Wyniki wyszukiwania

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Apolipoprotein E genotypes in sporadic early and late-onset Alzheimer's disease

100%

Kowalska A., Florczak J., Pruchnik-Wolinska D., Kraszewski A., Wender M.

Archivum Immunologiae et Therapiae Experimentalis

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1998

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tom 46

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nr 3

2

The effect of nebivolol on atherogenesis in apoE - knockout mice

72%

Kus K., Gajda M., Pyka-Fosciak G., Toton-Zuranska J., Pawlowska M., Suski M., Niepsuj A., Nowak B., Wolkow P., Olszanecki R., Jawien J., Korbut R.

Journal of Physiology and Pharmacology

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2009

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tom 60

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nr 4

163-165

Nebivolol is a novel beta1-blocker with a nitric oxide (NO) - potentiating, vasodilatory effect that is unique among beta-blockers. It was already shown that nebivolol ameliorates atherosclerosis in cholesterol-fed rabbits. We, therefore, wanted to investigate whether this is the case in the fine experimental model of atherosclerosis: apolipoprotein E (apoE)- knockout mice. Nebivolol attenuated atherogenesis, measured both by "en face" method (9.23±1.8% vs. 14.6±2.1%) and "cross-section" method (63125±8455 µm2 vs. 91416±8357 m2). This is the first report showing the effect of nebivolol on atherogenesis in gene-targeted mice.

3

Significant deterioration of anti-atherogenic efficacy of nebivolol in a double (apolipoprotein E and endothelial nitric oxide synthase) knockout mouse model of atherosclerosis in comparison to single (apolipoprotein E) knockout model

72%

Kus K., Wisniewska A., Toton-Zuranska J., Olszanecki R., Jawien J., Korbut R.

Journal of Physiology and Pharmacology

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2014

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tom 65

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nr 6

4

AVE 0991 - angiotensin-(1-7) receptor agonist, inhibits atherogenesis in apoE - knockout mice

72%

Toton-Zuranska J., Gajda M., Pyka-Fosciak G., Kus K., Pawlowska M., Niepsuj A., Wolkow P., Olszanecki R., Jawien J., Korbut R.

Journal of Physiology and Pharmacology

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2010

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tom 61

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nr 2

Recent evidence shows that the renin-angiotensin system is a crucial player in atherosclerotic processes. It was also proved that Ang II promotes atherogenesis. Angiotensin-(1-7) [Ang-(1-7)] opposites Ang II action. Therefore, we would like to find out whether Ang-(1-7) receptor agonist: AVE 0991, could ameliorate atherosclerosis progression in an experimental model of atherosclerosis: apolipoprotein E (apoE) - knockout mice. AVE 0991 inhibited atherogenesis, measured both by “en face” method (7.63±1.6% vs. 14.6±2.1%) and “cross-section” method (47 235±7 546 µm2 vs. 91 416±8 357 µm2). This is the first report showing the effect of AVE 0991 on atherogenesis in gene-targeted mice.

5

Heart rate reduction with ivabradine in the early phase of atherosclerosis is protective in the endothelium of ApoE-deficient mice

72%

Aquila G., Morelli M. B., Vieceli Dalla Sega F., Fortini F., Nigro P., Caliceti C., Ferracin M., Negrini M., Pannuti A., Bonara M., Pinton P., Ferrari R., Rizzo P.

Journal of Physiology and Pharmacology

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2018

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tom 69

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nr 1

6

ApoE polymorphism in Polish patients with Alzheimer's disease

72%

Lalowski M. M., Czyzewski K., Pfeffer A., Barcikowska M., Kwiecinski H.

Acta Neurobiologiae Experimentalis

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1998

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tom 58

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nr 1

7

Involvement of plasma proteins in liposome-hepatocyte interactions

72%

Yan X., Scherphof G. L., Kamps J. A. A. M.

Cellular and Molecular Biology Letters

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2005

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tom 10

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nr Suppl.

8

Inhibition of nuclear factor-kappaB attenuates atherosclerosis in apoE-LDLR - double knockout mice

72%

Jawien J., Gajda M., Mateuszuk L., Olszanecki R., Jakubowski A., Szlachcic A., Karabiowska M., Korbut R.

