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Biomedical subjects

R Randazzo

Publications and source records attributed to R Randazzo.

13 recordsLinked to original sources
PubMed1992

Renal pelvic transitional cell carcinoma. The role of the kidney in tumor-node-metastasis staging.

Renal pelvic carcinoma is a rare tumor. There are several staging systems currently in use based on a bladder cancer staging model. An analysis of the American Cancer Society, Illinois Division, experience with 611 cases of renal pelvic transitional cell carcinoma suggested that the kidney parenchyma may be a determinant in the anatomic spread of disease. A tumor-node-metastasis system for renal pelvic (separate from ureteral) cancer is recommended.

Carcinoma, Transitional Cell↗
PubMed1992

Renal pelvic cancer: a review of 611 patients treated in Illinois 1975-1985. Cancer Incidence and End Results Committee.

Renal pelvic transitional cell carcinoma constitutes about 7 percent of all kidney cancer. This report is a summary of 611 Illinois patients with this tumor treated between 1975 and 1985. Overall, the five-year relative survival rate was 62 percent and the observed five-year rate was 48 percent. Stage was a major determinant of survival, as expected, in these cancer patients. The Illinois experience is reviewed and compared with the accumulated literature experience with renal pelvic cancers since 1944.

Age Factors↗
PubMed1989

Cytogenetic manifestations associated with the reversion, by gene amplification, at the HGPRT locus in V79 Chinese hamster cells.

Some HGPRT spontaneous revertants were isolated from a mutant line (E2) of V79 Chinese hamster cells and phenotypically characterized. Dot-Blot hybridization with a 32P-labelled HGPRT probe revealed an increase in the number of HGPRT sequences in some of these revertants, suggesting the occurrence of gene amplification. Cytogenetic analysis performed in three of these revertants showed a characteristic abnormally banding region (ABR) on the elongated p arm of the X chromosome. In situ hybridization in one revertant (RHE2) showed that the amplified sequences reside on the p+ arm of the X chromosome in two different localizations. Because of the very probably clonal origin of the revertant, these features indicate that the amplified sequences might rearrange after their integration into the chromosome.

Animals↗
PubMed1988

Chromosome aberrations associated with CAD gene amplification in Chinese hamster cultured cells.

Eleven sublines with increasing resistance to N-phosphonacetyl-L-aspartate (PALA) were isolated from the V79,B7 Chinese hamster cell line. Aspartate transcarbamylase activity and CAD gene copy number increased with increasing resistance of sublines. In situ hybridization with a DNA probe for the CAD gene showed that the amplified sequences resided in the terminal region of a marker chromosome with elongated q arms. This region stained homogeneously after G-banding. A high incidence of both numerical and structural chromosome aberrations was found in PALA-resistant cells. In hyperdiploid and polyploid cells, containing 2 copies of the marker chromosome, dicentrics were found at a very high frequency. As indicated by in situ hybridization and G-banding, they originated from a rearrangement involving 2 homologous marker chromosomes.

Animals↗
PubMed1987

Modulation of induced reversion frequency by nucleotide pool imbalance as a tool for mutant characterization.

Addition of thymidine (TdR) or deoxycytidine (CdR) to the culture medium during posttreatment incubation affected the frequency of mutagen-induced reversion in three hypoxanthine-guanine phosphoribosyl transferase-deficient mutants of V79 Chinese hamster cells. With two of the mutants (E20 and I3), reversions induced by N-ethylnitrosourea, ethyl methanesulfonate, and methyl methanesulfonate were enhanced by TdR and were either decreased (E20) or not affected (I3) by CdR. With the third mutant (E21), alkylating agent-induced reversions were enhanced by CdR and decreased by TdR. Finally, 6-amino-2-hydroxypurine induced reversions were enhanced by TdR in mutant I3 and were decreased by TdR or deoxyadenosine (AdR) and enhanced by CdR in mutant E21. An attempt was made to reconcile these results with simple mutation mechanisms, based on either G:C to A:T or A:T to G:C transitions. It is suggested that the present approach may add useful information to studies of specific revertibility of mammalian cell mutants with known mutagens.

Animals↗
PubMed1984

Recovery of V79 cell clones with different phenotypes in aminopterin- or azaserine-containing media used for the selection of HGPRT revertants.

Three 6-thioguanine (6TG)-resistant mutants were mutagen-treated and selected for clones capable of growing in 2 selective media: HAT medium, containing aminopterin (AP) and HAS medium, containing L-azaserine (AS). Both 6TG-sensitive, wild-type clones and 6TG-resistant mutants were found among colonies growing in HAT medium, while only 6TG-sensitive clones grew in HAS medium. Time for expression was required by 6TG-resistant but not by 6TG-sensitive clones, that were fully expressed immediately after treatment. All HAT-resistant, 6TG-resistant clones which were analyzed proved to be resistant to AP. These data were interpreted as follows: in HAT medium, both HGPRT+ revertants and double mutants (HGPRT-, AP-resistant) were selected, while only HGPRT+ revertants were selected in HAS medium. Not all 6TG-resistant mutants were able to produce both classes of HAT-resistant clones.

Aminopterin↗
PubMed1984

Instantaneous renal arterial pressure-flow relations in anesthetized dogs.

