Aleksandra Korcz

Angiotensin-converting enzyme (ACE, I/D) gene polymorphism and susceptibility to abdominal aortic aneurysm or aortoiliac occlusive disease.

BACKGROUND The purpose of this study was to examine the role of polymorphism in angiotensin converting enzyme gene (ACE, I/D) in the development of abdominal aortic aneurysm (AAA) or aortoiliac occlusive disease (AIOD). MATERIALS AND METHODS We investigated 829 individuals in 4 groups: AAA (n = 133), AIOD (n = 152), control (n = 152), and a random Polish population group (n = 392). ACE I/D gene polymorphism analysis was performed by polymerase chain reaction and gel electrophoresis. The genotype distribution was in Hardy-Weinberg equilibrium. RESULTS The genotype distribution and allele frequency of ACE I/D were not significantly different between patients with AAA or AIOD and the control or the population group. Significant differences were found between the following groups: 1) hypertensive patients with AAA and normotensive patients with AAA (OR = 3.08 95% CI 1.22-7.79, P = 0.0147); 2) hypertensive patients with AAA and the population group (OR = 2.56; 95% CI 1.27-5.16, P = 0.0066). Since the majority of subjects were male, these associations were also true when only male hypertensive subjects with AAA were compared with male normotensive patients with AAA or to male population group. No relation of the ACE gene polymorphism to hypertension in the AIOD group was found. CONCLUSIONS ACE I/D gene polymorphism is not a susceptibility factor to aortoiliac occlusive disease; however it may be an important factor in the development of AAA when coexisting with hypertension.

Risk factors in abdominal aortic aneurysm and in Polish population aortoiliac occlusive disease and differences between them [corrected].

Abdominal aortic aneurysm (AAA) and aortoiliac occlusive disease (AIOD) are multifactorial vascular disorders caused by complex genetic and environmental factors. The purpose of this study was to define risk factors of AAA and AIOD in the Polish population and indicate differences between diseases.

Species-specific Inhibitory Effect of Lupine Alkaloids on Translation in Plants

Summary The following lupine alkaloids: lupanine, 13-OH-lupanine, and angustifoline isolated fromthe seeds of L. angustifolius cv. Mirela, and commercial sparteine have been tested for their effect on selected steps of protein biosynthesis: aminoacylation of tRNA Phe and enzymatic binding of Phe-tRNA Phe to poly-U programmed ribosomes. We found that only one of these two steps-namely the binding reaction, is effected by alkaloids. Following this observation, evidence is presented that the inhibitory properties of these alkaloids are species-specific. Higher inhibitory effect (two- to ten-fold) was observed on wheat germ system (alkaloid-free) in comparison to the translational system originating from bitter lupine ( L. albus cv. Pop). On the basis of these observations we concluded that the sensitivity of the system is correlated with the presence of endogenous alkaloids which probably participate in internal interactions.

Lupin ferritin: Purification and characterization, biosynthesis and regulation of in vitro synthesis in plant system

Summary Ferritin from lupin seedlings was isolated and purified to homogeneity. Identification was performed by iron-specific staining, determination of physico-chemical properties and electron microscopy. The molecular weight of lupen ferritin under native conditions was about 500 kDa; this protein consists of three subunits (MW: 28 kDa, 26.5 kDa and 22.5 kDa). The biosynthesis of lupen ferritin has been tested ≪in vivo≫ in roots of lupen seedlings and in the ≪in vitro≫ translation system of wheat germ. During in vitro and in vivo biosynthesis ferritin is synthesized as a dominant 31 kDa or 28 kDa polypeptide, respectively. The transcriptional mechanism of ferritin biosynthesis regulation is supported by observation of higher syntheses of this protein by poly A + RNA isolated from lupin growing on FeSO 4 (in comparison to control — water conditions). Addition of the 22.5 kDa subunit to the in vitro translation system of wheat germ causes a reduction of ferritin syntheses whereas the 28 kDa subunit has no effect, This observation suggests the parallel existence of an autoregulatory mechanism of ferritin biosynthesis at the translational level.

Elongation Factor 1 in Norway Maple Seeds during the Breaking of Dormancy

Summary Elongation factor 1 is a protein responsible for the binding of AA-tRNA to the ribosomal Asite. During the breaking of dormancy of the Norway maple seeds we found significant changes of the total and specific activity of the elongation factor 1. These observations are in strict correlation with data concerning the changes in the level of polyamine concentration. Experiments carried out with EF1 from embryo axes and from cotyledons, showed basic differences in the kinetics of the binding reaction. In connection with our previous publications concerning the effect of alkaloids on the translation process and changes of polyamine concentration during stratification, we suggest that polyamines can be regulators of the translation process by modulating the activity of elongation factor 1.

Gene polymorphism -418 G/C of tissue inhibitor of metalloproteinases 2 is associated with abdominal aortic aneurysm.

OBJECTIVE The pathogenesis of abdominal aortic aneurysm (AAA) is connected with abnormal extracellular matrix remodeling, with the assistance of extracellular matrix metalloproteinases and tissue inhibitors of metalloproteinases (TIMPs). A decrease in tissue inhibitor of metalloproteinases 2 (TIMP2) gene expression was detected in AAA patients. Recently, a -418 G/C (rs8179090) polymorphism of the TIMP2 gene promoter, influencing the transcription rate of the gene, has been described. This study investigated whether the -418 G/C gene polymorphism is associated with AAA in the Polish population. METHODS The TIMP2 gene promoter polymorphism was evaluated by polymerase chain reaction, followed by restriction enzyme analysis and pyrosequencing in 128 patients affected by AAA and in 180 individuals included as references. The control group was directly matched to patients according to known risk factors for vascular diseases. RESULTS The frequency of the C allele was significantly higher in AAA patients than in the control group (odds ratio [OR], 2.516; P = .0005). The distribution of genotypes also differed significantly between the groups (CC + CG vs GG: OR, 2.906; P = .0037) or was close to being significantly different (CC vs GG + GC: OR, 2.144; P = .0501). A similar trend was observed in men but not in women. The multivariate logistic regression analysis indicated the TIMP2 gene promoter polymorphism is risk factor of AAA in the Polish population, with an adjusted OR of 4.99, when applied to a dominant inheritance model. CONCLUSIONS Our study supports the hypothesis that TIMP2 and the -418G/C polymorphism located in the promoter of the TIMP2 gene are important in AAA pathophysiology.