Polymorphism of the IL-8 gene and the risk of ovarian cancer.

Ovarian cancer still represents a challenge in gynecological oncology. Most patients are diagnosed in an advanced tumor stage. No specific screening or prevention strategies for ovarian cancer exist as of yet. Interleukin 8 (IL-8) is a pro-inflammatory chemokine known for its angiogenetic activity, and is supposedly responsible for tumor-associated angiogenesis in several malignant tumors. The aim of the study was to investigate the susceptibility of patients with an IL-8 gene polymorphism to developing ovarian cancer. Four single nucleotide polymorphisms (SNPs) (IL-8 -251, IL-8 +781, IL-8 +1633 and IL-8 +2767) of the IL-8 gene were screened, using the PCR method in 268 patients with ovarian cancer and 426 healthy women as a control group. Significant associations were noted in patients with the IL-8 +781 (T/T) genotype (p=0.0048) with increased frequencies of ovarian cancer, while women with the IL-8 +781 (C/C) allele suffer from ovarian cancer significantly less frequently (p=0.0003). Furthermore, the IL-8 +2767 (T/T) genotype is also associated with a higher risk of ovarian cancer (p=0.0177). Our results indicate, for the first time, that IL-8 polymorphism is associated with ovarian cancer.

N-acetylation and debrisoquine type oxidation polymorphism in Caucasians--with reference to age and sex.

Phenotypes of the N-acetylation and debrisoquine type oxidation polymorphism were determined with sulfamethazine and debrisoquine in 145 healthy volunteers (31-80 years, 64 males, 81 females) of a North-East German area. Seventeen (11.7%) were poor metabolizers of debrisoquine and 81 (55.9%) slow acetylators of sulfamethazine. No significant correlations between the frequencies of oxidation and acetylation phenotypes, age, and sex were found. Only a tendency of rapid acetylators to accumulate among individuals above 60 years was noticed. Parameters of phenotyping were not influenced by sex. With age, metabolic ratios of N-acetylation but not of oxidation phenotyping increased. The urinary excretion (0-8 hours) of debrisoquine, sulfamethazine and their metabolites was strikingly reduced in the elderly. Misclassifications of acetylation phenotyping cannot be excluded because of the age dependent kinetics of the test drug.

[A concentration measuring error-induced calculation error in determining uric acid clearance in dialysis: a simulation study]. / Durch Konzentrationsmessfehler verursachte Kalkulationsfehler bei der Berechnung der Harnstoffclearance unter Dialyse: Eine Simulationsstudie.

Three calculation methods to estimation of the total clearance of dialysis patients are evaluated. The basis of calculation are concentration values of urea in blood versus dialysate. The variation coefficient of the measurement errors is 5 percent. The error formation in three estimation formulas is examined. The formula [formula: see text] is most suitable, if as evaluation criteria the variation coefficient of the estimation error are used. The parameters like dialysate flow, blood flow, ultrafiltration rate and dialysate volume are of relative value.

Interactions of dihydralazine with furosemide in hypertonic patients.

In 9 hypertensive patients stage II we studied whether dihydralazine, which is known to increase the renal blood flow, influences the elimination of furosemide (40 mg i.v.) when given additionally over a period of 2 weeks (75 mg daily). The results were compared with data from 9 healthy volunteers. The most important alterations in hypertonics were significantly increased half-lives (28.0 +/- 3.7 and 35.1 +/- 5.7 min), distribution coefficients (0.105 +/- 0.017 and 0.132 +/- 0.028 ml/g) and unchanged plasma clearances (2.62 +/- 0.33 and 2.59 +/- 0.27 ml min-1 X kg-1). Pretreatment with dihydralazine resulted in normalization of distribution coefficients (0.134 +/- 0.027 and 0.102 +/- 0.020 ml/g), decrease in plasma clearance (2.55 +/- 0.29 and 2.08 +/- 0.23 ml min-1 X kg-1) without alterations in half-lives (36.3 +/- 6.0 and 34.2 +/- 7.0 min). The authors conclude that the effects after dihydralazine co-medication are only distribution mediated.

The influence of the acetylator phenotype for the clinical use of dihydralazine.

Dihydralazine is a substrate of the human N-acetyltransferase. Therefore the acetylator phenotype could influence the pharmacodynamic response of dihydralazine and/or side effects of this drug. In this study it could be shown that: among patients with dihydralazine incompatibility slow acetylators preponderated; the risk of early side effects was higher in females than in males; and the ratio of fast/slow acetylators was higher in dihydralazine treated patients than in patients treated with other antihypertensives. Dihydralazine should be given very cautiously to female hypertonic patients that are slow acetylators.

On a nonparametric test of location.

The aim of this paper is to give some corrections to the article of Matos and Heppes "A simple nonparametric procedure: the Maximin-test", published in 1981, volume 19 of this journal.

Albumin binding of photobilirubin II.

Photobilirubin II, a stereoisomer of bilirubin, binds to human serum albumin at a single binding site (K = 2.2 x 10(6)M-1), presumably the high-affinity bilirubin-binding site. Binding in the secondary (class II) binding sites is of minor importance. The results are discussed with respect to photometabolism of bilirubin and as a possible source of error in the determination of bilirubin unbound to albumin.

The genetic linkage between the PKU locus and the loci for amylase 1, amylase 2, Fy, PGM 1, and Rh and the question of assignment of the PKU locus to chromosome no. 1.

The alpha-amylase loci Amy 1 and Amy 2 and other loci on chromosome 1 were investigated for their linkage relationship to the PKU locus. Ten families were informative for the study of linkage between PKU/Amy, 20 for PKU-Fy, 11 for PKU/PGM 1, and 10 for PKU/Rh linkage. The probabilities of linkage at different recombinant fractions were calculated according to Bayes' theorem. The results are in striking contrast with those of Kamaryt et al. who found strong evidence for close linkage between the amylase loci and the PKU locus, whereas with our results close linkage can be excluded; loose linkage is possible but unlikely. The results are discussed with regard to the genetic heterogeneity of phenylketonuria.