Instantaneous renal arterial pressure-flow (P/ Qra ) relations were investigated in 11 anesthetized dogs using the nonpulsatile fall in aortic pressure and renal arterial flow ( Qra ) during cardiac arrest caused by vagal stimulation. We found that P/ Qra relations were linear with an extrapolated zero flow intercept (Ped, effective downstream pressure) of 20.8 +/- 1.9 mmHg and the reciprocal of the slope (Ra, arterial resistance) of 0.6 +/- 0.04 mm Hg X ml-1 X min. These values are markedly lower than the values found in similar experiments in coronary and femoral arteries. Raising renal venous pressure (5 dogs) decreased Qra and elevated Ra and Ped in the ipsilateral renal artery while decreasing Qra and elevating Ra but not Ped in the contralateral renal artery. Carotid artery occlusion (6 dogs) decreased Qra and elevated Ra and Ped. Alpha-Adrenergic blockade (4 dogs) lowered Ped and Ra. Arterial resistance seems to be more important for change in P/Q relations in the renal arterial bed than it is in other arterial beds investigated so far. We suggest that the effective downstream pressure to renal arterial flow is downstream from the glomerular capillaries. The location of the "vascular waterfall " phenomenon appears to be between the intrarenal veins and the veins outside the capsule.

Anesthesia, General↗
PubMed1977

Anti-inflammatory agents in experimental atherosclerosis. Part 2. Failure of antihypertensive drugs to exacerbate atherosclerotic plaque formation.

Hypertension is associated with an increased incidence of generalized vascular disease. Antihypertensive drug therapy, while decreasing overall mortality due to cerebral hemorrhage, myocardial hypertrophy or renal failure, paradoxically does not appear to reduce the incidence of coronary atherosclerosis. This study investigates whether the drugs, as a possible side effect, may have an adverse influence on the development of atherosclerotic plaques. Groups of rabbits were fed an atherogenic diet containing 1% cholesterol for 12 weeks. Two commonly used antihypertensive agents (methyldopa and chlorthalidone) were added to the diet of some groups at levels of 100 mg and 10 mg per day respectively. No significant increase in total atherosclerotic plaque area was produced by either of the drugs tested singly or in combination. Plasma renin levels were only mildly elevated and in this experimental system there was no correlation between renin activity and atherosclerotic plaque intensity. There is thus no evidence from this study that antihypertensive drugs have any adverse effects on atherosclerotic plaque formation. While the ineffectiveness of these drugs against coronary atherosclerosis may indicate that normalization of pressure cannot arrest changes already initiated, it also supports the possibility that association of atherosclerosis with hypertension may be symptomatic of a common underlying defect not correlated by normalizing blood pressure.

Animals↗
PubMed1976

Localized mutagenesis in Streptomyces coelicolor A3 (2).

Nutritional mutants (co-mutants) were scored among nitrosoguanidine-induced revertants of four mutations in Streptomyces coelicolor A3 (2). All co-mutations were due to mutations in genes linked to the revertant locus. The co-mutant loci were located in a region of about 20 map units around the revertant locus (co-mutation region). Revertants for different loci showed co-mutation patterns different from each other and from that of random nitrosoguanidine-induced forward mutations. Mutations appeared to be completely abolished outside the co-mutation region (mutation restriction).

Cell Nucleus↗
PubMed1973

Comutation in Streptomyces.

Up to 6% of N-methyl-N'-nitro-N-nitrosoguanidine-induced back mutations in the hisA locus of Streptomyces coelicolor were forward mutations (comutations) in another closely linked his locus.

Alleles↗
PubMedDate not supplied

Anti-inflammatory drugs in experimental atherosclerosis. Part 5. Influence of cortisone acetate on short-term and long-term cholesterol fluxes in atherosclerotic aorta.

Previous studies in this series have shown that cortisone and other anti-inflammatory drugs inhibit atherosclerotic plaque development in cholesterol-fed rabbits. The present study was designed to investigate the influence of cortisone on the processes of cholesterol influx and efflux in the aorta wall. Forty-seven New Zealand white rabbits were fed a 1% cholesterol diet for periods up to 12 weeks. In addition 23 of the animals were fed 5 mg cortisone acetate daily. At 0, 5 and 12 weeks, groups were fed a tracer dose of [3H]cholesterol. Plasma cholesterol specific radioactivity was measured at intervals during the next 10 days. Total aorta cholesterol and its specific activity were measured by killing groups of animals at 2 days and 10 days. Atherosclerotic plaque intensity at 12 weeks, measured planimetrically, averaged 68 +/- 12% in controls vs. only 6 +/- 3% in cortisone-treated animals. During the period between 5 and 12 weeks, net cholesterol accumulation by chemical analysis averaged only 11 micrograms/g aorta/day in cortisone-treated animals vs. 117 micrograms/g in controls. [3H]cholesterol influx (measured during a brief 2-day exposure) at 5 weeks averaged 206 and 199 micrograms/g tissue/day and at 12 weeks 586 micrograms and 281 micrograms/day in control and cortisone-treated animals, respectively. Measured over a longer 10-day period, however, the apparent influx of [3H]cholesterol was much less in cortisone-treated animals, averaging only 53 micrograms/day compared to 269 micrograms/day in controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