Journal of Physiology and Pharmacology

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2005

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tom 56

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nr 3

Nuclear factor - B (NF-B) is a good therapeutic target for cardiovascular disease and numerous efforts are being made to develop safe NF-B inhibitors. Nowadays many authors address NF-B as a major therapeutic target in atherosclerosis, especially for preventive measures, in the light of two main hypothesis of atherosclerosis: oxidation and inflammation. We hypothesized that ammonium pyrrolidinedithioocarbamate (PDTC) - a well-known inhibitor of NF-B could inhibit the development of atherosclerosis in this experimental model. We used apoE/LDLR - DKO mouse model, which is considered as a one of the best models to study the anti-atherosclerotic effect of drugs. In this model PDTC inhibited atherogenesis, measured both by "en face" method (25,15±2,9% vs. 15,63±0,6%) and "cross-section" method (565867±39764 µm2 vs. 291695±30384 µm2). Moreover, PDTC did not change the profile of cholesterol and triglycerides in blood. To our knowledge, this is the first report that shows the effect of PDTC on atherogenesis in gene-targeted apoE/LDLR - double knockout mice.

9

Triple immunofluorescence labeling of atherosclerotic plaque components in apoE-LDLR mice

58%

Gajda M., Jawien J., Mateuszuk L., Lis G. J., Radziszewski A., Chlopicki S., Litwin J. A.

Folia Histochemica et Cytobiologica

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2008

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tom 46

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nr 2

143-146

10

Comparison of acetaminophen toxicity in primary hepatocytes isolated from transgenic mice with different apolipoprotein E alleles

58%

Mezera V., Kucera O., Moravcova A., Peterova E., Rousar T., Rychtrmoc D., Sobotka O., Cervinkova Z.

Journal of Physiology and Pharmacology

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2015

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tom 66

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nr 6

11

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Effect of caloric restriction on liver function in young and old ApoE/LDLr-/- mice

58%

Kostogrys R. B., Franczyk-Zarow M., Manterys A., Wybranska I.

Roczniki Państwowego Zakładu Higieny

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2018

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tom 69

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nr 1

Background. Caloric restriction (CR) leads to decrease metabolic intensity, which results in a reduction of oxygen consumption and the amount of free radicals. This can affect the function of the liver. Studies show that caloric restriction does not alter or significantly increase the enzyme activity associated with gluconeogenesis, but the effect was different according to the age of the model animals. Objective. The aim of the study was to determine the effect of caloric restriction on liver function in young and old ApoE/ LDLr-/- mice. Material and methods. Dietary experiments were performed on 2 and 5 month old male ApoE/LDLr-/- mice. Animals were divided into 3 experimental groups (n=6) and fed AIN’93G diet for 8 and 5 weeks, respectively. Control animals were fed ad libitum (AL) and housed in a colony cages. These animals were checked for dietary intake. The second group were also fed ad libitum but the animals were kept individually in cages (stress AL- sAL). Similarly to sAL group, the animals from the CR group were kept individually but received a 30% less diet compared to AL group. At the end of the experiment animals were euthanized and the blood, liver and adipose tissue have been collected. Alanine aminotransferase (ALT) as well as aspartate aminotransferase (AST) were measured in plasma. Fatty acid profile was evaluated (relative %) in adipose tissue (GC-MS). Liver’s stetosis was assessed. Results were analyzed statistically (ANOVA, STATISTICA v.10.0). Results. CR ApoE/LDLr-/- mice showed significantly lower body weight compared to animals, both AL and sAL. There were no significant differences between ALT and AST in both younger and older animals. However, negative tendencies were more pronounced in younger animals. In young animals CR significantly increased liver weight compared to AL (4.14 vs 3.73g/100g). In adipose tissue fatty acid profile differed in CR mice compared to control in young animals. Conclusions. Caloric restriction did not affect liver enzymes in mice. Caloric restriction showed similar but not identical metabolic activity in young and old mice.

12

The effect of doxycycline on atherogenesis in apoE-knockout mice

58%

Pawlowska M., Gajda M., Pyka-Fosciak G., Toton-Zuranska J., Niepsuj A., Kus K., Bujak-Gizycka B., Suski M., Olszanecki R., Jawien J., Korbut R.

