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Wyszukujesz frazę "Borkowska, Anna" wg kryterium: Autor

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    Wyświetlanie 1-7 z 7
    Tytuł:
    AS-30D hepatoma as a model to study on insulin resistance in vitro
    Autorzy:
    Wierzbicka-Bregier, Katarzyna
    Brutkowski, Wojciech
    Borkowska, Anna
    Milewski, Krzysztof
    Zabłocki, Krzysztof
    Powiązania:
    https://bibliotekanauki.pl/articles/1039458.pdf
    Data publikacji:
    2013
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    AS-30D hepatoma
    insulin resistance
    palmitate
    rosiglitazone
    Opis:
    Studies on insulin resistance of liver cells are often performed with the use of various hepatoma cell lines. Such an approach allows investigating selected biochemical pathways at the cellular level. However, possible modifications of metabolic processes due to the neoplastic nature of such cells must be considered. Expanding the diversity of hepatoma cell lines used in metabolic studies could deliver new data for comparison with those obtained for other cell lines and should reduce the risk of misleading conclusions. In this study rat hepatoma AS-30D cells were tested as a potential model for studies on palmitate-induced insulin resistance. It was found that insulin-induced Akt kinase phosphorylation was substantially reduced in cells incubated with palmitate at a concentration as low as 75 µM. This effect was not accompanied by excessive reactive oxygen species (ROS) generation or increased Jun N-terminal kinase (JNK) phosphorylation. Moreover, preincubation of AS-30D cells with rosiglitazone, an antidiabetic agonist of peroxisome proliferator-activated receptor gamma (PPARγ), efficiently prevented the palmitate-induced insulin resistance. We conclude that AS-30D hepatoma cells may be used as a model sensitive to insulin and vulnerable to palmitate-induced insulin resistance.
    Źródło:
    Acta Biochimica Polonica; 2013, 60, 4; 635-640
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Fecal lactoferrin, a marker of intestinal inflammation in children with inflammatory bowel disease
    Autorzy:
    Borkowska, Anna
    Liberek, Anna
    Łuczak, Grażyna
    Jankowska, Agnieszka
    Plata-Nazar, Katarzyna
    Korzon, Maria
    Kamińska, Barbara
    Powiązania:
    https://bibliotekanauki.pl/articles/1039002.pdf
    Data publikacji:
    2015
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    fecal lactoferrin
    inflammatory bowel disease
    children
    Opis:
    The aim of this study was to analyze the usefulness of fecal lactoferrin in the diagnosis and monitoring of inflammatory bowel disease (IBD) in children. The study included 52 children with IBD (24 with Crohn's disease and 28 with ulcerative colitis) aged between 0.92 and 18 years, and 41 IBD-free controls of similar age. Fecal concentration of lactoferrin was determined with a quantitative immunoenzymatic test. Fecal concentration of lactoferrin in children with IBD was significantly higher than in the controls. The cut-off value of fecal lactoferrin concentration optimally distinguishing between the children with IBD and the controls was identified as 13 μg/g. The sensitivity and specificity of this cut-off value equaled 80.7% and 92.7%, respectively, and its positive and negative prognostic values were 96.8% and 63.3%, respectively. Patients diagnosed with moderate Crohn's disease had significantly higher fecal concentrations of lactoferrin than children with the mild or inactive disease. Similarly, children with moderate ulcerative colitis showed significantly higher fecal concentrations of lactoferrin than individuals with the mild condition. No significant relationship was found between the fecal concentration of lactoferrin and the severity of endoscopic lesions. Patients with IBD and a positive result of fecal occult blood test were characterized by significantly higher concentrations of lactoferrin than the individuals with IBD and a negative result of this test. In conclusion, fecal concentration of lactoferrin seems to be a useful parameter for diagnosis and monitoring of IBD in children.
    Źródło:
    Acta Biochimica Polonica; 2015, 62, 3; 541-545
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Coexistence of type 1 diabetes mellitus and spinal muscular atrophy in an 8-year-old girl: a case report
    Autorzy:
    Borkowska, Anna
    Jankowska, Agnieszka
    Szlagatys-Sidorkiewicz, Agnieszka
    Sztangierska, Beata
    Liberek, Anna
    Plata-Nazar, Katarzyna
    Kamińska, Barbara
    Powiązania:
    https://bibliotekanauki.pl/articles/1039156.pdf
    Data publikacji:
    2015
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    Spinal muscular atrophy
    diabetes mellitus
    children
    Opis:
    The spinal muscular atrophy is a rare autosomal recessive genetic disease characterized by the progressive loss of muscular strength. In its natural course the disease leads to death. Diabetes mellitus type 1 is an autoimmune metabolic disorder characterized by the disturbed insulin synthesis. This is a case report of an 8-year-old girl suffering from Werdnig Hoffman disease in whom DM1 was diagnosed. The unspecific clinical manifestation and diagnostic difficulties are presented in this paper. To the authors' knowledge, this is the first publication concerning the co-existence of these two medical conditions.
