Agnieszka Brandt
Gdańsk Medical University
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Publication
Featured researches published by Agnieszka Brandt.
Journal of Clinical Lipidology | 2014
Małgorzata Myśliwiec; Mieczysław Walczak; Ewa Małecka-Tendera; Anna Dobrzańska; Barbara Cybulska; Krzysztof J. Filipiak; Artur Mazur; Przemysława Jarosz-Chobot; Agnieszka Szadkowska; Andrzej Rynkiewicz; Alicja Chybicka; Piotr Socha; Agnieszka Brandt; Joanna Bautembach-Minkowska; Tomasz Zdrojewski; Janusz Limon; Samuel S. Gidding; Maciej Banach
Familial hypercholesterolemia (FH) affects on average 1 in 500 individuals in European countries, and it is estimated that FH in Poland may affect more than 80,000 people. However, in Poland, only about 20% of the population is estimated to have been diagnosed with FH, of which only a small number receive adequate treatment. FH results in more rapid development of atherosclerosis and is associated with a high risk of cardiovascular events. Atherosclerosis develops beginning in childhood in patients with FH and reaches advanced stages before clinical manifestations develop. Inadequate diagnostics and treatment of FH in Polish children suggests a need for raising the level of awareness and understanding of the condition in both society and among health professionals. These recommendations present the current epidemiological status, guidelines for diagnosing FH in Polish children and adolescents, and effective treatment options.
Immunologic Research | 2016
Monika Ryba-Stanisławowska; Paulina Werner; Agnieszka Brandt; Małgorzata Myśliwiec; Jolanta Myśliwska
Th17, Th22 and Th9 are recently discovered effector populations that may contribute to the pathogenesis of autoimmune and inflammatory diseases. The presented study aimed to investigate the link between Th22 and Th9 subsets in type 1 diabetes, as this disease involves different subsets of CD4+ T lymphocytes. The study groups consisted of 23 patients with type 1 diabetes and 11 healthy individuals. All subjects had CD4+IL-22 Th22 and CD4+IL-9 Th9 lymphocytes investigated by flow cytometry. In addition, the plasma concentrations of IL-22 as well as IL-9 were analyzed. Our study demonstrated that Th9 and Th22 cell counts as well as their plasma cytokines were upregulated in patients with type 1 and correlated with HbA1c and CRP values. Taking these all into account, one can conclude that Th22 and Th9 lymphocyte activities may contribute to chronic, low-level inflammation that is considered an integral part of type 1 diabetes.
Mediators of Inflammation | 2016
Monika Ryba-Stanisławowska; Paulina Werner; Maria Skrzypkowska; Agnieszka Brandt; Jolanta Myśliwska
IL-33 is an IL-1 cytokine family member, with ability to induce both Th1 and Th2 immune responses. It binds to ST2 receptor, whose deficiency is associated with enhanced inflammatory response. The most recent studies have shown the immunoregulatory effect of IL-33 on Tregs in animal models. As type 1 diabetes is an autoimmune, inflammatory disease, where Treg defects have been described, we aimed to analyze the in vitro influence of recombinant IL-33 on quantitative properties of regulatory CD4+CD25highFOXP3+ T cells. CD4+CD25highFOXP3+ as well as CD4+CD25highFOXP3+ST2+ Tregs were analyzed by flow cytometry. In a group of patients with type 1 diabetes in vitro IL-33 treatment induced regulatory CD4+CD25highFOXP3+ cell frequencies as well as upregulating the surface expression of ST2 molecule. In addition, the number of CD4+CD25highFOXP3+ cells carrying ST2 receptor increased significantly. Similar effect was observed in case of the FOXP3 expression. We did not observe any significant changes in IL-33 treated cells of healthy controls. The level of ST2 was higher in serum of patients with type 1 diabetes in comparison to their healthy counterparts. We propose that IL-33 becomes an additional immunostimulatory factor used to induce Treg expansion in future clinical trials of adoptive therapy in type 1 diabetes.
Mediators of Inflammation | 2014
Monika Ryba-Stanisławowska; Karolina Rybarczyk-Kapturska; Agnieszka Brandt; Małgorzata Myśliwiec; Jolanta Myśliwska
Purpose. The study aimed to investigate the influence of estrogen receptor α (ER-α) genotypes on inflammatory response and development of microvascular complications in girls with type 1 diabetes. Methods. 152 young regularly menstruating girls with diagnosed type 1 diabetes and 84 young, healthy menstruating girls were recruited. ER-α genotyping was carried out by PCR. Serum concentrations of 17β-estradiol, as well as IL-6, TNF-α, VEGF, and IL-10, were measured. CD4+Foxp3+ TH17 cells were isolated and analyzed by flow cytometry. Results. Type 1 diabetic girls carrying TT genotype were characterized by the lowest serum estradiol level and IL-10 and highest IL-6, TNF-α , and VEGF. The association between the level of certain cytokine and the genetic variant of estrogen receptor α polymorphism was analyzed. Frequencies of CD4+Foxp3+ TH17 cells were also enhanced in TT bearing girls with type 1 diabetes and correlated with the level of analyzed cytokines. In addition, the correlation between serum estradiol level and cytokine concentrations was observed. Conclusions. We propose that TT variant of estrogen receptor α polymorphism may be associated with enhanced inflammatory response, which in turn may lead to acceleration of diabetic retino- and nephropathy in girls with type 1 diabetes. This finding may help the physicians to predict the onset and progression of diabetic microvascular complications.