Journal of Physiology and Pharmacology

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2011

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tom 62

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nr 2

Doxycycline at subantimicrobial doses inhibits matrix metalloproteinases (MMPs) activity, and is the only MMP inhibitor which is widely available in clinical practice. The aim of the study was to reveal whether non-specific MMPs inhibition by tetracycline could ameliorate development of atherosclerosis in apolipoprotein E (apoE)-knockout mice. Doxycycline (1.5 mg/ kg b.w./day) administered orally attenuated atherogenesis, measured both by "en face" method (10.25±1.7% vs. 15.7±2.0%, p<0.05) and "cross-section" method (66,254±7,468 µm2 vs. 90,687±8,521 µm2, p<0.05). In-situ zymography showed decrease of the extent of non-specific gelatinase activity in doxycycline-treated mice This is the first report to date describing the effect of doxycycline on atherogenesis in apoE-targeted mice.

13

Apolipoprotein E4 allele is associated with substantial changes in the plasma lipids and hyaluronic acid content in patients with nonalcoholic fatty liver disease

58%

Stachowska E., Maciejewska D., Ossowski P., Drozd A., Ryterska K., Banaszczak M., Milkiewicz M., Raszeja-Wyszomirska J., Slebioda M., Milkiewicz P., Jelen H.

Journal of Physiology and Pharmacology

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2013

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tom 64

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nr 6

14

The effect of montelukast on atherogenesis in APOE-LDLR-double knockout mice

58%

Jawien J., Gajda M., Wolkow P., Zuranska J., Olszanecki R., Korbut R.

Journal of Physiology and Pharmacology

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2008

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tom 59

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nr 3

633-639

We have shown that inhibitors of five lipoxygenase activating protein (FLAP) - MK-886 and BAYx1005 inhibit atherosclerosis in apolipoprotein E / LDL receptor - double knockout mice. We, therefore, investigated whether cysteinyl leukotrienes receptor inhibitor - montelukast, given at a dose of 0.125 µg per 100 mg of body weight per day during 16 weeks, could also attenuate atherogenesis. In apoE/LDLR - DKO mouse model montelukast significantly decreased atherogenesis, measured both by "en face" method (25.5±2.% vs. 17.23 ± 1.8%) and "cross-section" method (455 494 ± 26 477 µm2 vs. 299 201 ± 20 373 µm2). The results were, however, less pronounced, comparing to FLAP inhibitors. This is the first report showing the effect of montelukast on atherogenesis in gene-targeted mice.

15

Dysregulation of calcium in Alzheimer's disease

58%

Brzyska M., Elbaum D.

Acta Neurobiologiae Experimentalis

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2003

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tom 63

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nr 3

Ograniczanie wyników

Apolipoprotein E genotypes in sporadic early and late-onset Alzheimer's disease

The effect of nebivolol on atherogenesis in apoE - knockout mice

Significant deterioration of anti-atherogenic efficacy of nebivolol in a double (apolipoprotein E and endothelial nitric oxide synthase) knockout mouse model of atherosclerosis in comparison to single (apolipoprotein E) knockout model

AVE 0991 - angiotensin-(1-7) receptor agonist, inhibits atherogenesis in apoE - knockout mice

Heart rate reduction with ivabradine in the early phase of atherosclerosis is protective in the endothelium of ApoE-deficient mice

ApoE polymorphism in Polish patients with Alzheimer's disease

Involvement of plasma proteins in liposome-hepatocyte interactions

Inhibition of nuclear factor-kappaB attenuates atherosclerosis in apoE-LDLR - double knockout mice

Triple immunofluorescence labeling of atherosclerotic plaque components in apoE-LDLR mice

Comparison of acetaminophen toxicity in primary hepatocytes isolated from transgenic mice with different apolipoprotein E alleles

Effect of caloric restriction on liver function in young and old ApoE/LDLr-/- mice

The effect of doxycycline on atherogenesis in apoE-knockout mice

Apolipoprotein E4 allele is associated with substantial changes in the plasma lipids and hyaluronic acid content in patients with nonalcoholic fatty liver disease

The effect of montelukast on atherogenesis in APOE-LDLR-double knockout mice

Dysregulation of calcium in Alzheimer's disease