    Źródło:
    Acta Biochimica Polonica; 2015, 62, 1; 167-168
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Time-dependent effect of leptin on renal Na+,K+-ATPase activity
    Autorzy:
    Marciniak, Andrzej
    Jamroz-Wiśniewska, Anna
    Borkowska, Ewelina
    Bełtowski, Jerzy
    Powiązania:
    https://bibliotekanauki.pl/articles/1041321.pdf
    Data publikacji:
    2005
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    mitogen-activated protein kinases
    leptin
    obesity
    arterial hypertension
    hydrogen peroxide
    Na+,K+-ATPase
    Opis:
    Leptin, secreted by adipose tissue, is involved in the pathogenesis of arterial hypertension, however, the mechanisms through which leptin increases blood pressure are incompletely elucidated. We investigated the effect of leptin, administered for different time periods, on renal Na+,K+-ATPase activity in the rat. Leptin was infused under anesthesia into the abdominal aorta proximally to the renal arteries for 0.5-3 h. Leptin administered at doses of 1 and 10 µg/min per kg for 30 min decreased the Na+,K+-ATPase activity in the renal medulla. This effect disappeared when the hormone was infused for ≥1 h. Leptin infused for 3 h increased the Na+,K+-ATPase activity in the renal cortex and medulla. The stimulatory effect was abolished by a specific inhibitor of Janus kinases (JAKs), tyrphostin AG490, as well as by an NAD(P)H oxidase inhibitor, apocynin. Leptin increased urinary excretion of hydrogen peroxide (H2O2) between 2 and 3 h of infusion. The effect of leptin on renal Na+,K+-ATPase and urinary H2O2 was augmented by a superoxide dismutase mimetic, tempol, and was abolished by catalase. In addition, infusion of H2O2 for 30 min increased the Na+,K+-ATPase activity. Inhibitors of extracellular signal regulated kinases (ERKs), PD98059 or U0126, prevented Na+,K+-ATPase stimulation by leptin and H2O2. These data indicate that leptin, by acting directly within the kidney, has a delayed stimulatory effect on Na+,K+-ATPase, mediated by JAKs, H2O2 and ERKs. This mechanism may contribute to the abnormal renal Na+ handling in diseases associated with chronic hyperleptinemia such as diabetes and obesity.
    Źródło:
    Acta Biochimica Polonica; 2005, 52, 4; 803-809
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Nitric oxide - superoxide cooperation in the regulation of renal Na+,K+-ATPase.
    Autorzy:
    Bełtowski, Jerzy
    Marciniak, Andrzej
    Jamroz-Wiśniewska, Anna
    Borkowska, Ewelina
    Powiązania:
    https://bibliotekanauki.pl/articles/1041505.pdf
    Data publikacji:
    2004
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    H+,K+-ATPase
    Sch 28080
    superoxide anion
    Na+,K+-ATPase
    nitric oxide
    oxidative stress
    Opis:
    The aim of this study was to investigate whether endogenous superoxide anion is involved in the regulation of renal Na+,K+-ATPase and ouabain-sensitive H+,K+-ATPase activities. The study was performed in male Wistar rats. Compounds modulating superoxide anion concentration were infused under general anaesthesia into the abdominal aorta proximally to the renal arteries. The activity of ATPases was assayed in isolated microsomal fraction. We found that infusion of a superoxide anion-generating mixture, xanthine oxidase (1 mU/min per kg) + hypoxanthine (0.2 μmol/min per kg), increased the medullary Na+,K+-ATPase activity by 49.5% but had no effect on cortical Na+,K+-ATPase and either cortical or medullary ouabain-sensitive H+,K+-ATPase. This effect was reproduced by elevating endogenous superoxide anion with a superoxide dismutase inhibitor, diethylthiocarbamate. In contrast, a superoxide dismutase mimetic, TEMPOL, decreased the medullary Na+,K+-ATPase activity. The inhibitory effect of TEMPOL was abolished by inhibitors of nitric oxide synthase (L-NAME), soluble guanylate cyclase (ODQ) and protein kinase G (KT5823). The stimulatory effect of diethylthiocarbamate was not observed in animals pretreated with a synthetic cGMP analogue, 8-bromo-cGMP. An inhibitor of NAD(P)H oxidase, apocynin (1 μmol/min per kg), decreased the Na+,K+-ATPase activity in the renal medulla and its effect was prevented by L-NAME, ODQ or KT5823. In contrast, a xanthine oxidase inhibitor, oxypurinol, administered at the same dose was without effect. These data suggest that NAD(P)H oxidase-derived superoxide anion increases Na+,K+-ATPase activity in the renal medulla by reducing the availability of NO. Excessive intrarenal generation of superoxide anion may upregulate medullary Na+,K+-ATPase leading to sodium retention and blood pressure elevation.