Molecular Immunology | 2011
Monika Ryba; Ewa Malinowska; Karolina Rybarczyk-Kapturska; Agnieszka Brandt; Małgorzata Myśliwiec; Jolanta Myśliwska
Type 1 diabetes is considered as pluricausal disease, whose etiology involves genetic predisposition as well as environmental factors that contribute to disease progression and pathogenesis. Women are believed to be more susceptible to develop autoimmune diseases, which may depend in part on the influence of sex hormones on the immune system. It was shown that estrogens may protect against the development of autoimmune disease by inducing the expansion of regulatory T cell pool and upregulating Foxp3 expression. Foxp3 is a transcription factor that controls the development and suppressive function of naturally occurring regulatory T cells CD4(+)Foxp3(+). Longstanding diabetes type 1 has features of low-grade chronic inflammation which may influence regulatory T cell subset by reducing their numbers or/and inhibiting their suppressive potential. As diabetic type 1 patients are differentiated with regard to metabolic factors, level of glycemic control and systemic inflammatory state, we aimed to examine if this can be associated with IVSI-397T>C estrogen receptor α polymorphism. We examined 93 young regularly menstruating girls with diagnosed type 1 diabetes and 49 healthy age-matched control individuals. The PvuII polymorphism of the ER-α gene was analyzed as well as the serum TNF level and the level of CD4(+)Foxp3(+) regulatory T cells in these individuals. Girls with type 1 diabetes had lower level of CD4(+)Foxp3(+) Tregs than their healthy counterparts. Regulatory T cells from these patients showed also lower expression of Foxp3 than Tregs in healthy, control group. In addition, DM1 girls bearing the CC genotypes showed the highest level of CD4(+)Foxp3(+) Tregs and the lowest TNF serum level in comparison to girls carrying CT or TT genotype. The CC DM1 carriers had also higher serum level of estrogens than girls bearing CT or TT genotype. We propose that different variants of IVS1-397 estrogen receptor α polymorphism may become additional genetic factor that influences regulatory conditions during diabetes type 1 in females.
International Journal of Endocrinology | 2014
Włodzimierz Łuczyński; Wojciech Fendler; Anna Ramatowska; Agnieszka Szypowska; Agnieszka Szadkowska; Wojciech Mlynarski; Miron Chumiecki; Przemysława Jarosz-Chobot; Joanna Chrzanowska; Anna Noczyńska; Agnieszka Brandt; Małgorzata Myśliwiec; Barbara Głowińska-Olszewska; Pawel Bernatowicz; Oksana Kowalczuk; Artur Bossowski
The objective was to compare the impact of clinical and genetic factors on body mass index (BMI) in children with type 1 diabetes (T1DM) without severe obesity. A total of 1,119 children with T1DM (aged 4–18 years) were qualified to take part in the study. All children were genotyped for variants of FTO, MC4R, INSIG2, FASN, NPC1, PTER, SIRT1, MAF, IRT1, and CD36. Results. Variants of FTO showed significant association with BMI-SDS in the T1DM group. The main factors influencing BMI-SDS in children with T1DM included female gender (P = 0.0003), poor metabolic control (P = 0.0001), and carriage of the A allele of the FTO rs9939609 gene (P = 0.02). Conclusion. Our research indicates, when assessing, the risk of overweight and obesity carriage of the A allele in the rs9939609 site of the FTO gene adds to that of female gender and poor metabolic control. This trial is registered with ClinicalTrials.gov (NCT01279161).
Endokrynologia Polska | 2015
Marta Buraczewska; Ewa Szymańska; Agnieszka Brandt; Przemysława Jarosz-Chobot; Jolanta Sykut-Cegielska; Ewa Barg; Maciej Borowiec; Wojciech Mlynarski; Małgorzata Myśliwiec
INTRODUCTION Congenital hyperinsulinism of Infancy (CHI) comprises heterogenic defects of insulin secretion with diverse molecular aetiology, histological features, severity of symptoms, and response to pharmacotherapy. The study aimed to establish the first clinical characteristics of Polish patients with CHI and to propose a novel clinical algorithm allowing the prioritisation of genetic and radiology studies, based on patients characteristics and response to pharmacotherapy. MATERIAL AND METHODS Thirty-one patients with CHI were recruited from five reference centres in Poland. Clinical and biochemical parameters were statistically evaluated and compared to those of a control group (n = 30). RESULTS CHI predisposes to increased birth weight (p = 0.004), lower Apgar score (p = 0.004), perinatal complications (74%), and neurological implications (48%). Diagnostic process and therapy were inconsistent. A trial of pharmacotherapy was applied in 21 patients (68%), and diagnostic imaging with 18F-L-DOPA PET was performed in only 3. Eighteen patients (58%) were surgically treated, including 8 infants (44%) aged less than 2 months. Depending on the type of resection, further hypoglycaemia was observed postoperatively in 50% (n = 9) and hyperglycaemia in 39% (n = 7) of cases. Based on foregoing results, a clinical algorithm was proposed. CONCLUSIONS Standardisation of clinical management with the use of pharmacotherapy, genetic screening, and diagnostic imaging will allow the optimisation of therapy and minimisation of treatment complications.
