assays revealed cell response that was proportional to the tubulin gene and heterozygosity status. Acquired tubulin mutations in conjunction with LOH for the wt tubulin resulted in a highly resistant phenotype, revealing a new mechanism for taxane resistance.

Alleles↗