Wyniki wyszukiwania

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Polskie regulacje prawne w zakresie ochrony środowiska przed zanieczyszczeniami pochodzenia rolniczego w świetle integracji z Unią Europejską

100%

Rynkiewicz A.

Zeszyty Edukacyjne. Rolnictwo Polskie i Ochrona Jakości Wody

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2005

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tom 10

2

Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik

Ogród Warzywny Polska sp. z o.o. – produkcja i przechowalnictwo ziemniaków z ugruntowaną marką

51%

Rynkiewicz A., Lesniak P., Pieczulewicz A., Urbanowicz J.

Ziemniak Polski

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2022

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tom 32

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nr 1

3

Lipids and hypertension

51%

Rynkiewicz A., Bellwon J., Rotkiewicz-Wozniak R.

Polish Journal of Food and Nutrition Sciences

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1998

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tom 07

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nr 2

4

Biopreparaty dobre na wszystko

38%

Rynkiewicz A.

Ekopartner

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1992

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nr 01

15-16

5

Postawa ciała dzieci w wieku 7–9 lat – badania wstępne

33%

Bezulska A., Kupczyk J., Kurianska-Wołoszyn J., Milcuszek M., Rynkiewicz A., Rynkiewicz M., Woloszyn A., Rynkiewicz T.

Aktywność Ruchowa Ludzi w Różnym Wieku

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2019

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tom 3-4[43-44]

6

Angiotensin converting enzyme gene polymorphism is associated with severity of coronary artery disease in men with high total cholesterol levels

33%

Borzyszkowska J., Stanislawska-Sachadyn A., Wirtwein M., Sobiczewski W., Ciecwierz D., Targonski R., Gruchala M., Rynkiewicz A., Limon J.

Journal of Applied Genetics

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2012

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tom 53

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nr 2

This study examines whether renin-angiotensin-aldosterone system gene polymorphisms: ACE (encoding for angiotensin converting enzyme) c.2306-117_404 I/D, AGTR1 (encoding for angiotensin II type-1 receptor) c.1080*86A>C and CYP11B2 (encoding for aldosterone synthase) c.-344C>T are associated with the extension of coronary atherosclerosis in a group of 647 patients who underwent elective coronary angiography. The extension of CAD was evaluated using the Gensini score. The polymorphisms were determined by PCR and RFLP assays. The associations between genotypes and the extent of coronary atherosclerosis were tested by the Kruskal-Wallis test, followed by pairwise comparisons using Wilcoxon test. The population has been divided into groups defined by: sex, smoking habit, past myocardial infarction, BMI (>, ? 25), age (>, ? 55), diabetes mellitus, level of total cholesterol (>, ? 200 mg/dl), LDL cholesterol (>, ? 130 mg/dl), HDL cholesterol (>, ? 40 mg/dl), triglycerides (>, ? 150 mg/dl). Significant associations between the ACE c.2306-117_404 I/D polymorphism and the Gensini score in men with high total cholesterol levels (PKruskal-Wallis =0.008; Padjusted=0.009), high level of LDL cholesterol (PKruskal-Wallis =0.016; Padjusted=0.028) and low level of HDL cholesterol (PKruskal-Wallis=0.04; Padjusted=0.055) have been found. No association between the AGTR1 c.1080*86A>C and CYP11B2 c.-344C>T and the Gensini score has been found. These results suggest that men who carry ACE c.2306-117_404 DD genotype and have high total cholesterol, high LDL cholesterol and low HDL cholesterol levels may be predisposed to the development of more severe CAD.

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Molecular characterization of Polish patients with familial hypercholesterolemia: novel and recurrent LDLR mutations

27%

Chmara M., Wasag B., Zuk M., Kubalska J., Wegrzyn A., Bednarska-Makaruk M., Pronicka E., Wehr H., Defesche J. C., Rynkiewicz A., Limon J.

Journal of Applied Genetics

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2010

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tom 51

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nr 1

95-106

Autosomal dominant hypercholesterolemia (ADH) is caused by mutations in the genes coding for the low-density lipoprotein receptor (LDLR), apolipoprotein B-100 (APOB), or proprotein convertase subtilisin/kexin type 9 (PCSK9). In this study, a molecular analysis of LDLR and APOB was performed in a group of 378 unrelated ADH patients, to explore the mutation spectrum that causes hypercholesterolemia in Poland. All patients were clinically diagnosed with ADH according to a uniform protocol and internationally accepted WHO criteria. Mutational analysis included all exons, exon-intron boundaries and the promoter sequence of the LDLR, and a fragment of exon 26 of APOB. Additionally, the MLPA technique was applied to detect rearrangements within LDLR. In total, 100 sequence variations were identified in 234 (62%) patients. Within LDLR, 40 novel and 59 previously described sequence variations were detected. Of the 99 LDLR sequence variations, 71 may be pathogenic mutations. The most frequent LDLR alteration was a point mutation p.G592E detected in 38 (10%) patients, followed by duplication of exons 4-8 found in 16 individuals (4.2%). Twenty-five cases (6.6%) demonstrated the p.R3527Q mutation of APOB. Our findings imply that major rearrangements of the LDLR gene as well as 2 point mutations (p.G592E in LDLR and p.R3527Q in APOB) are frequent causes of ADH in Poland. However, the heterogeneity of LDLR mutations detected in the studied group confirms the requirement for complex molecular studies of Polish ADH patients.

Ograniczanie wyników

Polskie regulacje prawne w zakresie ochrony środowiska przed zanieczyszczeniami pochodzenia rolniczego w świetle integracji z Unią Europejską

Ogród Warzywny Polska sp. z o.o. – produkcja i przechowalnictwo ziemniaków z ugruntowaną marką

Lipids and hypertension

Biopreparaty dobre na wszystko

Postawa ciała dzieci w wieku 7–9 lat – badania wstępne

Angiotensin converting enzyme gene polymorphism is associated with severity of coronary artery disease in men with high total cholesterol levels

Molecular characterization of Polish patients with familial hypercholesterolemia: novel and recurrent LDLR mutations