    Źródło:
    Acta Biochimica Polonica; 2004, 51, 4; 933-942
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Bidirectional regulation of renal cortical Na+,K+-ATPase by protein kinase C.
    Autorzy:
    Bełtowski, Jerzy
    Marciniak, Andrzej
    Jamroz-Wiśniewska, Anna
    Borkowska, Ewelina
    Wójcicka, Grażyna
    Powiązania:
    https://bibliotekanauki.pl/articles/1041555.pdf
    Data publikacji:
    2004
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    phosphatidylinositol-3-kinase
    protein kinase C
    cytochrome P450-dependent arachidonate metabolites
    Na+,K+-ATPase
    Opis:
    We examined the role of protein kinase C (PKC) in the regulation of Na+,K+- ATPase activity in the renal cortex. Male Wistar rats were anaesthetized and the investigated reagents were infused into the abdominal aorta proximally to the renal arteries. A PKC-activating phorbol ester, phorbol 12,13-dibutyrate (PDBu), had a dose-dependent effect on cortical Na+,K+-ATPase activity. Low dose of PDBu (10-11 mol/kg per min) increased cortical Na+,K+-ATPase activity by 34.2%, whereas high doses (10-9 and 10-8 mol/kg per min) reduced this activity by 22.7% and 35.0%, respectively. PDBu administration caused changes in Na+,K+-ATPase Vmax without affecting K0.5 for Na+, K+ and ATP as well as Ki for ouabain. The effects of PDBu were abolished by PKC inhibitors, staurosporine, GF109203X, and Gö 6976. The inhibitory effect of PDBu was reversed by pretreatment with inhibitors of cytochrome P450-dependent arachidonate metabolism, ethoxyresorufin and 17-octadecynoic acid, inhibitors of phosphatidylinositol 3-kinase (PI3K), wortmannin and LY294002, and by actin depolymerizing agents, cytochalasin D and latrunculin B. These results suggest that PKC may either stimulate or inhibit renal cortical Na+,K+-ATPase. The inhibitory effect is mediated by cytochrome P450-dependent arachidonate metabolites and PI3K, and is caused by redistribution of the sodium pump from the plasma membrane to the inactive intracellular pool.
    Źródło:
    Acta Biochimica Polonica; 2004, 51, 3; 757-772
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
    Tytuł:
    Phenotype modifiers of spinal muscular atrophy: the number of SMN2 gene copies, deletion in the NAIP gene and probably gender influence the course of the disease
    Autorzy:
    Jędrzejowska, Maria
    Milewski, Michał
    Zimowski, Janusz
    Borkowska, Janina
    Kostera-Pruszczyk, Anna
    Sielska, Danuta
    Jurek, Marta
    Hausmanowa-Petrusewicz, Irena
    Powiązania:
    https://bibliotekanauki.pl/articles/1040639.pdf
    Data publikacji:
    2009
    Wydawca:
    Polskie Towarzystwo Biochemiczne
    Tematy:
    SMN2 gene copy number
    SMA modifiers
    NAIP deletion
    gender influence
    Opis:
    Spinal muscular atrophy (SMA) is an autosomal recessive neuromuscular disorder caused by mutations of the SMN1 gene. It is characterized by significant phenotype variability. In this study, we analyzed possible phenotype modifiers of the disease - the size of the deletion in the SMA region, the number of SMN2 gene copies, as well as the effect of gender. Among the factors analyzed, two seem to influence the SMA phenotype: the number of SMN2 gene copies and a deletion in the NAIP gene. A higher number of SMN2 copies makes the clinical symptoms more benign, and the NAIP gene deletion is associated with a more severe phenotype. The influence of gender remains unclear. In a group of 1039 patients, 55% of whom were male, the greatest disproportion was in the SMA1 (F/M = 0.78) and SMA3b (F/M = 0.45) forms. In SMA1 a deletion in the NAIP gene was seen twice as frequently in girls compared to boys. In three patients, we observed genotypes atypical for the chronic forms of SMA: two patients with SMA3a and 3b had a deletion of the NAIP gene, and a third patient with SMA2 had one copy of the SMN2 gene.
    Źródło:
    Acta Biochimica Polonica; 2009, 56, 1; 103-108
    0001-527X
    Pojawia się w:
    Acta Biochimica Polonica
    Dostawca treści:
    Biblioteka Nauki
    Artykuł
      Wyświetlanie 1-7 z 7

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