Kardiologia Polska | 2013
Małgorzata Myśliwiec; Mieczysław Walczak; Ewa Małecka-Tendera; Anna Dobrzańska; Barbara Cybulska; Krzysztof J. Filipiak; Artur Mazur; Przemysława Jarosz-Chobot; Agnieszka Szadkowska; Andrzej Rynkiewicz; Alicja Chybicka; Piotr Socha; Agnieszka Brandt; Jolanta Kubalska; Joanna Bautembach-Minkowska; Janusz Limon; Tomasz Zdrojewski; Maciej Banach
1Katedra i Klinika Pediatrii, Diabetologii i Endokrynologii, Gdanski Uniwersytet Medyczny, Gdansk 2Klinika Pediatrii, Endokrynologii, Diabetologii, Chorob Metabolicznych i Kardiologii Wieku Rozwojowego, Pomorski Uniwersytet Medyczny, Szczecin 3Klinika Pediatrii, Endokrynologii i Diabetologii Dzieciecej, Śląski Uniwersytet Medyczny, Katowice 4Klinika Patologii Noworodka, Instytut Pediatrii, Centrum Zdrowia Dziecka, Warszawa 5Instytut Żywności i Żywienia, Warszawa 6I Katedra i Klinika Kardiologii, Warszawski Uniwersytet Medyczny, Warszawa 7Wydzial Medyczny, Uniwersytet Rzeszowski, Rzeszow 8Klinika Pediatrii, Hematologii, Onkologii i Diabetologii, Łodzki Uniwersytet Medyczny, Łodź 9I Katedra i Klinika Kardiologii, Gdanski Uniwersytet Medyczny, Gdansk 10Katedra i Klinika Transplantacji Szpiku, Onkologii i Hematologii Dzieciecej, Wroclawski Uniwersytet Medyczny, Wroclaw 11Klinika Gastroenterologii, Hepatologii i Żywienia Dzieci, Centrum Zdrowia Dziecka, Warszawa 12Zaklad Genetyki, Instytut Psychiatrii i Neurologii, Warszawa 13Zaklad Prewencji i Dydaktyki, Katedra Nadciśnienia Tetniczego i Diabetologii, Gdanski Uniwersytet Medyczny, Gdansk 14Katedra i Zaklad Biologii i Genetyki, Gdanski Uniwersytet Medyczny, Gdansk 15Katedra Nefrologii i Nadciśnienia Tetniczego, Łodzki Uniwersytet Medyczny, Łodź
Molecular and Cellular Endocrinology | 2017
Bartosz Słomiński; Urszula Ławrynowicz; Jolanta Myśliwska; Monika Ryba-Stanisławowska; Maria Skrzypkowska; Agnieszka Brandt
AIM The aim of the study was to assess the relationship between the CCR5-Δ32 polymorphism and the risk of diabetic retinopathy (DR) in patients with DM1. METHODS We examined 420 patients and 350 healthy controls. The analysis concerned CCR5-Δ32 polymorphism as well as levels of serum inflammatory markers (CRP, TNF-α), adhesion molecules (VCAM, ICAM-1, ICAM-3) and CCR5 ligand (MCP-1). RESULTS We found a negative association between DM1 and Δ32 allele. Moreover, the frequency of Δ32 allele was higher in a group with DR in comparison to control subjects without this complication. We also found that Δ32 carriers had the highest levels of: HbA1c, inflammatory markers, adhesion molecules and CCR5 ligand. CONCLUSIONS The findings of our studies suggest that the CCR5-Δ32 polymorphism is associated with DM1 such that the Δ32 allele protects against the development of DM1 and increases the risk of DR in patients who have already developed the disease.
Journal of Diabetes and Its Complications | 2015
Bartosz Słomiński; Jolanta Myśliwska; Agnieszka Brandt
BACKGROUND AND AIMS The effect of estrogens is mediated by activation of estrogen receptors (ERs), which are expressed in many tissues. Because ER-α gene polymorphisms may exert different effects in childhood, in the present study we analyzed associations between the IVS1 -397T>C polymorphism and indicators of inflammatory response as well as late complications in boys with type 1 diabetes mellitus (DM1). METHODS AND RESULTS We examined 108 young boys with DM1 and 64 healthy age-matched control individuals. ER-α genotyping, as well as the CRP and IL-6 serum level and blood pressure, was analyzed. In our study boys with CC genotype had lower blood pressure and IL-6 and CRP serum levels. Similar results were obtained for DM1 boys with microvascular complications - the blood pressure and serum level of IL-6, but not CRP, were still lower in the CC patients. CONCLUSIONS Our findings suggest that the presence of -397T allele may indicate macro- and microvascular complications in DM1 boys, before the occurrence of first clinical symptoms.